{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,4]],"date-time":"2025-11-04T10:12:55Z","timestamp":1762251175145},"reference-count":34,"publisher":"Society for Neuroscience","issue":"33","license":[{"start":{"date-parts":[[2007,2,16]],"date-time":"2007-02-16T00:00:00Z","timestamp":1171584000000},"content-version":"vor","delay-in-days":184,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J. Neurosci."],"published-print":{"date-parts":[[2006,8,16]]},"abstract":"<jats:p>Stargazer (<jats:italic>stg<\/jats:italic>) mutant mice fail to express stargazin [transmembrane AMPA receptor regulatory protein \u03b32 (TARP\u03b32)] and consequently experience absence seizure-like thalamocortical spike-wave discharges that pervade the hippocampal formation via the dentate gyrus (DG). As in other seizure models, the dentate granule cells of<jats:italic>stg<\/jats:italic>develop elaborate reentrant axon collaterals and transiently overexpress brain-derived neurotrophic factor. We investigated whether GABAergic parameters were affected by the<jats:italic>stg<\/jats:italic>mutation in this brain region. GABA<jats:sub>A<\/jats:sub>receptor (GABAR) \u03b14 and \u03b23 subunits were consistently upregulated, GABAR \u03b4 expression appeared to be variably reduced, whereas GABAR \u03b11, \u03b22, and \u03b32 subunits and the GABAR synaptic anchoring protein gephyrin were essentially unaffected. We established that the \u03b14\u03b2\u03b32 subunit-containing, flunitrazepam-insensitive subtype of GABARs, not normally a significant GABAR in DG neurons, was strongly upregulated in<jats:italic>stg<\/jats:italic>DG, apparently arising at the expense of extrasynaptic \u03b14\u03b2\u03b4-containing receptors. This change was associated with a reduction in neurosteroid-sensitive GABAR-mediated tonic current. This switch in GABAR subtypes was not reciprocated in the tottering mouse model of absence epilepsy implicating a unique, intrinsic adaptation of GABAergic networks in<jats:italic>stg<\/jats:italic>.<\/jats:p><jats:p>Contrary to previous reports that suggested that TARP\u03b32 is expressed in the dentate, we find that TARP\u03b32 was neither detected in<jats:italic>stg<\/jats:italic>nor control DG. We report that TARP\u03b38 is the principal TARP isoform found in the DG and that its expression is compromised by the stargazer mutation. These effects on GABAergic parameters and TARP\u03b38 expression are likely to arise as a consequence of failed expression of TARP\u03b32 elsewhere in the brain, resulting in hyperexcitable inputs to the dentate.<\/jats:p>","DOI":"10.1523\/jneurosci.1088-06.2006","type":"journal-article","created":{"date-parts":[[2006,8,16]],"date-time":"2006-08-16T19:42:55Z","timestamp":1155757375000},"page":"8600-8608","source":"Crossref","is-referenced-by-count":31,"title":["Aberrant GABA<sub>A<\/sub>Receptor Expression in the Dentate Gyrus of the Epileptic Mutant Mouse Stargazer"],"prefix":"10.1523","volume":"26","author":[{"given":"Helen L.","family":"Payne","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Peter S.","family":"Donoghue","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"William M. 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