Identification of oxytoxin cells in the rat supraoptic nucleus by their response to cholecystokinin injection

Leng, Gareth; Way, Stanley; Dyball, R. E. J.

doi:10.1016/0304-3940(91)90847-m

Cited by 62 publications

(46 citation statements)

References 11 publications

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“…Selective effects of peripherally administered CCK on the activity of central neurons have been described previously (26). Leng et al (26) reported that CCK differentially influenced the discharge of neurons in the supraoptic nucleus of hypothalamus.…”

Section: Discussionmentioning

confidence: 82%

“…A change in discharge rate in response to CCK was measured by comparing the resting level of discharge prior to CCK administration with the discharge rate directly corresponding to the nadir of the depressor response. The doses of CCK were chosen on the basis of previous reports (26,31,41) and also by performing preliminary experiments that determined the threshold for the effects of CCK on arterial blood pressure, RVLM unit discharge, and sympathetic nerve discharge.…”

Section: Methodsmentioning

confidence: 99%

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Cholecystokinin selectively affects presympathetic vasomotor neurons and sympathetic vasomotor outflow

Sartor

Verberne

2002

American Journal of Physiology-Regulatory, Integrative and Comp

102

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To determine whether CCK influences sympathetic vasomotor function, we examined the effect of systemic CCK administration on mean arterial blood pressure (MAP), heart rate (HR), lumbar sympathetic nerve discharge (LSND), splanchnic sympathetic nerve discharge (SSND), and the discharge of presympathetic neurons of the rostral ventrolateral medulla (RVLM) in ␣-chloralose-anesthetized rats. CCK (1-8 g/kg iv) reduced MAP, HR, and SSND and transiently increased LSND. Vagotomy abolished the effects of CCK on MAP and SSND as did the CCK-A receptor antagonist devazepide (0.5 mg/kg iv). The bradycardic effect of CCK was unaltered by vagotomy but abolished by devazepide. CCK increased superior mesenteric arterial conductance but did not alter iliac conductance. CCK inhibited a subpopulation (ϳ49%) of RVLM presympathetic neurons whereas ϳ28% of neurons tested were activated by CCK. The effects of CCK on RVLM neuronal discharge were blocked by devazepide. RVLM neurons inhibited by exogenous CCK acting via CCK-A receptors on vagal afferents may control sympathetic vasomotor outflow to the gastrointestinal tract vasculature. blood pressure; splanchnic sympathetic nerve; lumbar sympathetic nerve; rat CHOLECYSTOKININ (CCK) is a gastrointestinal hormone with actions including gastrointestinal vasodilatation (18), reduced gut motility, gastric acid secretion, and pancreatic secretion (3, 28). In the central nervous system, it is one of the most abundant neuropeptides, probably playing a major role in satiety as well as anxiety-related behavior (6, 38). Of the two types of CCK receptors, the A-type (CCK-A receptor) is predominantly found in the periphery, although it is also present in discrete brain regions and has a higher affinity for the sulfated octapeptide form of CCK. In the brain, the B-type receptor (CCK-B receptor) predominates and has a high affinity for both the sulfated and nonsulfated forms of CCK (13).Peripherally, CCK has been implicated in postprandial intestinal hyperemia because systemic administration of the peptide produces intestinal vasodilatation (18). In contrast, its effects on the vascular resistance of forelimb, skin, or muscle have been found to be negligible (10), suggesting that the actions of CCK may target specific vascular beds.CCK receptors are located on vagal afferents (11, 35) and in the nucleus of solitary tract (NTS) (7, 35), a major site of termination of vagal afferents. Although peptides generally do not permeate the blood-brain barrier, CCK may potentially act on neurons of the area postrema, a circumventricular organ with neuronal cell bodies lying outside the blood brain barrier but with projections to several areas within the brain (6). There are also regions within the NTS and the dorsal nucleus of vagus nerve that have altered blood-brain barrier properties potentially facilitating the access of peptides such as CCK (6). Thus CCK may act either directly on the central nervous system to influence sympathetic vasomotor function and/or peripherally via vagal afferent fibers, conveying ...

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Section: Discussionmentioning

confidence: 82%

Section: Methodsmentioning

confidence: 99%

Cholecystokinin selectively affects presympathetic vasomotor neurons and sympathetic vasomotor outflow

Sartor

Verberne

2002

American Journal of Physiology-Regulatory, Integrative and Comp

102

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“…In agreement with the higher levels of NO IF and cGMPir found in VP neurones, blockade of NO production with 7-NI, a relatively specific blocker of the nNOS isoform (Moore et al 1993;MacKenzie et al 1994), resulted in a stronger excitation in phasically active as compared to continuously active MNCs. While the expression of phasic and continuous firing patterns in vivo distinguishes VP from OT neurones, respectively (Poulain & Wakerley, 1982;Leng et al 1991), the use of firing patterns to classify MNCs in vitro is more conflicting. While the expression of phasic activity in vitro is still a consistent feature found in the majority of VP neurones (Yamashita et al 1983;Cobbett et al 1986;Armstrong et al 1994), continuous activity, though more often associated with OT neurones (Yamashita et al 1987;Yang & Hatton, 1994), does not conclusively differentiate between the two (Armstrong, 1995).…”

Section: Basally Produced No Modulates Ongoing Firing Activity Of Sonmentioning

confidence: 99%

Cellular sources, targets and actions of constitutive nitric oxide in the magnocellular neurosecretory system of the rat

