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Stimulating Hypothesis - Revision history
2024-03-28T18:49:28Z
Revision history for this page on the wiki
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128.97.66.134 at 21:33, 15 July 2010
2010-07-15T21:33:04Z
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<tr><td class='diff-marker'>−</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div><div style="float:left; padding:10px; background:yellow; border:2px solid black;font-size:large;">[[<del class="diffchange diffchange-inline">AIRB</del>| Back <del class="diffchange diffchange-inline">to Main </del>Page]]</div></div></td><td class='diff-marker'>+</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><div style="float:left; padding:10px; background:yellow; border:2px solid black;font-size:large;">[[<ins class="diffchange diffchange-inline">:Category:Causes</ins>| Back<ins class="diffchange diffchange-inline">]]</div></ins></div></td></tr>
<tr><td colspan="2"> </td><td class='diff-marker'>+</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins class="diffchange diffchange-inline"><div style="float:right; padding:10px; background:yellow; border:2px solid black;font-size:large;">[[:Category:Welcome| Home </ins>Page]]</div></div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div><br><br><br><br></div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div><br><br><br><br></div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>====References====</div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>====References====</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>1. Kelleher RJ 3rd et. al. '''The autistic neuron: troubled translation?'''Cell. 2008 Oct 31;135(3):401-6. PMID 18984149</div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>1. Kelleher RJ 3rd et. al. '''The autistic neuron: troubled translation?'''Cell. 2008 Oct 31;135(3):401-6. PMID 18984149</div></td></tr>
<tr><td colspan="2"> </td><td class='diff-marker'>+</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>2. Rubenstein JL.'''Three hypotheses for developmental defects that may underlie some forms of autism spectrum disorder.'''Curr Opin Neurol. 2010 Apr;23(2):118-23. PMID 20087182</div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>2. Rubenstein JL.'''Three hypotheses for developmental defects that may underlie some forms of autism spectrum disorder.'''Curr Opin Neurol. 2010 Apr;23(2):118-23. PMID 20087182</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>3. Uhlhaas PJ et. al. '''Neural synchrony and the development of cortical networks.'''Trends Cogn Sci. 2010 Feb;14(2):72-80. PMID 20080054</div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>3. Uhlhaas PJ et. al. '''Neural synchrony and the development of cortical networks.'''Trends Cogn Sci. 2010 Feb;14(2):72-80. PMID 20080054</div></td></tr>
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128.97.66.134
http://lcni-3.uoregon.edu/phenowiki/index.php?title=Stimulating_Hypothesis&diff=3625&oldid=prev
128.97.66.134: /* 75pxGenetics */
2010-06-10T20:49:02Z
<p><span dir="auto"><span class="autocomment">75pxGenetics</span></span></p>
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<td colspan='2' style="background-color: white; color:black; text-align: center;">Revision as of 20:49, 10 June 2010</td>
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<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==[[Image:Anaphase_IF.gif|75px]]Genetics==</div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==[[Image:Anaphase_IF.gif|75px]]Genetics==</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>A central component in this theory are the variants in [[Neuroligins/Neurexins/Shank3|Neuroligins and Neurexins ]] that have been found in ASD probands.  [[Neuroligins/Neurexins/Shank3|Neuroligins and Neurexins]] are likely to be the centrally organizing molecules for excitatory [[Serotoninergic, GABAergic, and glutamatergic pathways|glutamatergic and inhibitory GABAergic]] synapses in the mammalian brain.  Studies have shown that mutant mice with the R451C Nlgn3 mutation have increased GABAergic synapses and inhibitory currents.  In addition, MeCP2 knockout mice, Caps2 knowckout mice, mice exposed to prenatla valproate treatment, and many other models have imbalances of inhibition and excitation.<sup>1</sup></div></td><td class='diff-marker'>+</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>A central component in this theory are the variants in [[Neuroligins/Neurexins/Shank3|Neuroligins and Neurexins ]] that have been found in ASD probands.  [[Neuroligins/Neurexins/Shank3|Neuroligins and Neurexins]] are likely to be the centrally organizing molecules for excitatory [[Serotoninergic, GABAergic, and glutamatergic pathways|glutamatergic and inhibitory GABAergic]] synapses in the mammalian brain.  