Depolarizing action of cholecystokinin on rat supraoptic neurones in vitro.

Abstract

SUMMARY1. Cholecystokinin is co-localized within the oxvtocin-and, to a lesser extent, vasopressin-synthesizing magnocellular neurones in the hypothalamic supraoptic anid paraventricular nuclei. These nuclei are also protminent binding sites for cholecystokinin. In the present study we used in-tracellular current-and voltageclamp recordings from fifty-seven supraoptic nucleus cells, inaintained in superfused explants of rat hypothalamus, to assess their membrane responses to exogenous cholecystokinin and define the nature of their cholecystokinin receptors.2. In a majority of the fifty-seven cells tested, bolus infuisions into the superfusion media of cholecystokinin fragments (maximum concentrations estimated at 0(3-15 AM) were

Direct hypertonic stimulation of the rat supraoptic nucleus increases c-fos expressionin glial cells rather than magnocellular neurones

“…We have previously shown that CCK microinjected into the SON stimulates release of OT within the SON, as well as from the posterior pituitary (Neumann et al 1994). When applied directly CCK excites the firing rate of both OT and VP SON neurones (Jarvis et al 1992), so the expression of Fos induced in the present study could be a result of activation of a particular post-CCK receptor mechanism, since the excitation by direct hypertonic stimulation was ineffective.…”

“…To further test responsiveness of the c-fos gene in SON neurones, the effect of peripheral hypertonic stimulation and of microinjection of cholecystokinin-8S (CCK) into the SON were studied. CCK acts directly on SON neurones to increase their firing rate (Jarvis et al 1992) and their secretory activity, including release within the SON (Neumann et al 1994). A group of lactating rats was included, since glial cells are involved in the reorganisation of the SON in lactation (Tweedle and Hatton 1982;Theodosis and Poulain 1984), to examine whether this affected their responsiveness to direct hypertonic stimulation.…”

Cholecystokinin Increases GABA Release by Inhibiting a Resting K+Conductance in Hippocampal Interneurons

“…Also, Cox et al (1995) reported the inhibition of a voltage-independent K ϩ leak current by CCK-8S in rat reticular thalamic neurons. In addition to this mechanism, CCK can produce membrane depolarization, associated with a decrease in membrane resistance, through activation of a nonselective cation conductance (Dodd and Kelly, 1981;Jarvis et al, 1992;Wu and Wang, 1996a,b). However, in the present study we did not observe CCK-activated currents with reversal potentials consistent with this mechanism.…”

“…Both receptors couple to G-proteins (Wank et al, 1994), and their relative distributions in the CNS and peripheral nervous system correlate well with CCK immunoreactivity (Dockray, 1987;Hays et al, 1980;Innis and Snyder, 1980). Cholecystokinin receptors have been shown to interact with several different cellular transduction systems in central and peripheral tissues, including the activation of phospholipase C (Kuwahara et al, 1993;Lee et al, 1993;Wu and Wang, 1996b), the modulation of potassium and calcium channels (Boden and Hill, 1988;Buckett and Saint, 1989;Miyoshi et al, 1991;Branchereau et al, 1993;Cox et al, 1995;Liu et al, 1995), and activation of nonselective cation channels (Dodd and Kelly, 1981;Jarvis et al, 1992).…”

Opioid tolerance and dependence in the magnocellular oxytocin system: a physiological mechanism?

“…In this respect, CCK has an excitatory action on supraoptic oxytocin (and vasopressin) neurones in vitro (Jarvis, Bourque & Renaud, 1992). Whether such an action of CCK, perhaps released from the dendrites of oxytocin neurones, is pronounced in morphine tolerance remains to be investigated.…”