Epilepsy, Hyperalgesia, Impaired Memory, and Loss of Pre- and Postsynaptic GABA sub(B) Responses in Mice Lacking GABA sub(B(1))

GABA sub(B) ( gamma -aminobutyric acid type B) receptors are important for keeping neuronal excitability under control. Cloned GABA sub(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 functi...

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Published in:Neuron (Cambridge, Mass.) Mass.), 2001-07, Vol.31 (1), p.47-58
Main Authors: Schuler, V, Luescher, C, Blanchet, C, Klix, N, Sansig, G, Klebs, K, Schmutz, M, Heid, J, Gentry, C, Urban, L, Fox, A, Spooren, W, Jaton, A-L, Bettler, B
Format: Article
Language:English
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hyperalgesia
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Summary:GABA sub(B) ( gamma -aminobutyric acid type B) receptors are important for keeping neuronal excitability under control. Cloned GABA sub(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 sub(B(1)) subunit are viable, exhibit spontaneous seizures, hyperalgesia, hyperlocomotor activity, and memory impairment. Upon GABA sub(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 sub(B) responses in null mutant mice. This demonstrates that GABA sub(B(1)) is an essential component of pre- and postsynaptic GABA sub(B) receptors and casts doubt on the existence of proposed receptor subtypes.
ISSN:0896-6273