Studies have shown that mutant mice with the R451C Nlgn3 mutation have increased <ins class="diffchange diffchange-inline">[[Serotoninergic, GABAergic, and glutamatergic pathways|</ins>GABAergic synapses<ins class="diffchange diffchange-inline">]] </ins>and inhibitory currents.  In addition, MeCP2 knockout mice, Caps2 knowckout mice, mice exposed to prenatla valproate treatment, and many other models have imbalances of inhibition and excitation.<sup>1</sup></div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>It is unknown whether these changes represent changes in synaptic signaling, or are just responses from a change in homeostasis. However, given that many of the susceptibility genes in ASD affect synapse formation signaling.  Additionally, several of the genes also affect cortical interneurons.<sup>2</sup></div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>It is unknown whether these changes represent changes in synaptic signaling, or are just responses from a change in homeostasis. However, given that many of the susceptibility genes in ASD affect synapse formation signaling.  Additionally, several of the genes also affect cortical interneurons.<sup>2</sup></div></td></tr>
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128.97.66.134
http://lcni-3.uoregon.edu/phenowiki/index.php?title=Stimulating_Hypothesis&diff=3624&oldid=prev
128.97.66.134: /* Stimulating Hypothesis */
2010-06-10T20:45:56Z
<p><span dir="auto"><span class="autocomment">Stimulating Hypothesis</span></span></p>
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<td colspan='2' style="background-color: white; color:black; text-align: center;">Revision as of 20:45, 10 June 2010</td>
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<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>'''Neural Synchrony and the development of cortical networks'''</div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>'''Neural Synchrony and the development of cortical networks'''</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'>−</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>Neural synchronization is imperative in the successful synchronization of different areas of the brain for proper development.  Evidence shows that neural synchronization of oscillations is involved in synaptic plasticity. Oscillations during both resting state and cognitive tasks show that gamma oscillations start to appear during childhood and temporal coordination is refined until early adulthood. This co-occurs with changes in the myelination of cortico-cortical connections and the development of GABAergic transmissions.  </div></td><td class='diff-marker'>+</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>Neural synchronization is imperative in the successful synchronization of different areas of the brain for proper development.  Evidence shows that neural synchronization of oscillations is involved in synaptic plasticity. Oscillations during both resting state and cognitive tasks show that gamma oscillations start to appear during childhood and temporal coordination is refined until early adulthood. This co-occurs with changes in the myelination of cortico-cortical connections and the development of <ins class="diffchange diffchange-inline">[[Serotoninergic, </ins>GABAergic<ins class="diffchange diffchange-inline">, and glutamatergic pathways|GABAergic]] </ins>transmissions.  </div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>It may be that abnormal brain maturation during the early prenatal and postnatal periods results in cortical circuits which cannot support the frequency high frequency oscillations that appear typically during infancy. As a result, the temporal precision that is required for specific firing patterns during development is disturbed and the activity dependent selection of specific cortical circuits during development is absent for children with ASD. <sup>3</sup></div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>It may be that abnormal brain maturation during the early prenatal and postnatal periods results in cortical circuits which cannot support the frequency high frequency oscillations that appear typically during infancy. As a result, the temporal precision that is required for specific firing patterns during development is disturbed and the activity dependent selection of specific cortical circuits during development is absent for children with ASD. <sup>3</sup></div></td></tr>
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128.97.66.134
http://lcni-3.uoregon.edu/phenowiki/index.php?title=Stimulating_Hypothesis&diff=3455&oldid=prev
64.134.232.19 at 22:53, 25 April 2010
2010-04-25T22:53:30Z
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<td colspan='2' style="background-color: white; color:black; text-align: center;">Revision as of 22:53, 25 April 2010</td>
