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
Neuronjournal_title
Neuronauthors
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 derdoi
10.1016/s0896-6273(01)00345-2subject
Has Abstractpub_date
2001-07-19 00:00:00pages
47-58issue
1eissn
0896-6273issn
1097-4199pii
S0896-6273(01)00345-2journal_volume
31pub_type
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