Cortical GABAergic neurons and cerebellar Purkinje cells respond to ischemia-pathogenic factors differently.
GABAergic neurons in the central nervous system are vulnerable to hazard situations, such as ischemia and toxic substances, under which their dysfunction results in neuronal excitotoxicity and subsequently cell death. How ischemia-related pathogenic factors influence the functions of different GABAergic neurons remains to be documented. We investigated this issue at cortical GABAergic neurons and cerebellar Purkinje cells in brain slices by whole-cell recordings. Our results demonstrate that ischemia, cellular Ca(2+)-overload and acidosis lower the spike capacity of cortical GABAergic neurons, but elevate that of cerebellar Purkinje cells. These changes of spike encoding at two types of GABAergic cells are associated with the different effects of three factors on spike refractory periods and threshold potentials, which are mediated by voltage-gated sodium channels. Mechanisms underlying such differences are discussed.
Department of Neurology, the Fourth Affiliated Hospital in Harbin Medical University, Harbin, Heilongjiang 150001, China.
Shuyan
S
Zhang
Zichao
Z
Yang
Zixin
Z
Zhang
Zhongren
Z
Sun
D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism* / Q000473:pathology; D002525:Cerebellar Cortex / Q000378:metabolism* / Q000473:pathology; D002540:Cerebral Cortex / Q000378:metabolism* / Q000473:pathology; D007395:Interneurons / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D008822:Mice, Transgenic; D009498:Neurotoxins / Q000378:metabolism; D009924:Organ Culture Techniques; D011689:Purkinje Cells / Q000378:metabolism* / Q000473:pathology; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
D009498:Neurotoxins; D005680:gamma-Aminobutyric Acid