Tolerance to Acute Ethanol Inhibition of Peptide Hormone Release in the Isolated Neurohypophysis

Knott, Thomas; Dayanithi, Govindan; Coccia, Vincent; Custer, Edward E.; Lemos, Jos?? R.; Treistman, Steven N.

doi:10.1097/00000374-200007000-00020

Cited by 9 publications

(10 citation statements)

References 10 publications

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“…As expected TRH secretion was stimulated by cell swelling (Najvirtova et al, 2002(Najvirtova et al, , 2003Kiss et al, 2005), while oxytocin, neurohormone engaged in water and salt regulation, was not released after cell swelling-inducing stimulus (Najvirtova et al, 2003). This is in good agreement with observations that ethanol inhibits the release of oxytocin from the posterior pituitary induced by high K + (Knott et al, 2000) or suckling (Subramanian, 1999) and that hypotonic stimuli hyperpolarize magnocellular neurosecretory cells via stretchinactivated channels (Bourque and Oliet, 1997). Excitatory effects of some peptides in these cells are also due to stimulation of stretch-inactivated channels (Chakfe and Bourque, 2000).…”

Section: Introductionsupporting

confidence: 84%

The Effect of Swelling on TRH and Oxytocin Secretion From Hypothalamic Structures

et al. 2006

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1. Cell swelling induces exocytosis of material stored in secretory vesicles resulting in a secretory burst of peptidic hormones or enzymes from various types of cells including endocrine cells and neurons. We have previously shown that swelling-induced exocytosis possesses limited selectivity; hypotonic medium evokes TRH but not oxytocin release from hypothalamic paraventricular nucleus (PVN) and neurohypophysis (NH). 2. It is the aim of this study to ascertain whether the swelling-induced oxytocin secretion could be unmasked by the inhibition of specific osmotic response using Ca(2+)-free medium and GdCl(3), an inhibitor of stretch activated channels. 3. Oxytocin release from the PVN was stimulated by the hypotonic medium only in the presence of 50 or 100 microM GdCl(3.) Oxytocin release from supraoptic nucleus (SON) was also stimulated by the Ca(2+)-free hypotonic medium in the presence of GdCl(3). Oxytocin secretion from the NH was not stimulated even in the presence of GdCl(3), both in Ca(2+) containing and Ca(2+)-free medium. TRH response to swelling-inducing stimulus was not affected by the presence of GdCl(3). 4. An intranuclear oxytocin secretion to hyposmotic stimulation within the PVN and the SON could be unmasked by the inhibiting specific response by GdCl(3). At these conditions general secretory response to swelling-inducing stimuli emerged. Secretion of oxytocin from the NH was not affected by any of these treatments. 5. Peptides and proteins released after cell swelling can play an important role in the pathophysiology of ischemia and could be mediators of local or remote preconditioning. Disruption of mechanosensitive gating in magnocellular neurosecretory cells could result in an inadequate secretory response (e.g. stimulation instead of inhibition and vice versa) of hormones engaged in water and salt metabolism regulation.

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Section: Introductionsupporting

confidence: 84%

The Effect of Swelling on TRH and Oxytocin Secretion From Hypothalamic Structures

et al. 2006

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“…Plasma levels of AVP and OT in animals, including humans, are depressed after acute exposure to ethanol, increasing diuresis. These phenomena appear to reflect ethanol's inhibition of AVP release, which can be observed in vitro (Knott et al, 2000). However, animals previously exposed to an ethanol-containing diet develop tolerance to acute ethanol-induced reduction of AVP and OT release.…”

Section: Alcohol Tolerance In Bk Channels Of Neuronal Terminalsmentioning

confidence: 91%

“…The NH consists of numerous MCN terminals, from which 2 peptide hormones, arginine-vasopressin (AVP, also known as antidiuretic hormone) and oxytocin (OT), are released. The release of these hormones is modulated by ethanol (Knott et al, 2000). Plasma levels of AVP and OT in animals, including humans, are depressed after acute exposure to ethanol, increasing diuresis.…”