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<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>Estrogens can regulate the expression of glutamic acid decarboxylase, thus modulating GABA signaling, as well as modulating whether GABA is excitatory or inhibitory through the cotransporter KCC2.  Androgens can predispose males to GABA mediated excitoxicity. Thus, sex hormones could modulate the excitatory/inhibotyr balance, perhaps sensitizing the male brain to ASD, and play a role in explaining while ASD occurs in males 4 times as often as it occurs in females.   </div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>Estrogens can regulate the expression of glutamic acid decarboxylase, thus modulating GABA signaling, as well as modulating whether GABA is excitatory or inhibitory through the cotransporter KCC2.  Androgens can predispose males to GABA mediated excitoxicity. Thus, sex hormones could modulate the excitatory/inhibotyr balance, perhaps sensitizing the male brain to ASD, and play a role in explaining while ASD occurs in males 4 times as often as it occurs in females.   </div></td></tr>
<tr><td colspan="2"> </td><td class='diff-marker'>+</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr>
<tr><td colspan="2"> </td><td class='diff-marker'>+</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">'''Neural Synchrony and the development of cortical networks'''</ins></div></td></tr>
<tr><td colspan="2"> </td><td class='diff-marker'>+</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr>
<tr><td colspan="2"> </td><td class='diff-marker'>+</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Neural synchronization is imperative in the successful synchronization of different areas of the brain for proper development.  Evidence shows that neural synchronization of oscillations is involved in synaptic plasticity. Oscillations during both resting state and cognitive tasks show that gamma oscillations start to appear during childhood and temporal coordination is refined until early adulthood. This co-occurs with changes in the myelination of cortico-cortical connections and the development of GABAergic transmissions. </ins></div></td></tr>
<tr><td colspan="2"> </td><td class='diff-marker'>+</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr>
<tr><td colspan="2"> </td><td class='diff-marker'>+</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">It may be that abnormal brain maturation during the early prenatal and postnatal periods results in cortical circuits which cannot support the frequency high frequency oscillations that appear typically during infancy. As a result, the temporal precision that is required for specific firing patterns during development is disturbed and the activity dependent selection of specific cortical circuits during development is absent for children with ASD. <sup>3</sup></ins></div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==[[Image:Brain_MRI_T1_movie.gif|75px]]Neuroimaging==</div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==[[Image:Brain_MRI_T1_movie.gif|75px]]Neuroimaging==</div></td></tr>
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<td colspan="2" class="diff-lineno">Line 28:</td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>1. Kelleher RJ 3rd et. al. '''The autistic neuron: troubled translation?'''Cell. 2008 Oct 31;135(3):401-6. PMID 18984149</div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>1. Kelleher RJ 3rd et. al. '''The autistic neuron: troubled translation?'''Cell. 2008 Oct 31;135(3):401-6. PMID 18984149</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>2. Rubenstein JL.'''Three hypotheses for developmental defects that may underlie some forms of autism spectrum disorder.'''Curr Opin Neurol. 2010 Apr;23(2):118-23. PMID 20087182</div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>2. Rubenstein JL.'''Three hypotheses for developmental defects that may underlie some forms of autism spectrum disorder.'''Curr Opin Neurol. 2010 Apr;23(2):118-23. PMID 20087182</div></td></tr>
<tr><td colspan="2"> </td><td class='diff-marker'>+</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr>
<tr><td colspan="2"> </td><td class='diff-marker'>+</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">3. Uhlhaas PJ et. al. '''Neural synchrony and the development of cortical networks.'''Trends Cogn Sci. 2010 Feb;14(2):72-80. PMID 20080054</ins></div></td></tr>
</table>
64.134.232.19
http://lcni-3.uoregon.edu/phenowiki/index.php?title=Stimulating_Hypothesis&diff=3275&oldid=prev
128.97.66.134 at 22:43, 25 March 2010
2010-03-25T22:43:11Z
<p></p>
<table class='diff diff-contentalign-left'>
