caa a22 4500 477038328 CHVBK 20180405111310.0 cr unu---uuuuu 170330e19960801xx s 000 0 eng 10.1007/BF02740750 doi (NATIONALLICENCE)springer-10.1007/BF02740750 The role of GABAB mechanisms in animal models of absence seizures [Elektronische Daten] [Sarah Caddick, David Hosford] Generalized absence seizures in humans are a unique type of epilepsy characterized by a synchronous, bilateral 3-Hz spike and wave discharge emanating from a cortical and thalamic network within the brain. The availability of a number of pharmacological and genetic animal models has provided us with the means with which to investigate the cellular and molecular mechanisms underlying these seizures. Over the last few years a significant amount of research in these models has focused on the role of the inhibitory GABAB receptors, which have been previously described in a number of brain areas as being responsible for a long-lasting hyperpolarization and depression in neurotransmitter release. Initial studies provided evidence that the GABAB receptor was capable of generating the low threshold calcium spike required for initiation of the burst firing, leading researchers to hypothesize that the GABAB receptors, played a significant role in these seizures. Subsequent research took advantage of the new generation of GABAB antagonists that became available in the early 1990s and demonstrated that in a number of models the seizures could be abolished by the administration of one of these compounds. Further biochemical, molecular, and electrophysiological experiments have been carried out to determine the exact involvement of GABAB receptors and their mechanism of action. The current evidence and interpretations of this work are presented here. Humana Press Inc, 1996 Generalized absence seizures nationallicence GABAB receptors nationallicence animal models nationallicence pre- and postsynaptic mechanisms nationallicence lh/lh nationallicence GAERS nationallicence GHB nationallicence low threshold calcium spikes nationallicence Caddick Sarah Division of Neurology, Duke University Medical Center and Durham VAMC, Bldg 16, Rm 20, VAMC, 508 Fulton St, 27705, Durham, NC aut Hosford David Division of Neurology, Duke University Medical Center and Durham VAMC, Bldg 16, Rm 20, VAMC, 508 Fulton St, 27705, Durham, NC aut Molecular Neurobiology Humana Press 13/1(1996-08-01), 23-32 0893-7648 13:1<23 1996 13 12035 https://doi.org/10.1007/BF02740750 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF02740750 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Caddick Sarah Division of Neurology, Duke University Medical Center and Durham VAMC, Bldg 16, Rm 20, VAMC, 508 Fulton St, 27705, Durham, NC aut NATIONALLICENCE 700 1- Hosford David Division of Neurology, Duke University Medical Center and Durham VAMC, Bldg 16, Rm 20, VAMC, 508 Fulton St, 27705, Durham, NC aut NATIONALLICENCE 773 0- Molecular Neurobiology Humana Press 13/1(1996-08-01), 23-32 0893-7648 13:1<23 1996 13 12035 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer