{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T21:06:36Z","timestamp":1789938396580,"version":"4.0.1"},"reference-count":42,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[1999,5,1]]},"abstract":"<jats:p>Electrophysiological recordings and calcium measurements in striatal large aspiny interneurons in response to combined O<jats:sub>2<\/jats:sub>\/glucose deprivation. The effects of combined O<jats:sub>2<\/jats:sub>\/glucose deprivation were investigated on large aspiny (LA) interneurons recorded from a striatal slice preparation by means of simultaneous electrophysiological and optical recordings. LA interneurons were visually identified and impaled with sharp microelectrodes loaded with the calcium (Ca<jats:sup>2+<\/jats:sup>)-sensitive dye bis-fura-2. These cells showed the morphological, electrophysiological, and pharmacological features of large striatal cholinergic interneurons. O<jats:sub>2<\/jats:sub>\/glucose deprivation induced a membrane hyperpolarization coupled to a concomitant increase in intracellular Ca<jats:sup>2+<\/jats:sup>concentration ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>). Interestingly, this [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>elevation was more pronounced in dendritic branches rather than in the somatic region. The O<jats:sub>2<\/jats:sub>\/glucose-deprivation-induced membrane hyperpolarization reversed its polarity at the potassium (K<jats:sup>+<\/jats:sup>) equilibrium potential. Both membrane hyperpolarization and [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>rise were unaffected by TTX or by a combination of ionotropic glutamate receptors antagonists,d-2-amino-5-phosphonovaleric acid and 6cyano-7-nitroquinoxaline-2,3-dione. Sulfonylurea glibenclamide, a blocker of ATP-sensitive K<jats:sup>+<\/jats:sup>channels, markedly reduced the O<jats:sub>2<\/jats:sub>\/glucose-deprivation-induced membrane hyperpolarization but failed to prevent the rise in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>. Likewise, charybdotoxin, a large K<jats:sup>+<\/jats:sup>-channel (BK) inhibitor, abolished the membrane hyperpolarization but did not produce detectable changes of [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>elevation. A combination of high-voltage-activated Ca<jats:sup>2+<\/jats:sup>channel blockers significantly reduced both the membrane hyperpolarization and the rise in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>. In a set of experiments performed without dye in the recording electrode, either intracellular bis-( o-aminophenoxy)- N,N,N\u2032,N\u2032-tetraacetic acid or external barium abolished the membrane hyperpolarization induced by O<jats:sub>2<\/jats:sub>\/glucose deprivation. The hyperpolarizing effect on membrane potential was mimicked by oxotremorine, an M2-like muscarinic receptor agonist, and by baclofen, a GABA<jats:sub>B<\/jats:sub>receptor agonist. However, this membrane hyperpolarization was not coupled to an increase but rather to a decrease of the basal [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>. Furthermore glibenclamide did not reduce the oxotremorine- and baclofen-induced membrane hyperpolarization. In conclusion, the present results suggest that in striatal LA cells, O<jats:sub>2<\/jats:sub>\/glucose deprivation activates a membrane hyperpolarization that does not involve ligand-gated K<jats:sup>+<\/jats:sup>conductances but is sensitive to barium, glibenclamide, and charybdotoxin. The increase in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>is partially due to influx through voltage-gated high-voltage\u2013activated Ca<jats:sup>2+<\/jats:sup>channels.<\/jats:p>","DOI":"10.1152\/jn.1999.81.5.2508","type":"journal-article","created":{"date-parts":[[2017,12,25]],"date-time":"2017-12-25T05:06:31Z","timestamp":1514178391000},"page":"2508-2516","source":"Crossref","is-referenced-by-count":40,"title":["Electrophysiological Recordings and Calcium Measurements in Striatal Large Aspiny Interneurons in Response to Combined O<sub>2<\/sub>\/Glucose Deprivation"],"prefix":"10.1152","volume":"81","author":[{"given":"Antonio","family":"Pisani","sequence":"first","affiliation":[{"name":"Clinica Neurologica, Dipartimento di Neuroscienze, Universit\u00e0 di Roma Tor Vergata, 00133 Rome;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paolo","family":"Calabresi","sequence":"additional","affiliation":[{"name":"Clinica Neurologica, Dipartimento di Neuroscienze, Universit\u00e0 di Roma Tor Vergata, 00133 Rome;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Diego","family":"Centonze","sequence":"additional","affiliation":[{"name":"Clinica Neurologica, Dipartimento di Neuroscienze, Universit\u00e0 di Roma Tor Vergata, 00133 Rome;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Girolama A.","family":"Marfia","sequence":"additional","affiliation":[{"name":"Clinica Neurologica, Dipartimento di Neuroscienze, Universit\u00e0 di Roma Tor Vergata, 00133 Rome;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Giorgio","family":"Bernardi","sequence":"additional","affiliation":[{"name":"Clinica Neurologica, Dipartimento di Neuroscienze, Universit\u00e0 di Roma Tor Vergata, 00133 Rome;"},{"name":"IRCCS Ospedale S. 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