Stern

Zhang

2005

The Journal of Physiology

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Nitric oxide (NO) is a key activity-dependent modulator of the magnocellular neurosecretory system (MNS) during conditions of high hormonal demand. In addition, recent studies support the presence of a functional consitutive NO tone. The aim of this study was to identify the cellular sources, targets, signalling mechanisms and functional relevance of constitutive NO production within the supraoptic nucleus (SON). Direct visualization of intracellular NO, along with neuronal nitric oxide synthase (nNOS) and cGMP immunohistochemisty, was used to study the cellular sources and targets of NO within the SON, respectively. Our results support the presence of a strong NO basal tone within the SON, and indicate that vasopressin (VP) neurones constitute the major neuronal source and target of basal NO. NO induced-fluorescence and cGMP immunoreactivity (cGMPir) were also found in the glia and microvasculature of the SON, suggesting that they contribute as sources/targets of NO within the SON. cGMPir was also found in association with glutamic acid decarboxylase 67 (GAD67)-and vesicular glutamate transporter 2 (VGLUT2)-positive terminals. Glutamate, acting on NMDA and possibly AMPA receptors, was found to be an important neurotransmitter driving basal NO production within the SON. Finally, electrophysiological recordings obtained from SON neurones in a slice preparation indicated that constitutive NO efficiently restrains ongoing firing activity of these neurones. Furthermore, phasically active (putative VP) and continuously firing neurones appeared to be influenced by NO originating from different sources. The potential roles for basal NO as an autocrine signalling molecule, and one that bridges neuronal-glial-vascular interactions within the MNS are discussed.

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“…The lack of a strict association of neurones with DAPs and spike clustering over this time frame suggests another mechanism is involved. In vivo, continuous activity can characterize both cell types, as judged by the response to stimuli selective for VP or OT release or inhibition (Brimble & Dyball, 1977;Poulain et al 1977;Renaud et al 1987;Leng et al 1991;, but is more characteristic of putative OT neurones. Typically, putative VP neurones exhibit this behaviour either in transition to phasic bursting, injection, and double-labelled seven of these ten with an A few of the OT neurones exhibiting a DAP in this study could be made to fire phasically in a manner similar to VP neurones by adjusting membrane potential.…”

Section: Firing Patterns Of Ot and Vp Neuronesmentioning

confidence: 99%

“…This tradition, based so strongly on the earlier, elegant studies in vivo of Wakerley and others (Poulain & Wakerley, 1982), has perhaps placed undue importance on a single facet of a cell's behaviour for in vitro studies, and this behaviour, which in the whole animal is under the complex control of a mixture of synaptic inputs and intrinsic membrane properties, may not be as selectively expressed in a significant percentage of neurones in vitro, at least, certainly not at all times. Even in vivo, physiological tests may yield ambiguous results for 10-15 % of the neurones (Leng et al 1991). It has recently been possible to record intracellularly, albeit briefly, from supraoptic neurones in vivo (Dyball, Tasker, Wuarin & Dudek, 1991; Bourque &G , and an understanding of the differences in synaptic inputs between the two cells could be forthcoming with improvements in this technique.…”

Section: Firing Patterns Of Ot and Vp Neuronesmentioning

confidence: 99%

Electrophysiological characteristics of immunochemically identified rat oxytocin and vasopressin neurones in vitro.

Armstrong¹,

Smith²,

Tian³

1994

The Journal of Physiology

158

174

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1. Intracellular recordings were made from supraoptic neurones in vitro from hypothalamic explants prepared from adult male rats. Neurones were injected with biotinylated markers, and of thirty-nine labelled neurones, nineteen were identified immunocytochemically as containing oxytocin-neurophysin and twenty as containing vasopressin-neurophysin. 2. Vasopressin and oxytocin neurones did not differ in their resting membrane potential, input resistance, membrane time constant, action potential height from threshold, action potential width at half-amplitude, and spike hyperpolarizing after-potential amplitude. Both cell types exhibited spike broadening during brief, evoked spike trains (6-8 spikes), but the degree of broadening was slightly greater for vasopressin neurones. When hyperpolarized below -75 mV, all but one neurone exhibited a transient outward rectification to depolarizing pulses, which delayed the occurrence of the first spike.3. Both cell types exhibited a long after-hyperpolarizing potential (AHP) following brief spike trains evoked either with a square wave pulse or using 5 ms pulses in a train. There were no significant differences between cell types in the size of the AHP evoked with nine spikes, or in the time constant of its decay. The maximal AHP evoked by a 180 ms pulse was elicited by an average of twelve to thirteen spikes, and neither the size of this maximal AHP nor its time constant of decay were different for the two cell types.4. In most oxytocin and vasopressin neurones the AHP, and concomitantly spike frequency adaptation, were markedly reduced by the bee venom apamin and by d-tubocurarine, known blockers of a Ca2+-mediated K+ conductance. However, a minority of neurones, of both cell types, were relatively resistant to both agents.

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Identification of oxytoxin cells in the rat supraoptic nucleus by their response to cholecystokinin injection

Cited by 62 publications

References 11 publications

Cholecystokinin selectively affects presympathetic vasomotor neurons and sympathetic vasomotor outflow

Cholecystokinin selectively affects presympathetic vasomotor neurons and sympathetic vasomotor outflow

Cellular sources, targets and actions of constitutive nitric oxide in the magnocellular neurosecretory system of the rat

Electrophysiological characteristics of immunochemically identified rat oxytocin and vasopressin neurones in vitro.

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