{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,5]],"date-time":"2025-10-05T16:59:39Z","timestamp":1759683579575,"version":"3.41.0"},"reference-count":34,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[1997,11,1]]},"abstract":"<jats:p>Miura, Masami, Masatomo Yoshioka, Hiroyoshi Miyakawa, Hiroshi Kato, and Ken-Ichi Ito. Properties of calcium spikes revealed during GABA<jats:sub>A<\/jats:sub>receptor antagonism in hippocampal CA1 neurons from guinea pigs. J. Neurophysiol. 78: 2269\u20132279, 1997. Intracellular electrical responses and changes in intracellular calcium concentration ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>) in response to activation of synaptic inputs and to DC injections were recorded simultaneously from CA1 pyramidal neurons ( n = 42) in guinea pig hippocampal slices. In the presence of the \u03b3-aminobutyric acid-A (GABA<jats:sub>A<\/jats:sub>) receptor antagonists, bicuculline (25 \u03bcM) and picrotoxin (10 \u03bcM), broad (&gt;20 ms) all-or-none spikes were induced by activation of synaptic inputs (20 pulses, 30 Hz) and were accompanied by a simultaneous rapid and large rise in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>(34 of 34 cells). By contrast, direct depolarizing current (0.7 nA, 1 s) induced spikes having short duration, during which time the spike firing pattern was observed not to be significantly affected. When Na<jats:sup>+<\/jats:sup>channels were blocked by QX-314 applied intracellularly through the recording microelectrode in the presence of GABA<jats:sub>A<\/jats:sub>receptor antagonists, broad spikes were frequently generated by activation of synaptic inputs (32 of 33 cells). These broad spikes were blocked by Cd<jats:sup>2+<\/jats:sup>(200 \u03bcM) or in Ca<jats:sup>2+<\/jats:sup>-free medium (6 of 6 cells) but were resistant to either tetrodotoxin (TTX; 1 \u03bcM; 6 of 6 cells) or QX-314, whereas short-duration spikes were blocked by both TTX andQX-314. Based on these findings we conclude that broad and short-duration spikes are Ca<jats:sup>2+<\/jats:sup>and Na<jats:sup>+<\/jats:sup>spikes, respectively. To investigate the properties of the Ca<jats:sup>2+<\/jats:sup>spikes, antagonists of a voltage-operated Ca<jats:sup>2+<\/jats:sup>channel were applied to the evoked responses. Nifedipine (30 \u03bcM), a L-type Ca<jats:sup>2+<\/jats:sup>channel blocker, suppressed the generation of Ca<jats:sup>2+<\/jats:sup>spikes, whereas Ni<jats:sup>2+<\/jats:sup>(100 \u03bcM), theT- and R-type Ca<jats:sup>2+<\/jats:sup>channel blocker, and \u03c9-agatoxin-IVA (\u03c9-Aga-IVA, 60 nM), a P-type Ca<jats:sup>2+<\/jats:sup>channel blocker, had little effect on the generation of Ca<jats:sup>2+<\/jats:sup>spikes. Nifedipine suppressed the rise in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>induced by synaptic inputs up to 26% of the control in the soma and 18\u201332% in the dendrites ( n = 5), respectively, whereas Ni<jats:sup>2+<\/jats:sup>suppressed the rise by 12\u201327% ( n = 5) in both soma and dendrites. \u03c9-Aga-IVA showed little effect (less than a 10% change; n = 7). These results suggest that the GABA<jats:sub>A<\/jats:sub>inhibitory system tonically suppresses dendritic Ca<jats:sup>2+<\/jats:sup>spikes, and the L-type Ca<jats:sup>2+<\/jats:sup>channel plays a major role in the generation of Ca<jats:sup>2+<\/jats:sup>spikes and in Ca<jats:sup>2+<\/jats:sup>influx.<\/jats:p>","DOI":"10.1152\/jn.1997.78.5.2269","type":"journal-article","created":{"date-parts":[[2017,12,25]],"date-time":"2017-12-25T06:14:15Z","timestamp":1514182455000},"page":"2269-2279","source":"Crossref","is-referenced-by-count":16,"title":["Properties of Calcium Spikes Revealed During GABA<sub>A<\/sub>Receptor Antagonism in Hippocampal CA1 Neurons From Guinea Pigs"],"prefix":"10.1152","volume":"78","author":[{"given":"Masami","family":"Miura","sequence":"first","affiliation":[{"name":"Department of Physiology, Yamagata University School of Medicine, Yamagata 990-23; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masatomo","family":"Yoshioka","sequence":"additional","affiliation":[{"name":"Department of Physiology, Yamagata University School of Medicine, Yamagata 990-23; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hiroyoshi","family":"Miyakawa","sequence":"additional","affiliation":[{"name":"Laboratory of Life Science, School of Life Science, Tokyo College of Pharmacy, Hachioji 192-03, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hiroshi","family":"Kato","sequence":"additional","affiliation":[{"name":"Department of Physiology, Yamagata University School of Medicine, Yamagata 990-23; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ken-Ichi","family":"Ito","sequence":"additional","affiliation":[{"name":"Department of Physiology, Yamagata University School of Medicine, Yamagata 990-23; and"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1993.sp019838"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/jn.1993.69.6.1966"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.02-11-01614.1982"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/361315a0"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/368823a0"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.15-04-02777.1995"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/jn.1995.73.6.2553"},{"key":"B8","doi-asserted-by":"crossref","first-page":"476","DOI":"10.1016\/S0022-3565(25)32969-1","volume":"220","author":"Connors B. 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