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http://purl.uniprot.org/citations/8388308http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/8388308http://www.w3.org/2000/01/rdf-schema#comment"This study begins to explore possible mechanisms underlying the role of GABAB receptors in absence seizures in lethargic (lh/lh) mice. To test the hypothesis that alterations intrinsic to the GABAB receptor underlie enhanced synaptic activation of these receptors in absence seizures, we measured GABA-displaceable [3H]baclofen binding to neocortical plasma membranes prepared from lh/lh and wild (+/+) age-matched congenic mice. The number (Bmax) of binding sites was significantly greater (20%) in lh/lh (4.2 pmol/mg protein, n = 43 pairs, P < 0.02) than in +/+ mice (3.3 pmol/mg protein) in an age-independent manner. Interestingly, the subset of lh/lh mice with greater seizure frequency (40-70 seizures/15 min, measured by bipolar electrodes implanted into neocortex; n = 11) had a significantly greater Bmax (P < 0.003) than the subset with lower seizure frequency (1-10 seizures/15 min; n = 11). The equilibrium dissociation constant (Kd) was unchanged (60 nM in both). The Kd of both strains was inhibited to an equal degree by the nonhydrolysable GTP analogue 5'-guanylimido-diphosphate [Gpp(NH)p]. The increased number of GABAB binding sites was selective, because binding to NMDA sites ([3H]glutamate binding) and to GABAA sites ([3H]muscimol binding) was not significantly different in the two strains. These data suggest that the increased number of GABAB receptors in lh/lh mice underlies enhanced synaptic activation of these receptors. Together with evidence that GABAB receptor activation can produce disinhibition, our data support a role for GABAB receptors in the expression of absence seizures in lh/lh mice."xsd:string
http://purl.uniprot.org/citations/8388308http://purl.org/dc/terms/identifier"doi:10.1016/0006-8993(93)90779-m"xsd:string
http://purl.uniprot.org/citations/8388308http://purl.uniprot.org/core/author"Cao Z."xsd:string
http://purl.uniprot.org/citations/8388308http://purl.uniprot.org/core/author"Lin F.H."xsd:string
http://purl.uniprot.org/citations/8388308http://purl.uniprot.org/core/author"Hosford D.A."xsd:string
http://purl.uniprot.org/citations/8388308http://purl.uniprot.org/core/date"1993"xsd:gYear
http://purl.uniprot.org/citations/8388308http://purl.uniprot.org/core/name"Brain Res"xsd:string
http://purl.uniprot.org/citations/8388308http://purl.uniprot.org/core/pages"101-106"xsd:string
http://purl.uniprot.org/citations/8388308http://purl.uniprot.org/core/title"Increased number of GABAB receptors in the lethargic (lh/lh) mouse model of absence epilepsy."xsd:string
http://purl.uniprot.org/citations/8388308http://purl.uniprot.org/core/volume"608"xsd:string
http://purl.uniprot.org/citations/8388308http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/8388308
http://purl.uniprot.org/citations/8388308http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/8388308
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http://purl.uniprot.org/uniprot/#_Q8R0S4-mappedCitation-8388308http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/8388308
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