Phasic firing enhances vasopressin release from the rat neurohypophysis

Dutton, Angela; Dyball, R. E. J.

doi:10.1113/jphysiol.1979.sp012781

Cited by 358 publications

(244 citation statements)

References 22 publications

(41 reference statements)

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“…Additionally, comparison of OVX and OVXϩE cells in the a.m. and the p.m. indicated changes in firing rates and patterns associated with estradiol negative and positive feedback, respectively, which were also consistent with the observed changes in LH levels. The relationship between electrical activity and hormone release has been demonstrated in magnocellular neurosecretory cells of the paraventricular (38,39) and supraoptic nuclei (40), as well as the GnRH system (41). Thus, it is likely that the changes observed here are directly related to, and indicative of, the increased GnRH release that is characteristic of the GnRH surge.…”

Section: Discussionmentioning

confidence: 74%

Diurnal and estradiol-dependent changes in gonadotropin-releasing hormone neuron firing activity

Christian

Mobley

Moenter

2005

Proc. Natl. Acad. Sci. U.S.A.

192

213

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A robust gonadotropin-releasing hormone (GnRH) surge is a prerequisite signal for the luteinizing hormone (LH) surge that triggers ovulation. In rodents, the GnRH surge is initiated by elevated estradiol and a diurnal switch in estrogen action from negative to positive feedback. The ability of constant estradiol treatment to induce daily LH surges was tested in adult mice that were ovariectomized (OVX) or OVX and treated with estradiol implants (OVX؉E). LH in OVX mice showed no time-of-day difference. In contrast, OVX؉E mice showed a large LH surge (8-to 124-fold relative to the a.m.) in p.m. samples on d 2-5 post-OVX؉E. Targeted extracellular recordings were used to examine changes in firing activity of GnRH neurons in brain slices. There was no time-of-day difference in cells from OVX mice. In contrast, OVX؉E cells recorded in the p.m. showed an increased mean firing rate and instantaneous firing frequency, which could increase GnRH release, and decreased duration of quiescence between bouts of firing, possibly reflecting increased pulse frequency, compared with cells recorded in the a.m. In the a.m., OVX؉E cells showed changes in GnRH neuron firing reflecting negative feedback compared with OVX cells, whereas in the p.m., OVX؉E cells exhibited changes suggesting positive feedback. These data indicate that differences in pattern and level of individual GnRH neuron firing may reflect the switch in estradiol action and underlie GnRH surge generation. The persistence of altered GnRH neuron activity in slices indicates that this approach can be used to study the neurobiological mechanisms of surge generation.luteinizing hormone ͉ mouse model ͉ surge ͉ electrophysiology ͉ neuroendocrinology

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Section: Discussionmentioning

confidence: 74%

Diurnal and estradiol-dependent changes in gonadotropin-releasing hormone neuron firing activity

Christian

Mobley

Moenter

2005

Proc. Natl. Acad. Sci. U.S.A.

192

213

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“…Increased coupling among oxytocin neurons in lactation is hypothesized to play a role in the synchronization of bursting among these cells that occurs just before each milk ejection during suckling of the pups (Hatton, 1997). The weak coupling (Yang and Hatton, 1988) among vasopressin neurons should not produce synchrony, but it appears to contribute importantly to their phasic bursting patterns of firing, which are eliminated by uncoupling agents (Li et al, 1998), patterns without which vasopressin release is inefficient or lacking (Dutton and Dyball, 1979). NO may influence vasopressin release via its effect on expanding the network of metabolically coupled neurons that fire phasically, although asynchronously.…”

Section: Possible Functional Rolesmentioning

confidence: 99%

Nitric Oxide via cGMP-Dependent Mechanisms Increases Dye Coupling and Excitability of Rat Supraoptic Nucleus Neurons

Yang

Hatton

1999

J. Neurosci.

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Unlike many neuron populations, supraoptic nucleus (SON) neurons are rich in both nitric oxide synthase (NOS) and the NO receptor-soluble guanylyl cyclase (GC), the activation of which leads to cGMP accumulation. Elevations in cGMP result in increased coupling among SON neurons. We investigated the effect of NO on dye coupling in SONs from male, proestrus virgin female, and lactating rats. In 167 slices 263 SON neurons were recorded; 210 of these neurons were injected intracellularly (one neuron per SON) with Lucifer yellow (LY). The typically minimal coupling seen in virgin females was increased nearly fourfold by the NO precursor, L-arginine, or the NO donor, sodium nitroprusside (SNP). L-Arginine-induced coupling was abolished by a NOS inhibitor. In slices from male and lactating rats who have a higher basal incidence of coupling, SNP increased coupling by approximately twofold over control ( p Ͻ 0.03). SNP effects were prevented by the NO scavenger hemoglobin (20 M) and by the selective blocker of NO-activated GC, ODQ (10 M). These results suggest that NO released from cells within the SON can expand the coupled network of neurons and that this action occurs via cGMP-dependent processes. Because increased coupling is associated with elevated SON neuronal excitability, we also studied the effects of 8-bromocGMP on excitability. In both phasically and continuously firing neurons 8-bromo-cGMP (1-2 mM), but not cGMP, produced membrane depolarizations accompanied by membrane conductance increases. Conductance increases remained when depolarizations were eliminated by current-clamping the membrane potential. Thus, NO-induced cGMP increases SON neuronal coupling and excitability. Key words: gap junctions; guanylyl cyclase inhibition; hemoglobin; L-NAME; ODQ; sodium nitroprusside; 8-bromo-cGMPStudies of the distribution of neuronal nitric oxide synthase (NOS) have shown this enzyme to be abundant in the dendrites, somata, and axon terminals of the neurons constituting the magnocellular hypothalamo -neurohypophysial system (Bredt et al., 1990;Dawson et al., 1991). Neurons of this system synthesize, transport, and release either oxytocin or vasopressin, and NOS has been found to be colocalized with both of these peptides (Sanchez et al., 1994). NO is a membrane-permeant neuronal messenger that is produced from L-arginine by the activation of NOS. T ypically, NO release from one cell type finds its way to its receptor, soluble guanylyl cyclase (sGC), in nearby (within 200 M) target cells of another type, activating this enzyme and elevating intracellular cGM P levels (Southam and Garthwaite, 1993;Wood and Garthwaite, 1994). Magnocellular neurons of the paraventricular and supraoptic (SON) nuclei are atypical in that they are rich not only in NOS but also in both the ␣1 and ␤1 subunits of sGC (Furuyama et al., 1993). Because this situation allows for NO activation of sGC within the same neuron as well as between any nearby magnocellular neurons, it is possible that NO plays an autoregulatory role in at least some of th...