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<td colspan='2' style="background-color: white; color:black; text-align: center;">Revision as of 22:43, 25 March 2010</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l1" >Line 1:</td>
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<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==Stimulating Hypothesis==</div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==Stimulating Hypothesis==</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>The stimulating hypothesis says that the imbalance between inhibitory and excitatory synaptic currents causes ASD. <del class="diffchange diffchange-inline"> A central component in this theory are the variants in [[Neuroligins/Neurexins/Shank3|Neuroligins and Neurexins ]] that have been found in ASD probands.  [[Neuroligins/Neurexins/Shank3|Neuroligins and Neurexins]] are likely to be the centrally organizing molecules for excitatory [[Serotoninergic, GABAergic, and glutamatergic pathways|glutamatergic and inhibitory GABAergic]] synapses in the mammalian brain.  Studies have shown that mutant mice with the R451C Nlgn3 mutation have increased GABAergic synapses and inhibitory currents.  In addition, MeCP2 knockout mice, Caps2 knowckout mice, mice exposed to prenatla valproate treatment, and many other models have imbalances of inhibition and excitation.<sup>1</sup></del></div></td><td class='diff-marker'>+</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>The stimulating hypothesis says that the imbalance between inhibitory and excitatory synaptic currents causes ASD.  </div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'>−</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div><del class="diffchange diffchange-inline">It is unknown whether these changes represent changes in synaptic </del>signaling, or <del class="diffchange diffchange-inline">are just responses from a change in homeostasis</del>. <del class="diffchange diffchange-inline">However</del>, <del class="diffchange diffchange-inline">given that many of </del>the <del class="diffchange diffchange-inline">susceptibility genes </del>in ASD <del class="diffchange diffchange-inline">affect synapse formation signaling</del>.  <del class="diffchange diffchange-inline">Additionally, several of the genes also affect cortical interneurons.<sup>2</sup></del></div></td><td class='diff-marker'>+</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins class="diffchange diffchange-inline">Estrogens can regulate the expression of glutamic acid decarboxylase, thus modulating GABA </ins>signaling, <ins class="diffchange diffchange-inline">as well as modulating whether GABA is excitatory </ins>or <ins class="diffchange diffchange-inline">inhibitory through the cotransporter KCC2</ins>. <ins class="diffchange diffchange-inline"> Androgens can predispose males to GABA mediated excitoxicity. Thus</ins>, <ins class="diffchange diffchange-inline">sex hormones could modulate </ins>the <ins class="diffchange diffchange-inline">excitatory/inhibotyr balance, perhaps sensitizing the male brain to ASD, and play a role </ins>in <ins class="diffchange diffchange-inline">explaining while </ins>ASD <ins class="diffchange diffchange-inline">occurs in males 4 times as often as it occurs in females</ins>.   </div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==[[Image:Brain_MRI_T1_movie.gif|75px]]Neuroimaging==</div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==[[Image:Brain_MRI_T1_movie.gif|75px]]Neuroimaging==</div></td></tr>
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<td colspan="2" class="diff-lineno">Line 8:</td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==[[Image:Anaphase_IF.gif|75px]]Genetics==</div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==[[Image:Anaphase_IF.gif|75px]]Genetics==</div></td></tr>
<tr><td colspan="2"> </td><td class='diff-marker'>+</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">A central component in this theory are the variants in [[Neuroligins/Neurexins/Shank3|Neuroligins and Neurexins ]] that have been found in ASD probands.  [[Neuroligins/Neurexins/Shank3|Neuroligins and Neurexins]] are likely to be the centrally organizing molecules for excitatory [[Serotoninergic, GABAergic, and glutamatergic pathways|glutamatergic and inhibitory GABAergic]] synapses in the mammalian brain.  Studies have shown that mutant mice with the R451C Nlgn3 mutation have increased GABAergic synapses and inhibitory currents.  In addition, MeCP2 knockout mice, Caps2 knowckout mice, mice exposed to prenatla valproate treatment, and many other models have imbalances of inhibition and excitation.<sup>1</sup></ins></div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td colspan="2"> </td><td class='diff-marker'>+</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">It is unknown whether these changes represent changes in synaptic signaling, or are just responses from a change in homeostasis. However, given that many of the susceptibility genes in ASD affect synapse formation signaling.  Additionally, several of the genes also affect cortical interneurons.<sup>2</sup></ins></div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>===Animal Models===</div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>===Animal Models===</div></td></tr>
