Difference between revisions of "Stimulating Hypothesis"
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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 and Neurexins that have been found in ASD probands. 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> | 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 and Neurexins that have been found in ASD probands. 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> | ||
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====References==== | ====References==== | ||
1. PMID 18984149 | 1. PMID 18984149 | ||
Revision as of 11:48, 5 November 2009
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 and Neurexins that have been found in ASD probands. 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.1