Section: Alcohol Tolerance In Bk Channels Of Neuronal Terminalsmentioning

confidence: 99%

Actions of Acute and Chronic Ethanol on Presynaptic Terminals

Roberto

Treistman

Pietrzykowski

et al. 2006

Alcoholism Clin & Exp Res

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This article presents the proceedings of a symposium entitled "The Tipsy Terminal: Presynaptic Effects of Ethanol" (held at the annual meeting of the Research Society on Alcoholism, in Santa Barbara, CA, June 27, 2005). The objective of this symposium was to focus on a cellular site of ethanol action underrepresented in the alcohol literature, but quickly becoming a "hot" topic. The chairs of the session were Marisa Roberto and George Robert Siggins. Our speakers were chosen on the basis of the diverse electrophysiological and other methods used to discern the effects of acute and chronic ethanol on presynaptic terminals and on the basis of significant insights that their data provide for understanding ethanol actions on neurons in general, as mechanisms underlying problematic behavioral effects of alcohol. The 5 presenters drew from their recent studies examining the effects of acute and chronic ethanol using a range of sophisticated methods from electrophysiological analysis of paired-pulse facilitation and spontaneous and miniature synaptic currents (Drs. Weiner, Valenzuela, Zhu, and Morrisett), to direct recording of ion channel activity and peptide release from acutely isolated synaptic terminals (Dr. Treistman), to direct microscopic observation of vesicular release (Dr. Morrisett). They showed that ethanol administration could both increase and decrease the probability of release of different transmitters from synaptic terminals. The effects of ethanol on synaptic terminals could often be correlated with important behavioral or developmental actions of alcohol. These and other novel findings suggest that future analyses of synaptic effects of ethanol should attempt to ascertain, in multiple brain regions, the role of presynaptic terminals, relevant presynaptic receptors and signal transduction linkages, exocytotic mechanisms, and their involvement in alcohol's behavioral actions. Such studies could lead to new treatment strategies for alcohol intoxication, alcohol abuse, and alcoholism.

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“…Previous work has explored the nature of alcohol tolerance in the BK channel within nerve terminals of the hypothalamic-neurohypophysial system (Knott et al, 2000(Knott et al, , 2001(Knott et al, , 2002Pietrzykowski et al, 2004). Ethanol tolerance in these BK channels is manifested as both decreased ethanol sensitivity occurring within 15 minutes of drug exposure (Component 1), and reduced BK current density evident at 6 hours that reaches maximal values after 24 hours (Component 2) .…”

mentioning

confidence: 99%

BK Channel Subunit Composition Modulates Molecular Tolerance to Ethanol

Feinberg-Zadek

Martin

Treistman

2008

Alcoholism Clin & Exp Res

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Thus, rapid tolerance in human BK occurs in cell-free membrane patches, independent of cytosolic second messengers, nucleotides or changes in free calcium. Alcohol pretreatment for 24 hours altered subsequent short-term plasticity of hSlo + beta(4) channels, suggesting a relationship between classes of tolerance. Finally, Component 2 reduction in current density showed a striking dependency on channel composition. Twenty-four hour exposure to 25 mM ethanol resulted in a down-regulation of BK current in hSlo and hSlo + beta(4) channels, but not in hSlo + beta(1) channels. The fact that hSlo + beta(1) channels show less sensitivity to acute challenge, in conjunction with less Component 1 and Component 2 tolerance, suggests subunit composition is an important factor for these elements of alcohol response.

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Tolerance to Acute Ethanol Inhibition of Peptide Hormone Release in the Isolated Neurohypophysis

Cited by 9 publications

References 10 publications

The Effect of Swelling on TRH and Oxytocin Secretion From Hypothalamic Structures

The Effect of Swelling on TRH and Oxytocin Secretion From Hypothalamic Structures

Actions of Acute and Chronic Ethanol on Presynaptic Terminals

BK Channel Subunit Composition Modulates Molecular Tolerance to Ethanol

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