</table>
128.97.66.134
http://lcni-3.uoregon.edu/phenowiki/index.php?title=Stimulating_Hypothesis&diff=3274&oldid=prev
128.97.66.134: /* References */
2010-03-25T22:34:56Z
<p><span dir="auto"><span class="autocomment">References</span></span></p>
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<td colspan='2' style="background-color: white; color:black; text-align: center;">Revision as of 22:34, 25 March 2010</td>
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<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>====References====</div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>====References====</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>1. PMID 18984149</div></td><td class='diff-marker'>+</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>1<ins class="diffchange diffchange-inline">. Kelleher RJ 3rd et. al. '''The autistic neuron: troubled translation?'''Cell. 2008 Oct 31;135(3):401-6</ins>. PMID 18984149</div></td></tr>
<tr><td colspan="2"> </td><td class='diff-marker'>+</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins class="diffchange diffchange-inline">2. Rubenstein JL.'''Three hypotheses for developmental defects that may underlie some forms of autism spectrum disorder.'''Curr Opin Neurol. 2010 Apr;23(2):118-23. PMID 20087182</ins></div></td></tr>
</table>
128.97.66.134
http://lcni-3.uoregon.edu/phenowiki/index.php?title=Stimulating_Hypothesis&diff=3273&oldid=prev
128.97.66.134: /* Stimulating Hypothesis */
2010-03-25T22:33:19Z
<p><span dir="auto"><span class="autocomment">Stimulating Hypothesis</span></span></p>
<table class='diff diff-contentalign-left'>
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<td colspan='2' style="background-color: white; color:black; text-align: center;">Revision as of 22:33, 25 March 2010</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l1" >Line 1:</td>
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<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==Stimulating Hypothesis==</div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==Stimulating Hypothesis==</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>The stimulating hypothesis says that the imbalance between inhibitory and excitatory synaptic currents causes ASD.  A central component in this theory are the variants in [[Neuroligins/Neurexins/Shank3|Neuroligins and Neurexins ]] that have been found in ASD probands.  [[Neuroligins/Neurexins/Shank3|Neuroligins and Neurexins]] are likely to be the centrally organizing molecules for excitatory [[Serotoninergic, GABAergic, and glutamatergic pathways|glutamatergic and inhibitory GABAergic]] synapses in the mammalian brain.  Studies have shown that mutant mice with the R451C Nlgn3 mutation have increased GABAergic synapses and inhibitory currents.  In addition, MeCP2 knockout mice, Caps2 knowckout mice, mice exposed to prenatla valproate treatment, and many other models have imbalances of inhibition and excitation.<sup>1</sup></div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>The stimulating hypothesis says that the imbalance between inhibitory and excitatory synaptic currents causes ASD.  A central component in this theory are the variants in [[Neuroligins/Neurexins/Shank3|Neuroligins and Neurexins ]] that have been found in ASD probands.  [[Neuroligins/Neurexins/Shank3|Neuroligins and Neurexins]] are likely to be the centrally organizing molecules for excitatory [[Serotoninergic, GABAergic, and glutamatergic pathways|glutamatergic and inhibitory GABAergic]] synapses in the mammalian brain.  Studies have shown that mutant mice with the R451C Nlgn3 mutation have increased GABAergic synapses and inhibitory currents.  In addition, MeCP2 knockout mice, Caps2 knowckout mice, mice exposed to prenatla valproate treatment, and many other models have imbalances of inhibition and excitation.<sup>1</sup></div></td></tr>
<tr><td colspan="2"> </td><td class='diff-marker'>+</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr>
<tr><td colspan="2"> </td><td class='diff-marker'>+</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">It is unknown whether these changes represent changes in synaptic signaling, or are just responses from a change in homeostasis. However, given that many of the susceptibility genes in ASD affect synapse formation signaling.  Additionally, several of the genes also affect cortical interneurons.<sup>2</sup></ins></div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==[[Image:Brain_MRI_T1_movie.gif|75px]]Neuroimaging==</div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==[[Image:Brain_MRI_T1_movie.gif|75px]]Neuroimaging==</div></td></tr>
