Effects of Tetrodotoxin on Osmotically Stimulated Central and Peripheral Vasopressin and Oxytocin Release

Ludwig, Mike; Callahan, Michael F.; Morris, Mariana

doi:10.1159/000127058

Cited by 51 publications

(32 citation statements)

References 31 publications

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“…2, in Shahar et al, 2004). In this regard, it is interesting to note that osmotically stimulated OXT and AVP release is also blocked by application of TTX to the HNS (Ludwig et al, 1995) and that the expected increased in Avp hnRNA under these conditions is also inhibited (see Fig. 1D in this paper).…”

Section: Discussionmentioning

confidence: 51%

Experimental approaches for the study of oxytocin and vasopressin gene expression in the central nervous system

Scordalakes

Yue

Gainer

2008

Progress in Brain Research

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Intron-specific probes measure heteronuclear RNA (hnRNA) levels and thus approximate the transcription rates of genes, in part because of the rapid turnover of this intermediate form of RNA in the cell nucleus. Previously, we used oxytocin (Oxt)-and vasopressin (Avp)-intron-specific riboprobes to measure changes in Oxt and Avp hnRNA levels in the supraoptic nucleus (SON) by quantitative in situ hybridization (ISH) after various classical physiological perturbations, including acute and chronic salt loading, and lactation. In the present experiments, we used a novel experimental model to study the neurotransmitter regulation of Oxt and Avp gene expression in the rat SON in vivo. Bilateral cannulae connected via tubing to Alzet osmotic mini-pumps were positioned over the SON. In every experiment, one SON was infused with PBS and served as the control SON in each animal, and the contralateral SON received infusions of various neurotransmitter agonists and antagonists. Using this approach, we found that Avp but not Oxt gene expression increased after acute (2-5 h) combined excitatory amino acid agonist and GABA antagonist treatment, similar to what we found after an acute hyperosmotic stimulus. Since both OXT and AVP are known to be comparably and robustly secreted in response to acute osmotic stimuli in vivo and glutamate agonists in vitro, our results indicate a dissociation between OXT secretion and Oxt gene transcription in vivo.

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Section: Discussionmentioning

confidence: 51%

Experimental approaches for the study of oxytocin and vasopressin gene expression in the central nervous system

Scordalakes

Yue

Gainer

2008

Progress in Brain Research

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“…2) Although experimental evidence from in vitro or electronmicroscopic studies is missing, OXT may directly act at the dendritic level to locally inhibit exocytotic processes related to AVP release. A dissociation of dendritic release and the electrical activity of neuropeptidergic neurons has been established (11,36). 3) Alternatively, OXT could modulate excitatory or inhibitory inputs to AVP neurons identified preor postsynaptically within the SON (7,8; for a review, see Ref.…”

Section: Discussionmentioning

confidence: 99%

“…It demonstrates the ability of neuronal cells to independently regulate neuropeptide release from various neuronal elements (axon terminals vs. dendrites and somata). With respect to dendritic release, it has been revealed that intrahypothalamic neuropeptide release can occur independently of the electrical activity (11,36), which is required for axonal neuropeptide secretion. Furthermore, locally released neurotransmitters/neuromodulators, including AVP itself (21,63), GABA (17,28,29) and taurine (15,26,52) were recently considered to regulate basal and stimulated activity of neurohypophyseal AVP (and also OXT) neurons and, thus, AVP secretion into blood.…”

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confidence: 99%

Oxytocin actions within the supraoptic and paraventricular nuclei: differential effects on peripheral and intranuclear vasopressin release

