Involvement of protein kinase C in NMDAR-dependent long-term potentiation in rat amygdala / 生理学报
Acta Physiologica Sinica
; (6): 737-742, 2008.
Article
em Zh
| WPRIM
| ID: wpr-302496
Biblioteca responsável:
WPRO
ABSTRACT
The mechanism of long-term potentiation (LTP) in basolateral amygdala (BLA) was explored using field potential recording in rat brain slice preparation. Field potentials (field excitatory post-synaptic potentials, fEPSPs) in BLA were evoked with sharpened steel bipolar stimulating electrodes placed in the external capsule (EC). Two theta burst stimulations (TBS, interval=10 min) induced LTP in BLA. TBS-induced synaptic potentiation lasted for more than 30 min after the second TBS. LTP in BLA was input-specific and was blocked by N-methyl-D-aspartate receptor (NMDAR) antagonist 2-amino-5-phosphonovaleric acid (APV). The effect of protein kinase C (PKC) on LTP was then determined using PKC inhibitor chelerythrine chloride. Bath application of chelerythringe chloride had no effect on basic field potentials and paired-pulse ratio (PPR). However, in the presence of chelerythrine chloride, two TBS failed to induce LTP. In contrast, bath application of chelerythrine chloride 10 min after the second TBS did not affect the maintenance of LTP in BLA. These results indicate that LTP is NMDAR-dependent and PKC is involved in the induction and early maintenance of LTP in BLA.
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1
Índice:
WPRIM
Assunto principal:
Farmacologia
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Técnicas In Vitro
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Proteína Quinase C
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2-Amino-5-fosfonovalerato
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Receptores de N-Metil-D-Aspartato
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Potenciação de Longa Duração
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Estimulação Elétrica
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Potenciais Sinápticos
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Tonsila do Cerebelo
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Metabolismo
Limite:
Animals
Idioma:
Zh
Revista:
Acta Physiologica Sinica
Ano de publicação:
2008
Tipo de documento:
Article