</table>
128.97.66.134
http://lcni-3.uoregon.edu/phenowiki/index.php?title=Stimulating_Hypothesis&diff=3272&oldid=prev
128.97.66.134 at 22:17, 25 March 2010
2010-03-25T22:17:33Z
<p></p>
<table class='diff diff-contentalign-left'>
<col class='diff-marker' />
<col class='diff-content' />
<col class='diff-marker' />
<col class='diff-content' />
<tr style='vertical-align: top;' lang='en'>
<td colspan='2' style="background-color: white; color:black; text-align: center;">← Older revision</td>
<td colspan='2' style="background-color: white; color:black; text-align: center;">Revision as of 22:17, 25 March 2010</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l1" >Line 1:</td>
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<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==Stimulating Hypothesis==</div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==Stimulating Hypothesis==</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>The stimulating hypothesis says that the imbalance between inhibitory and excitatory synaptic currents causes ASD.  A central component in this theory are the variants in [[Neuroligins/Neurexins/Shank3|Neuroligins and Neurexins ]] that have been found in ASD probands.  [[Neuroligins/Neurexins/Shank3|Neuroligins and Neurexins]] are likely to be the centrally organizing <del class="diffchange diffchange-inline">melecules </del>for excitatory glutamatergic and inhibitory GABAergic synapses in the mammalian brain.  Studies have shown that mutant mice with the R451C Nlgn3 mutation have increased GABAergic synapses and inhibitory currents.  In addition, MeCP2 knockout mice, Caps2 knowckout mice, mice exposed to prenatla valproate treatment, and many other models have imbalances of inhibition and excitation.<sup>1</sup></div></td><td class='diff-marker'>+</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>The stimulating hypothesis says that the imbalance between inhibitory and excitatory synaptic currents causes ASD.  A central component in this theory are the variants in [[Neuroligins/Neurexins/Shank3|Neuroligins and Neurexins ]] that have been found in ASD probands.  [[Neuroligins/Neurexins/Shank3|Neuroligins and Neurexins]] are likely to be the centrally organizing <ins class="diffchange diffchange-inline">molecules </ins>for excitatory <ins class="diffchange diffchange-inline">[[Serotoninergic, GABAergic, and glutamatergic pathways|</ins>glutamatergic and inhibitory GABAergic<ins class="diffchange diffchange-inline">]] </ins>synapses in the mammalian brain.  Studies have shown that mutant mice with the R451C Nlgn3 mutation have increased GABAergic synapses and inhibitory currents.  In addition, MeCP2 knockout mice, Caps2 knowckout mice, mice exposed to prenatla valproate treatment, and many other models have imbalances of inhibition and excitation.<sup>1</sup></div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==[[Image:Brain_MRI_T1_movie.gif|75px]]Neuroimaging==</div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==[[Image:Brain_MRI_T1_movie.gif|75px]]Neuroimaging==</div></td></tr>
</table>
128.97.66.134
http://lcni-3.uoregon.edu/phenowiki/index.php?title=Stimulating_Hypothesis&diff=3271&oldid=prev
128.97.66.134: /* Stimulating Hypothesis */
2010-03-25T22:14:40Z
<p><span dir="auto"><span class="autocomment">Stimulating Hypothesis</span></span></p>
<table class='diff diff-contentalign-left'>
<col class='diff-marker' />
<col class='diff-content' />
<col class='diff-marker' />
<col class='diff-content' />
<tr style='vertical-align: top;' lang='en'>
<td colspan='2' style="background-color: white; color:black; text-align: center;">← Older revision</td>
<td colspan='2' style="background-color: white; color:black; text-align: center;">Revision as of 22:14, 25 March 2010</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l1" >Line 1:</td>
<td colspan="2" class="diff-lineno">Line 1:</td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==Stimulating Hypothesis==</div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==Stimulating Hypothesis==</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>The stimulating hypothesis says that the imbalance between inhibitory and excitatory synaptic currents causes ASD.  A central component in this theory are the variants in [[Neuroligins/Neurexins/Shank3|Neuroligins and Neurexins ]] that have been found in ASD probands.  [[Neuroligins/Neurexins|Neuroligins and Neurexins<del class="diffchange diffchange-inline">/Shank3</del>]]are likely to be the centrally organizing melecules for excitatory glutamatergic and inhibitory GABAergic synapses in the mammalian brain.  