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Mechanisms of GABAB receptor exocytosis, endocytosis, and degradation


Benke, D (2010). Mechanisms of GABAB receptor exocytosis, endocytosis, and degradation. Advances in Pharmacology, 58:93-111.

Abstract

GABA(B) receptors belong to the family of G-protein-coupled receptors, which mediate slow inhibitory neurotransmission in the central nervous system. They are promising drug targets for a variety of neurological disorders and play important functions in regulating synaptic plasticity. Signaling strength is critically dependent on the availability of the receptors at the cell surface. Several distinct highly regulated trafficking mechanisms ensure the presence of adequate receptor numbers in the plasma membrane. The rate of exocytosis of newly synthesized receptors from the endoplasmic reticulum via the Golgi apparatus to the cell surface as well as the rates of their endocytosis and degradation determines the retention time of receptors at the cell surface. This chapter focuses on the recently emerged mechanisms of GABA(B) receptor exocytosis, endocytosis, recycling, and degradation.

Abstract

GABA(B) receptors belong to the family of G-protein-coupled receptors, which mediate slow inhibitory neurotransmission in the central nervous system. They are promising drug targets for a variety of neurological disorders and play important functions in regulating synaptic plasticity. Signaling strength is critically dependent on the availability of the receptors at the cell surface. Several distinct highly regulated trafficking mechanisms ensure the presence of adequate receptor numbers in the plasma membrane. The rate of exocytosis of newly synthesized receptors from the endoplasmic reticulum via the Golgi apparatus to the cell surface as well as the rates of their endocytosis and degradation determines the retention time of receptors at the cell surface. This chapter focuses on the recently emerged mechanisms of GABA(B) receptor exocytosis, endocytosis, recycling, and degradation.

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Additional indexing

Item Type:Journal Article, not refereed, further contribution
Communities & Collections:04 Faculty of Medicine > Institute of Pharmacology and Toxicology
07 Faculty of Science > Institute of Pharmacology and Toxicology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:2010
Deposited On:21 Dec 2010 14:18
Last Modified:05 Apr 2016 14:24
Publisher:Elsevier
ISSN:1054-3589
Publisher DOI:https://doi.org/10.1016/S1054-3589(10)58004-9
PubMed ID:20655479

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