1. Intracellular recordings were obtained from seventy‐two magnocellular neurosecretory cells (MNCs) in superfused explants of rat hypothalamus. The current underlying the after‐hyperpolarization (IAHP) following spike‐evoked trains of action potentials was characterized using the hybrid‐clamp technique. The activity‐dependent requirements for the genesis of the AHP were determined. The functional role of the conductance was investigated using saturating concentrations (50‐300 nM) of apamin, a selective blocker of the AHP in MNCs. 2. IAHP was reversibly abolished by the removal of extracellular Ca2+. The amplitude of IAHP varied linearly as a function of voltage and reversed at ‐100 +/‐ 3 mV in 3 mM external K+. Changes in the concentration of extracellular K+ resulted in shifts of the reversal potential consistent with Nernst equation predictions for a K+‐selective conductance. 3. Action potentials triggered by brief depolarizing pulses elicited an AHP during trains evoked at frequencies > 1 Hz. Onset of the AHP progressed exponentially, reaching a maximum after the first fifteen to twenty impulses. The steady‐state amplitude of the AHP increased logarithmically between 1 and 20 Hz. 4. Switching to voltage clamp during periods of continuous cell activity (firing rate > 4 Hz) confirmed the presence of an apamin‐sensitive Ca2(+)‐dependent K+ current. 5. Application of apamin produced a threefold increase in the mean firing rate of spontaneously active cells, but was without effect when applied to silent cells (firing rate < 0.5 Hz). 6. Apamin did not affect the ability of MNCs to fire in a phasic manner but caused a dramatic increase in the mean intraburst firing rate. Moreover, inhibition of IAHP by apamin strongly attenuated spike accommodation normally seen at the onset of phasic bursts. 7. While apamin did not enhance the amplitude of depolarizing after‐potentials following single spikes, post‐train plateau potentials and associated after‐discharges were enhanced. 8. The possible consequences of IAHP modulation are discussed in the context of the regulation of firing rate and pattern in MNCs.

1. The electrophysiological actions of neurotensin on magnocellular neurosecretory cells (MNCs) were examined during intracellular recording from seventy-three supraoptic nucleus neurones in superfused explants of rat hypothalamus. 2. Application of neurotensin tridecapeptide (NT(1-13); 1 nM to 3 mu M) caused a membrane depolarization and reversibly attenuated the after-hyperpolarization (AHP) which followed current-evoked spike trains. This effect was accompanied by increased firing frequency during depolarizing current pulses evoked from a fixed potential. 3. The effects of neurotensin could be mimicked by the C-terminal fragment, NT(8-13), but not by the N-terminal fragment, NT(1-8). 4. Depolarizing responses to NT(1-13) or NT(8-13), retained during K+ channel blockade with internal Cs+, were accompanied by increased membrane conductance. Current- and voltage-clamp analyses revealed that neurotensin-evoked depolarizations result partly from the activation of a non-selective cationic conductance reversing near -34 mV. 5. Depolarizing responses to neurotensin were retained in the presence of TTX or in Ca2+ free solutions, indicating the involvement of receptors located on the plasma membrane of MNCs themselves. 6. Through these effects endogenously released neurotensin may modulate excitability,activity patterns and secretion from the hypothalamo-neurohypophysial axis.