Studies have shown that mutant mice with the R451C Nlgn3 mutation have increased GABAergic synapses and inhibitory currents.  In addition, MeCP2 knockout mice, Caps2 knowckout mice, mice exposed to prenatla valproate treatment, and many other models have imbalances of inhibition and excitation.<sup>1</sup></div></td><td class='diff-marker'>+</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>The stimulating hypothesis says that the imbalance between inhibitory and excitatory synaptic currents causes ASD.  A central component in this theory are the variants in [[Neuroligins/Neurexins/Shank3|Neuroligins and Neurexins ]] that have been found in ASD probands.  [[Neuroligins/Neurexins<ins class="diffchange diffchange-inline">/Shank3</ins>|Neuroligins and Neurexins]] are likely to be the centrally organizing melecules for excitatory glutamatergic and inhibitory GABAergic synapses in the mammalian brain.  Studies have shown that mutant mice with the R451C Nlgn3 mutation have increased GABAergic synapses and inhibitory currents.  In addition, MeCP2 knockout mice, Caps2 knowckout mice, mice exposed to prenatla valproate treatment, and many other models have imbalances of inhibition and excitation.<sup>1</sup></div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==[[Image:Brain_MRI_T1_movie.gif|75px]]Neuroimaging==</div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==[[Image:Brain_MRI_T1_movie.gif|75px]]Neuroimaging==</div></td></tr>
</table>
128.97.66.134
http://lcni-3.uoregon.edu/phenowiki/index.php?title=Stimulating_Hypothesis&diff=3270&oldid=prev
128.97.66.134: /* Stimulating Hypothesis */
2010-03-25T22:14:02Z
<p><span dir="auto"><span class="autocomment">Stimulating Hypothesis</span></span></p>
<table class='diff diff-contentalign-left'>
<col class='diff-marker' />
<col class='diff-content' />
<col class='diff-marker' />
<col class='diff-content' />
<tr style='vertical-align: top;' lang='en'>
<td colspan='2' style="background-color: white; color:black; text-align: center;">← Older revision</td>
<td colspan='2' style="background-color: white; color:black; text-align: center;">Revision as of 22:14, 25 March 2010</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l1" >Line 1:</td>
<td colspan="2" class="diff-lineno">Line 1:</td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==Stimulating Hypothesis==</div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==Stimulating Hypothesis==</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>The stimulating hypothesis says that the imbalance between inhibitory and excitatory synaptic currents causes ASD.  A central component in this theory are the variants in [[<del class="diffchange diffchange-inline">Neuroligins and Neurexins |</del>Neuroligins/Neurexins/Shank3]] that have been found in ASD probands.  [[Neuroligins <del class="diffchange diffchange-inline">and </del>Neurexins |Neuroligins<del class="diffchange diffchange-inline">/</del>Neurexins/Shank3]]are likely to be the centrally organizing melecules for excitatory glutamatergic and inhibitory GABAergic synapses in the mammalian brain.  Studies have shown that mutant mice with the R451C Nlgn3 mutation have increased GABAergic synapses and inhibitory currents.  In addition, MeCP2 knockout mice, Caps2 knowckout mice, mice exposed to prenatla valproate treatment, and many other models have imbalances of inhibition and excitation.<sup>1</sup></div></td><td class='diff-marker'>+</td><td style="color:black; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>The stimulating hypothesis says that the imbalance between inhibitory and excitatory synaptic currents causes ASD.  A central component in this theory are the variants in [[Neuroligins/Neurexins/Shank3<ins class="diffchange diffchange-inline">|Neuroligins and Neurexins </ins>]] that have been found in ASD probands.  [[Neuroligins<ins class="diffchange diffchange-inline">/</ins>Neurexins|Neuroligins <ins class="diffchange diffchange-inline">and </ins>Neurexins/Shank3]]are likely to be the centrally organizing melecules for excitatory glutamatergic and inhibitory GABAergic synapses in the mammalian brain.  Studies have shown that mutant mice with the R451C Nlgn3 mutation have increased GABAergic synapses and inhibitory currents.  In addition, MeCP2 knockout mice, Caps2 knowckout mice, mice exposed to prenatla valproate treatment, and many other models have imbalances of inhibition and excitation.<sup>1</sup></div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==[[Image:Brain_MRI_T1_movie.gif|75px]]Neuroimaging==</div></td><td class='diff-marker'> </td><td style="background-color: #f9f9f9; color: #333333; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #e6e6e6; vertical-align: top; white-space: pre-wrap;"><div>==[[Image:Brain_MRI_T1_movie.gif|75px]]Neuroimaging==</div></td></tr>
</table>
128.97.66.134