Inhibition of transmitter release and long-term depression in the avian hippocampus
Data(s) |
01/01/2000
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Resumo |
Long-term depression has recently been shown to occur at glutamatergic synapses in the avian hippocampus and requires activation of calcium/calmodulin-dependent protein kinase II in the nerve terminal. Here using whole cell and intracellular recordings from brain slices, we show that the N-type calcium channel contributes significantly to glutamate release in the avian hippocampus. Activation of the metabotrobic gamma-aminobutyric acid (GABA)(B) receptor by the specific agonist baclofen blocks synaptic transmission. The action of baclofen was associated with a change in paired pulse facilitation indicating that it resulted from a reduction in the probability of transmitter release, In contrast, no change in paired pulse facilitation was observed following the induction of long-term depression. These results show that activation of GABA(B) receptors and long-term depression reduce transmitter release by distinct mechanisms. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved. |
Identificador | |
Idioma(s) |
eng |
Palavras-Chave | #Neurosciences #Long-term Depression #Transmitter Release #Protein Kinase #Gamma-aminobutyric Acids #Protein-interaction Site #Calcium Channels #Synaptic Transmission #Potentiation #Plasticity #Pigeons #Birds |
Tipo |
Journal Article |