Epilepsy, hyperalgesia, impaired memory, and loss of pre- and postsynaptic GABA(B) responses in mice lacking GABA(B(1)).

Abstract:

:GABA(B) (gamma-aminobutyric acid type B) receptors are important for keeping neuronal excitability under control. Cloned GABA(B) receptors do not show the expected pharmacological diversity of native receptors and it is unknown whether they contribute to pre- as well as postsynaptic functions. Here, we demonstrate that Balb/c mice lacking the GABA(B(1)) subunit are viable, exhibit spontaneous seizures, hyperalgesia, hyperlocomotor activity, and memory impairment. Upon GABA(B) agonist application, null mutant mice show neither the typical muscle relaxation, hypothermia, or delta EEG waves. These behavioral findings are paralleled by a loss of all biochemical and electrophysiological GABA(B) responses in null mutant mice. This demonstrates that GABA(B(1)) is an essential component of pre- and postsynaptic GABA(B) receptors and casts doubt on the existence of proposed receptor subtypes.

journal_name

Neuron

journal_title

Neuron

authors

Schuler V,Lüscher C,Blanchet C,Klix N,Sansig G,Klebs K,Schmutz M,Heid J,Gentry C,Urban L,Fox A,Spooren W,Jaton AL,Vigouret J,Pozza M,Kelly PH,Mosbacher J,Froestl W,Käslin E,Korn R,Bischoff S,Kaupmann K,van der

doi

10.1016/s0896-6273(01)00345-2

subject

Has Abstract

pub_date

2001-07-19 00:00:00

pages

47-58

issue

1

eissn

0896-6273

issn

1097-4199

pii

S0896-6273(01)00345-2

journal_volume

31

pub_type

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