Neumann¹,

Torner²,

Toschi³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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(FS), AVP is released somato-dendritically within the supraoptic nucleus (SON) and paraventricular nucleus (PVN), but not from neurohypophyseal terminals into blood. Together with AVP, oxytocin (OXT) is released within the SON and PVN. Here, we studied the role of intra-SON and intra-PVN OXT in the regulation of local AVP release and into the blood in male rats. Within the SON, bilateral retrodialysis of an OXT receptor antagonist (OXT-A) increased local AVP release in response to FS [60 s, 21°C, vehicle twofold, not significant (ns); OXT-A: 15-fold increase, P Ͻ 0.05] without significantly affecting basal AVP release. In addition, local OXT-A elevated plasma AVP secretion under basal conditions (twofold increase, P Ͻ 0.05) without further elevation after FS. Within the PVN, exposure to FS elevated local AVP release, reaching significance only in the OXT-A group (vehicle: 1.4-fold, ns; OXT-A: 1.6-fold increase, P ϭ 0.050). Bilateral OXT-A into the PVN did not affect peripheral AVP secretion either under basal or stress conditions. Basal ACTH concentrations tended to be elevated by local OXT-A within the PVN (1.7-fold increase, P ϭ 0.076). In contrast, the swim-induced ACTH secretion was attenuated after retrodialysis of OXT-A within both the SON (at 5 min) and PVN (at 15 min) (P Ͻ 0.05 both) compared with vehicle. The results demonstrate a receptormediated effect of OXT within the SON and PVN on local and neurohypophyseal AVP release, which depends upon the activity conditions. Further, while exerting an inhibitory effect on hypothalamo-pituitary-adrenal axis activity under basal conditions, hypothalamic OXT is essential for an adequate acute ACTH response.plasma; hypothalamo-pituitary-adrenal axis; dendritic release; microdialysis; swim stress THE NEUROPEPTIDES OXYTOCIN (OXT) and AVP are mainly synthesized in magnocellular neurons of the hypothalamic supraoptic nucleus (SON) and the paraventricular nucleus (PVN). They are released from neurohypophyseal axon terminals directly into the systemic circulation, but also in a somatodendritic fashion within the hypothalamus in response to relevant physiological stimuli, including parturition, suckling, osmotic challenge, and hemorrhage (for a review, see Ref. 33).Similarly, such local release within the SON and PVN has been described for both peptides, for instance, in response to various psychological stressors, such as forced swimming in male and female rats (for a review, see Ref. 16). However, upon stressor exposure, only OXT is simultaneously released from the dendrites within the hypothalamic nuclei and from neurohypophyseal terminals into blood, as revealed by intracerebral microdialysis in conjunction with blood sampling in conscious rats. In contrast, AVP secretion into blood remains unchanged despite its release within the PVN, SON, and/or septum, for example, during forced swimming or exposure to social defeat (13,14,44,60,61).The phenomenon of independent release patterns of AVP from dendrites within the SON/PVN and from neurohypophyseal terminals, in par...

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“…The reverse treatment, chronic hypernatremia, did not alter the survival of the axotomized MCNs in one study (Dohanics et al, 1996); however, in another study that used a chronic intermittent saltloading paradigm, there was an increase in the survival of MCN cells (Huang and Dellmann, 1996). In view of these reports, we tested the hypothesis that after axotomy, neural activity was neuroprotective in the HNS by directly inhibiting both electrical and synaptic activity unilaterally in the SON by local superfusion of TTX (Ludwig et al, 1995) in vivo. Each animal's contralateral SON served as the (noninhibited) control in these experiments.…”

Section: Discussionmentioning

confidence: 99%

Neural Activity Protects Hypothalamic Magnocellular Neurons against Axotomy-Induced Programmed Cell Death

Shahar¹,

House²,

Gainer³

2004

J. Neurosci.

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Axotomy typically leads to retrograde neuronal degeneration in the CNS. Studies in the hypothalamo-neurohypophysial system (HNS) have suggested that neural activity is supportive of magnocellular neuronal (MCN) survival after axotomy. In this study, we directly test this hypothesis by inhibiting neural activity in the HNS, both in vivo and in vitro, by the use of tetrodotoxin (TTX). After median eminence compression to produce axonal injury, unilateral superfusion of 3 M TTX into the rat supraoptic nucleus (SON), delivered with the use of a miniature osmotic pump for 2 weeks in vivo, produced a decrease in the number of surviving MCNs in the TTX-treated SON, compared with the contralateral untreated side of the SON. In vitro application of 2.5 M TTX for 2 weeks to the SON in organotypic culture produced a 73% decrease in the surviving MCNs, compared with untreated control cultures. Raising the extracellular KCl in the culture medium to 25 mM rescued the MCNs from the axotomy-and TTX-induced cell death. These data support the proposal that after axotomy, neural activity is neuroprotective in the HNS.

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Effects of Tetrodotoxin on Osmotically Stimulated Central and Peripheral Vasopressin and Oxytocin Release

Cited by 51 publications

References 31 publications

Experimental approaches for the study of oxytocin and vasopressin gene expression in the central nervous system

Experimental approaches for the study of oxytocin and vasopressin gene expression in the central nervous system

Oxytocin actions within the supraoptic and paraventricular nuclei: differential effects on peripheral and intranuclear vasopressin release

Neural Activity Protects Hypothalamic Magnocellular Neurons against Axotomy-Induced Programmed Cell Death

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