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Title

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

Authors
Schuler, V.
Klix, N.
Sansig, G.
Klebs, K.
Schmutz, M.
Heid, J.
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Published in Neuron. 2001, vol. 31, no. 1, p. 47-58
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.
Keywords AnimalsAnimals, NewbornAvoidance Learning/physiologyBaclofen/pharmacologyBody Temperature RegulationDelta Rhythm/drug effectsEpilepsy/ genetics/physiopathologyGABA Agonists/pharmacologyHippocampus/physiology/physiopathologyHyperalgesia/ genetics/physiopathologyMembrane Potentials/drug effects/physiologyMemory/ physiologyMemory Disorders/ genetics/physiopathologyMiceMice, Inbred BALB CMice, KnockoutMotor Activity/drug effects/physiologyMuscle Relaxation/drug effectsMuscle, Skeletal/drug effects/physiology/physiopathologyNeurons/ physiologyPain/physiopathologyPatch-Clamp TechniquesProtein SubunitsReceptors, GABA-B/deficiency/genetics/ physiology
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PMID: 11498050
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