PROTEINS FUNCTIONING IN SYNAPTIC TRANSMISSION AT THE SENSORY TO MOTOR SYNAPSE OF APLYSIA

被引：19

作者：

SKEHEL, A ^{[1
]}

ARMITAGE, BA ^{[1
]}

BARTSCH, D ^{[1
]}

HU, YH ^{[1
]}

KAANG, BK ^{[1
]}

SIEGELBAUM, SA ^{[1
]}

KANDEL, ER ^{[1
]}

MARTIN, KC ^{[1
]}

机构：

[1] COLUMBIA UNIV COLL PHYS & SURG, CTR NEUROBIOL & BEHAV, NEW YORK, NY 10032 USA

来源：

NEUROPHARMACOLOGY | 1995年 / 34卷 / 11期

关键词：

APLYSIA; SYNAPTIC TRANSMISSION; VAMP/SYNAPTOBREVIN; SYNAPTOTAGMIN;

D O I：

10.1016/0028-3908(95)00149-Z

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Over expression of Aplysia synaptotagmin in acutely dissected cholinergic neurons from the buccal ganglia, or in primary co-cultures of glutaminergic sensory neurons and motor neurons, causes a reduction synaptic transmission. Anti-sense oligonucleotide treatment of similar cultures produced an enhancement of synaptic transmission. The interaction between Aplysia VAMP/synaptobrevin and syntaxin is reconstructed using the yeast two hybrid system, and used to identify amino acid residues of VAMP/synaptobrevin that are required for this interaction. Point mutations around residue 50, close to the site of cleavage by botulinum toxins specifically disrupt the interaction with syntaxin. An additional VAMP/synaptobrevin binding protein, VAP33, is identified using the yeast two hybrid system. Intracellular injection of VAP33 specific antisera inhibits synaptic transmission in sensory-motor neuron co-cultures.

引用

页码：1379 / 1385

页数：7

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