{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T22:33:07Z","timestamp":1792189987098,"version":"4.4.0"},"reference-count":39,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2012,5,9]],"date-time":"2012-05-09T00:00:00Z","timestamp":1336521600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurochemistry"],"published-print":{"date-parts":[[2012,7]]},"abstract":"<jats:sec><jats:label\/><jats:p><jats:italic>J. Neurochem.<\/jats:italic> (2012) <jats:bold>122<\/jats:bold>, 48\u201357.<\/jats:p><\/jats:sec><jats:sec><jats:title>Abstract<\/jats:title><jats:p>Mouse superficial superior colliculus (SuSC) contains dense GABAergic innervation and diverse nicotinic acetylcholine receptor subtypes. Pharmacological and genetic approaches were used to investigate the subunit compositions of nicotinic acetylcholine receptors (nAChR) expressed on mouse SuSC GABAergic terminals. [<jats:sup>125<\/jats:sup>I]\u2010Epibatidine competition\u2010binding studies revealed that the \u03b13\u03b22* and \u03b16\u03b22* nicotinic subtype\u2010selective peptide \u03b1\u2010conotoxin MII\u2010blocked binding to 40\u2003\u00b1\u20035% of SuSC nAChRs. Acetylcholine\u2010evoked [<jats:sup>3<\/jats:sup>H]\u2010GABA release from SuSC crude synaptosomal preparations is calcium dependent, blocked by the voltage\u2010sensitive calcium channel blocker, cadmium, and the nAChR antagonist mecamylamine, but is unaffected by muscarinic, glutamatergic, P2X and 5\u2010HT3 receptor antagonists. Approximately 50% of nAChR\u2010mediated SuSC [<jats:sup>3<\/jats:sup>H]\u2010GABA release is inhibited by \u03b1\u2010conotoxin MII. However, the highly \u03b16\u03b22*\u2010subtype\u2010selective \u03b1\u2010conotoxin PIA did not affect [<jats:sup>3<\/jats:sup>H]\u2010GABA release. Nicotinic subunit\u2010null mutant mouse experiments revealed that ACh\u2010stimulated SuSC [<jats:sup>3<\/jats:sup>H]\u2010GABA release is entirely \u03b22 subunit\u2010dependent. \u03b14 subunit deletion decreased total function by &gt;90%, and eliminated \u03b1\u2010conotoxin MII\u2010resistant release. ACh\u2010stimulated SuSC [<jats:sup>3<\/jats:sup>H]\u2010GABA release was unaffected by \u03b23, \u03b15 or \u03b16 nicotinic subunit deletions. Together, these data suggest that a significant proportion of mouse SuSC nicotinic agonist\u2010evoked GABA\u2010release is mediated by a novel, \u03b1\u2010conotoxin MII\u2010sensitive \u03b13\u03b14\u03b22 nAChR. The remaining \u03b1\u2010conotoxin MII\u2010resistant, nAChR agonist\u2010evoked SuSC GABA release appears to be mediated via \u03b14\u03b22* subtype nAChRs.<\/jats:p><\/jats:sec>","DOI":"10.1111\/j.1471-4159.2012.07759.x","type":"journal-article","created":{"date-parts":[[2012,4,16]],"date-time":"2012-04-16T16:55:15Z","timestamp":1334595315000},"page":"48-57","source":"Crossref","is-referenced-by-count":11,"title":["A novel \u03b1\u2010conotoxin MII\u2010sensitive nicotinic acetylcholine receptor modulates [<sup>3<\/sup>H]\u2010GABA release in the superficial layers of the mouse superior colliculus"],"prefix":"10.1111","volume":"122","author":[{"given":"Tristan D.","family":"McClure\u2010Begley","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Charles R.","family":"Wageman","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sharon R.","family":"Grady","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael J.","family":"Marks","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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