Sil'kis I G
Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Moscow.
Zh Vyssh Nerv Deiat Im I P Pavlova. 2000 May-Jun;50(3):372-87.
It is known from the experimental data that at different cerebellar neurons there are voltage-dependent Ca2+ channels, NMDA receptors, metabotropic glutamate and GABAB receptors. This receptor arrangement ensures that activation of excitatory and inhibitory input results in changes in activity of protein kinases and phosphatases and subsequent modification of synaptic efficacy. The mechanism of synaptic plasticity is advanced that in accordance with the known experimental data concerning the modification of excitatory and inhibitory inputs to Purkinje cells, granule cells, and deep cerebellar nuclei cells. The mechanism is based on a postulate that phosphorylation/dephosphorylation of AMPA (GABAA) receptors on cerebellar cells causes the LTP/LTD of excitatory (LTD/LTP of inhibitory) transmission. It is assumed that modification rules for Purkinje cells, granule cells, and deep cerebellar nuclei cells, wherein cGMP-dependent protein kinase G is involved in synaptic plasticity, are distinct from those of hippocampal/neocortical cells, wherein cAMP-dependent protein kinase A is involved in synaptic plasticity, since cGMP (cAMP) concentration decreases (increases) with Ca2+ rise.
从实验数据可知，不同的小脑神经元存在电压依赖性Ca2+通道、NMDA受体、代谢型谷氨酸受体和GABAB受体。这种受体排列确保了兴奋性和抑制性输入的激活会导致蛋白激酶和磷酸酶活性的变化以及随后突触效能的改变。根据关于浦肯野细胞、颗粒细胞和小脑深部核团细胞兴奋性和抑制性输入修饰的已知实验数据，提出了突触可塑性的机制。该机制基于一个假设，即小脑细胞上AMPA（GABAA）受体的磷酸化/去磷酸化导致兴奋性（抑制性的长时程抑制/长时程增强）传递的长时程增强/长时程抑制。据推测，其中cGMP依赖性蛋白激酶G参与突触可塑性的浦肯野细胞、颗粒细胞和小脑深部核团细胞的修饰规则，与其中cAMP依赖性蛋白激酶A参与突触可塑性的海马/新皮层细胞的修饰规则不同，因为随着Ca2+升高，cGMP（cAMP）浓度降低（升高）。