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“…Because during lactation AVP neurons are more sensitive to hydric challenges (26), the study was performed on lactating rats to better differentiate AVP from OXY neurons. AVP neurons typically display phasic activity (succession of periods of activity, or ''bursts of spikes,'' and silences) (27,28). During lactation, this phasic pattern is reinforced, and the activation of AVP neurons leads to higher mean values of the activity quotient (Q) (percentage of time spent by the neuron in activity) than are observed in male rats (0.55 Ϯ 0.06 vs. 0.35 Ϯ 0.06 in males, P Ͻ 0.05, n ϭ 23 and 26 neurons, respectively).…”

Section: Electrical Activity Of Son Avp Neurons After Intraventriculamentioning

confidence: 99%

Apelin, a potent diuretic neuropeptide counteracting vasopressin actions through inhibition of vasopressin neuron activity and vasopressin release

Mota

Goazigo²,

Messari³

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

318

352

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Apelin, a recently isolated neuropeptide that is expressed in the supraoptic and the paraventricular nuclei, acts on specific receptors located on vasopressinergic neurons. The increased phasic pattern of these neurons facilitates sustained antidiuresis during dehydration or lactation. Here, we investigated whether apelin interacts with arginine vasopressin (AVP) to maintain body fluid homeostasis. We first characterized the predominant molecular forms of endogenous hypothalamic and plasma apelin as corresponding to apelin 13 and, to a lesser extent, to apelin 17. We then demonstrated that, in lactating rats, apelin was colocalized with AVP in supraoptic nucleus magnocellular neurons and given intracerebroventricularly inhibited the phasic electrical activity of AVP neurons. In lactating mice, intracerebroventricular administration of apelin 17 reduced plasma AVP levels and increased diuresis. Moreover, water deprivation, which increases systemic AVP release and causes depletion of hypothalamic AVP stores, decreased plasma apelin concentrations and induced hypothalamic accumulation of the peptide, indicating that AVP and apelin are conversely regulated to facilitate systemic AVP release and suppress diuresis. Opposite effects of AVP and apelin are likely to occur at the hypothalamic level through autocrine modulation of the phasic electrical activity of AVP neurons. Altogether, these data demonstrate that apelin acts as a potent diuretic neuropeptide counteracting AVP actions through inhibition of AVP neuron activity and AVP release. The coexistence of apelin and AVP in magnocellular neurons, their opposite biological effects, and regulation are likely to play a key role for maintaining body fluid homeostasis.A pelin is a bioactive peptide recently isolated from bovine stomach extracts (1). It was identified as the endogenous ligand of the human orphan G protein-coupled receptor APJ (1, 2), reported to act as a coreceptor of CD4 for human and simian immunodeficiency viruses (3, 4). Apelin is a 36-aa peptide derived from a 77-aa precursor, preproapelin, for which cDNAs have been cloned from humans, cattle, rats, and mice (1, 5, 6). The apelin precursor has a fully conserved C-terminal sequence between Trp-55 to Phe-77, including the C-terminal 17 (Lys-Phe-Arg-ArgGln-Arg-Pro-Arg-Leu-Ser-His-Lys-Gly-Pro-Met-Pro-Phe; K17F) and 13 (Gln-Arg-Pro-Arg-Leu-Ser-His-Lys-Gly-Pro-Met-Pro-Phe; Q13F) amino acid sequences. These molecular species, and the pyroglutamyl form of Q13F (pE13F), exhibit the highest activities on extracellular acidification rate (1) and strongly inhibit forskolinstimulated cAMP production in Chinese hamster ovary (CHO) cells expressing the human (5,7,8) or the rat (9) apelin receptor. These peptides also are highly potent inducers of rat apelin receptor internalization (10,11).In situ hybridization and RT-PCR studies have shown that the apelin precursor and apelin receptor mRNAs are expressed in various rat brain structures (6,8,9,12,13). Apelin-immunoreactive (IR) neurons are particularly abundant in ...

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Phasic firing enhances vasopressin release from the rat neurohypophysis

Cited by 358 publications

References 22 publications

Diurnal and estradiol-dependent changes in gonadotropin-releasing hormone neuron firing activity

Diurnal and estradiol-dependent changes in gonadotropin-releasing hormone neuron firing activity

Nitric Oxide via cGMP-Dependent Mechanisms Increases Dye Coupling and Excitability of Rat Supraoptic Nucleus Neurons

Apelin, a potent diuretic neuropeptide counteracting vasopressin actions through inhibition of vasopressin neuron activity and vasopressin release

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