Secretion of neurotransmitters is initiated by voltagegated calcium influx through presynaptic, voltage- gated N-type calcium channels. However, little is known about their cellular distribution in the mouse cerebellum. In the cerebellum, alpha1B immunoreactivity is found mainly on the cell bodies of all Purkinje cells. In addition, the immunoreactivity was detected on a subset of Purkinje cell dendrites, clustered to form a parasagittal array of bands. In the anterior lobe vermis, immunoreactive Purkinje cell dendrites form narrow stripes separated by broad bands of unstained dendrites. Moving caudally through the vermis, these stripes become thicker as a larger fraction of the Purkinje cell dendrites become immunoreactive. This localization study of the alpha1B pore-forming subunits in mouse cerebellum may guide future investigations of the role of calcium channels in neurological pathways.
Animals ; Calcium Channels, N-Type/*metabolism ; Cerebellum/cytology/*metabolism ; Dendrites/metabolism ; Immunohistochemistry ; Mice ; Mice, Inbred BALB C ; Purkinje Cells/metabolism

AIM AND METHODSWhole-cell recording technique was used to observe the changes of voltage-dependent ion channels and NMDA receptor currents of rat hippocampal neurons during primary culture.

RESULTSThere was no significant difference of voltage-dependent Na+ current (I(Na)) at 7 d, 14 d and 21 d in culture. It's the same for delayed rectifier K+ current (Ik). However, voltage-dependent Ca2+ current (I(Ca)) and its density were continuously and markedly increased. Further studies showed that the increase of I(Ca) was resulted from the increase of L-type voltage-dependent Ca2+ channels (L-VDCC). NMDA receptor current was also significantly increased with time of culture.

CONCLUSIONCa2+ influx through VDCC and NMIDA receptor is the fatal factor in the aging and death of hippocampal neurons.

Animals ; Animals, Newborn ; Calcium ; metabolism ; Calcium Channels, L-Type ; metabolism ; Cell Membrane ; metabolism ; Cells, Cultured ; Cellular Senescence ; Hippocampus ; cytology ; Ion Channels ; metabolism ; Neurons ; metabolism ; Patch-Clamp Techniques ; Rats ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate ; metabolism ; Time Factors

OBJECTIVE: To prove the existence neurons in the rat corpus callosum, the potential function of these neurons and their connection. METHODS: Immunohistochemistry was used performed to examine the expressions of NeuN, a mature neuron marker,and N-type voltage-dependent valcium channel alpha1-subunit (Cav2.2)in the section of the rat corpus callosum. Horseradish peroxidase (HRP) normal sodium solution (30%), the retrograde tracer,was injected under the frontal forceps of corpus callousm and HRP absorbed by the process of neurons in the brain slices was stained with tetramethyl benzidine. RESULTS: There were some NeuN positive cells in the rat corpus callosum and Cav2.2 was detected in some of these NeuN positive cells.Neurons with positive HRP were found in the rat corpus callosum and some of these neurons connected to the cortex or corpus striatum. CONCLUSION There are a few neurons in the corpus callosum of adult rats and some of them express Cav2.2. Neurons in the corpus callosum have connections with the brain cortex or corpora striatum.
Animals ; Calcium Channels, N-Type ; biosynthesis ; Corpus Callosum ; cytology ; metabolism ; DNA-Binding Proteins ; Male ; Nerve Tissue Proteins ; biosynthesis ; Neural Pathways ; physiology ; Neurons ; cytology ; Nuclear Proteins ; biosynthesis ; Random Allocation ; Rats ; Rats, Sprague-Dawley

To evaluate the effects of different antagonists on the release of cytochrome c from mitochondria to cytosol and the expression of Bcl-2 in mitochondria in rat hippocampus after ischemia, we examined Bcl-2 and cytochrome c expression by immunoblotting using 4-vessel occlusion (4-VO) as brain ischemia model. The results showed that after 24 h ischemia/reperfusion (I/R) cytochrome c decreased markedly in mitochondria, which was correspondingly increased in the cytosolic fraction. Bcl-2 expression was time-dependent, reaching its peak level after 6 h I/R. In all those samples, there were no alterations in the subcellular distribution of cytochrome oxidase, a mitochondrial respiratory chain protein. The decreases in Bcl-2 and cytochrome c in mitochondria were restored by pretreatment with non-competitive NMDA receptor antagonist ketamine or L-type voltage-gated Ca(2+) channel (L-VGCC) antagonist nifedipine at 20 min prior to ischemia. The results demonstrate that the release of cytochrome c from mitochondria to cytosol and the up-regulation of Bcl-2 are possibly mediated by NMDA receptors or L-VGCC following brain ischemia. Cytochrome c release may be injurious while Bcl-2 up-regulation may be protective to ischemic hippocampus.
Animals ; Brain Ischemia ; metabolism ; Calcium Channel Blockers ; pharmacology ; Calcium Channels, L-Type ; drug effects ; Cytochromes c ; metabolism ; Cytosol ; Hippocampus ; metabolism ; Ketamine ; pharmacology ; Male ; Mitochondria ; metabolism ; Nifedipine ; pharmacology ; Proto-Oncogene Proteins c-bcl-2 ; biosynthesis ; genetics ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate ; antagonists & inhibitors ; Up-Regulation