Difference between revisions of "Serotoninergic, GABAergic, and glutamatergic pathways"

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(Created page with '==Serotoninergic, GABAergic, and Glutamatergic pathways== '''Serotoninergic pathway''' '''GABAergic pathway''' '''Glutamatergic pathway''' <br><br><br><br> <div style…')
 
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'''Serotoninergic pathway'''
 
'''Serotoninergic pathway'''
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One group, Chugani et. al. has demonstrated that there are developmental differences in serotonin synthesis capacity between those with autism and those without.  Global brain values for autistic children, non-autistic children, and epileptic children without autism were obtained and trajectories were plotted for serotonin synthesis capacity.  It was found that for non-autistic children, serotonin synthesis capacity was greater than 200% of adult capacity until 5 years, when capacity then started declining until it reaches adult values.  For autistic children, serotonin synthesis capacity gradually increased between 2-11 years of age to 1 and a half times the normal values of an adult. 
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Pharmacological and knock-out experiments with mice show that serotonin can also affect synaptogenesis.  There is transient serotonergic innervation of the primary sensory cortex between postnatal days 2-14 during the period of synaptogenesis in the rat cortex. There is transient expression of high-affinity serotonin transporter and vesicular monoamine transporter by glutamergic thalamocortical neurons.  Thalamo-cortical neurons take up and store serotonin during this period but do not synthesis the neurotransmitter.  Depletion of serotonin stores delays the development of the barrel fields of the rat somatosensory cortex and decreases the size of barrel fields. Too much serotonin results in incrased tangential arborization of these axons resulting in the blurring of boundaries between cortical barrels. 
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There is also evidence that changes in the serotonin receptor 5HT1A can affect teh brain regions that are abnormal in autism.<sup>2</sup>
  
  
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====References====
 
====References====
 
1. Pardo, CA et. al.  '''The Neurobiology of Autism.'''Brain Pathol. 2007 Oct;17(4):434-47. PMID 17919129
 
1. Pardo, CA et. al.  '''The Neurobiology of Autism.'''Brain Pathol. 2007 Oct;17(4):434-47. PMID 17919129
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2. Chugani DC.'''Role of altered brain serotonin mechanisms in autism.'''Mol Psychiatry. 2002;7 Suppl 2:S16-7. PMID 12142936

Revision as of 12:56, 18 November 2009

Serotoninergic, GABAergic, and Glutamatergic pathways

Serotoninergic pathway

One group, Chugani et. al. has demonstrated that there are developmental differences in serotonin synthesis capacity between those with autism and those without. Global brain values for autistic children, non-autistic children, and epileptic children without autism were obtained and trajectories were plotted for serotonin synthesis capacity. It was found that for non-autistic children, serotonin synthesis capacity was greater than 200% of adult capacity until 5 years, when capacity then started declining until it reaches adult values. For autistic children, serotonin synthesis capacity gradually increased between 2-11 years of age to 1 and a half times the normal values of an adult.

Pharmacological and knock-out experiments with mice show that serotonin can also affect synaptogenesis. There is transient serotonergic innervation of the primary sensory cortex between postnatal days 2-14 during the period of synaptogenesis in the rat cortex. There is transient expression of high-affinity serotonin transporter and vesicular monoamine transporter by glutamergic thalamocortical neurons. Thalamo-cortical neurons take up and store serotonin during this period but do not synthesis the neurotransmitter. Depletion of serotonin stores delays the development of the barrel fields of the rat somatosensory cortex and decreases the size of barrel fields. Too much serotonin results in incrased tangential arborization of these axons resulting in the blurring of boundaries between cortical barrels.

There is also evidence that changes in the serotonin receptor 5HT1A can affect teh brain regions that are abnormal in autism.2


GABAergic pathway


Glutamatergic pathway







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References

1. Pardo, CA et. al. The Neurobiology of Autism.Brain Pathol. 2007 Oct;17(4):434-47. PMID 17919129

2. Chugani DC.Role of altered brain serotonin mechanisms in autism.Mol Psychiatry. 2002;7 Suppl 2:S16-7. PMID 12142936