Annals of the New York Academy of SciencesVolume 689, Issue 1 p. 512-519 Extrinsic and Intrinsic Modulatory Mechanisms Involved in Regulating the Electrical Activity of Supraoptic Neuronsa C. W. BOURQUE, C. W. BOURQUE Center for Research in Neuroscience Montreal General Hospital and McGill University 1650 Cedar Avenue Montreal, Quebec H3G 1A4 CanadaSearch for more papers by this authorS. H. R. OLIET, S. H. R. OLIET Center for Research in Neuroscience Montreal General Hospital and McGill University 1650 Cedar Avenue Montreal, Quebec H3G 1A4 CanadaSearch for more papers by this authorK. KIRKPATRICK, K. KIRKPATRICK Center for Research in Neuroscience Montreal General Hospital and McGill University 1650 Cedar Avenue Montreal, Quebec H3G 1A4 CanadaSearch for more papers by this authorD. RICHARD, D. RICHARD Center for Research in Neuroscience Montreal General Hospital and McGill University 1650 Cedar Avenue Montreal, Quebec H3G 1A4 CanadaSearch for more papers by this authorT. E. FISHER, T. E. FISHER Center for Research in Neuroscience Montreal General Hospital and McGill University 1650 Cedar Avenue Montreal, Quebec H3G 1A4 CanadaSearch for more papers by this author C. W. BOURQUE, C. W. BOURQUE Center for Research in Neuroscience Montreal General Hospital and McGill University 1650 Cedar Avenue Montreal, Quebec H3G 1A4 CanadaSearch for more papers by this authorS. H. R. OLIET, S. H. R. OLIET Center for Research in Neuroscience Montreal General Hospital and McGill University 1650 Cedar Avenue Montreal, Quebec H3G 1A4 CanadaSearch for more papers by this authorK. KIRKPATRICK, K. KIRKPATRICK Center for Research in Neuroscience Montreal General Hospital and McGill University 1650 Cedar Avenue Montreal, Quebec H3G 1A4 CanadaSearch for more papers by this authorD. RICHARD, D. RICHARD Center for Research in Neuroscience Montreal General Hospital and McGill University 1650 Cedar Avenue Montreal, Quebec H3G 1A4 CanadaSearch for more papers by this authorT. E. FISHER, T. E. FISHER Center for Research in Neuroscience Montreal General Hospital and McGill University 1650 Cedar Avenue Montreal, Quebec H3G 1A4 CanadaSearch for more papers by this author First published: July 1993 https://doi.org/10.1111/j.1749-6632.1993.tb55581.xCitations: 18 a This work was supported by the Medical Research Council of Canada. T. E. F. and K. K. are, respectively, recipients of a Fellowship and Studentship from FCAR. D. R. and S. H. R. O. are recipients of Studentships from the Heart and Stroke Foundation of Canada. C. W. B. is a Medical Research Council Scientist. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL References 1 Poulain, D. A. & J. B. Wakerley. 1982. Neuroscience 7: 773– 808. 2 Wakerley, J. B. & D. W. Lincoln. 1973. J. Endocrinol. 57: 477– 493. 3 Wakerley, J. B., D. A. Poulain & D. Brown. 1978. Brain Res. 148: 425– 440. 4 Bicknell, R. J. 1988. J. Exp. Biol. 139: 51– 65. 5 Bourque, C. W. 1991. Trends Neurosci. 14: 28– 30. 6 Bourque, C. W. & L. P. Renaud. 1991. Front. Neuroendocrinol. 11: 183– 212. 7 Bourque, C. W. & L. P. Renaud. 1991. Brain Res. 540: 349– 352. 8 Bourque, C. W. 1990 In Preparations of Vertebrate Central Nervous System in Vitro. H. Jahnsen, Ed.: 203– 232. John Wiley & Sons. Chichester . 9 Oliet, S. H. R. & C. W. Bourque. 1992. J. Physiol. 455: 291– 306. 10 Bourque, C. W., J. C. R. Randle & L. P. Renaud. 1985. J. Neurophysiol. 54: 1375– 1382. 11 Bourque, C. W. 1986. Neurosci. Lett. 70: 204– 209. 12 Bourque, C. W. 1987 In Organization of the Autonomic Nervous System: Central and Peripheral Mechanisms. J. Ciriello, F. R. Calaresu, L. P. Renaud & C. Polosa, Eds.: 387– 396. Alan R. Liss. New York . 13 Nowycky, M. C., A. P. Fox & R. W. Tsien. 1985. Nature 316: 440– 443. 14 Bourque, C. W. 1988. J. Physiol. 397: 331– 347. 15 Bourque, C. W. 1988. Soc. Neurosci. Abs. 14: p1089. 16 Kirkpatrick, K. & C. W. Bourque. 1991. Soc. Neurosci Abs. 17: p1188. 17 Leng, G., W. T. Mason & R. G. Dyer. 1982. Neuroendocrinology 34: 75– 82. 18 Mason, W. T. 1980. Nature 287: 154– 157. 19 Bourque, C. W. 1989. J. Physiol. 417: 263– 277. 20 Thrasher, T. N. & L. C. Keil. 1987. Am. J. Physiol. 253: R108– 120. 21 Richard, D. & C. W. Bourque. 1992. Neuroendocrinology 55: 609– 611. Citing Literature Volume689, Issue1The Neurohypophysis: A Window on Brain FunctionJuly 1993Pages 512-519 ReferencesRelatedInformation

Magnocellular neurosecretory cells (MNCs) display activity-dependent changes in spike duration to modulate Ca2+ influx both in their somata, and in their axon terminals in the neurohypophysis. This study reveals (i) that Ca2+ influx is required to mediate the expression of spike broadening, and (ii) that internal Ca2+ activates a delayed component of spike repolarization in MNCs of the rat supraoptic nucleus. This mechanism provides a rapid feedback control of spike-mediated Ca2+ influx in these neuroendocrine cells.