Effects of the Gabaergic Agent Sodium Valproate on the Arginine Vasopressin Responses to Hypertonic Stimulation and Upright Posture in Man

Chiodera, P.; Gnudi, A; Volpi, R.; Marchesi, Carlo; Marchesi, Matteo; Davoli, D; Capretti, L.; Coiro, V.

doi:10.1111/j.1365-2265.1989.tb00437.x

Cited by 18 publications

(6 citation statements)

References 17 publications

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“…However, valproate treatment produced an overall increase in plasma cortisol levels, as well as a decrease in heart rate and diastolic blood pressure, which may have masked the ability of cocaine cues to affect these measures. The decrease in cardiovascular activity is consistent with previous studies on valpoate and related GABA transaminase inhibitors in animals (Tanaka et al, 1992; Loscher, 1982) and humans (Chiodera et al, 1989; Isojarvi et al, 1998; Chong et al, 2001). The increase in cortisol levels is also consistent with prior studies on chronic valproate treatment in epileptic patients (Aydin et al, 2005; Vlasov et al, 2001).…”

Section: Discussionsupporting

confidence: 91%

Valproate treatment and cocaine cue reactivity in cocaine dependent individuals

Reid

Thakkar

2009

Drug and Alcohol Dependence

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Based on prior clinical trials indicating that γ-aminobutyric acid (GABA) based anticonvulsant medications reduce drug craving in cocaine dependent study participants, we tested the effects of valproate treatment on cue-induced cocaine craving. Crack cocaine dependent individuals (N=20) were tested in a randomized, placebo-controlled, within-subjects, crossover study design. Valproate treatment was titrated up to 1500 mg/day by Day 6 of treatment, cue testing was completed on Day 8 of treatment, and all study participants underwent a washout period of 5 days between active and placebo medication treatment periods. Testing included both cocaine and neutral cue exposure sessions, presented in a random and counterbalanced order. Main effects of cue exposure were found for subjective ratings of “desire to use cocaine now”, the cocaine craving index, cocaine-like high, and cocaine withdrawal. Treatment interaction effects were found with “desire to use cocaine now”, which underwent a greater increase following cocaine cue exposure in the valproate condition. Main effects of medication treatment were found, in which lower blood pressure and heart rate, and higher plasma cortisol levels, were associated with valproate treatment. Valproate treatment was also associated, at a trend level, with higher pre-test cocaine craving levels. The results demonstrate that cocaine cue reactivity is a robust phenomena across two assessment sessions, but fail to support the use of valproate as a means of reducing spontaneous and cue-induced cocaine craving. The use of valproate as a treatment for cocaine dependence is not supported.

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Section: Discussionsupporting

confidence: 91%

Valproate treatment and cocaine cue reactivity in cocaine dependent individuals

Reid

Thakkar

2009

Drug and Alcohol Dependence

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“…Therefore, and given the various reports about a GABAergic control of the release of AVP from the posterior pituitary (Bisset and Chowdrey, 1980;Knepel et al, 1980;Iovino et al, 1982Iovino et al, , 1983Unger et al, 1983;Wible et al, 1985a, b;Chowdrey and Bisset, 1988;Chiodera et al, 1989;Roberts and Robinson, 1991;Magnusson and Meyerson, 1993), one would have expected to measure reduced plasma AVP levels after temazepam treatment. However, at the dosages used here, temazepam failed to influence plasma AVP concentrations under basal and stress conditions.…”

Section: Temazepam Triggers Intra-pvn Release Of Avp T Welt Et Almentioning

confidence: 99%

Temazepam Triggers the Release of Vasopressin into the Rat Hypothalamic Paraventricular Nucleus: Novel Insight into Benzodiazepine Action on Hypothalamic–Pituitary–Adrenocortical System Activity During Stress

Welt

Engelmann

Renner

et al. 2006

Neuropsychopharmacol

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We investigated the influence of a representative classical benzodiazepine on the regulation of the hypothalamic-pituitary-adrenocortical (HPA) axis activity both under basal conditions and stress. Adult male Wistar rats were intravenously administered with temazepam (0.5, 1, and 3 mg/kg body weight) and plasma concentrations of corticotropin (ACTH) and vasopressin (AVP) were measured in blood samples collected via chronically implanted jugular venous catheters. Simultaneously, the release of AVP within the hypothalamic paraventricular nucleus (PVN) was monitored via microdialysis. Plasma AVP levels remained unaffected by the different treatment conditions. Temazepam blunted the stressor exposure-induced secretion of ACTH in a dose-dependent manner. Concurrently, and also in a dose-dependent manner temazepam enhanced the intra-PVN release of AVP, known to originate from magnocellular neurons of the hypothalamic neurohypophyseal system. Furthermore, temazepam did not affect the in vitro secretion of ACTH from the adenohypophyseal cells. Taken together, the results of this study suggest that temazepam modulates the central nervous regulation of the HPA axis by altering intra-PVN AVP release. An increasingly released AVP of magnocellular origin seems to provide a negative tonus on ACTH secretion most probably via inhibiting the release of ACTH secretagogues from the median eminence into hypophyseal portal blood.

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“…GABAergic terminals have been shown to synapse directly on neu rosecretory neurons in the supraoptic nucleus [32], and highaffmity GABA receptors have been localized in the same region [23]. Furthermore, Chiodera et al [10] have recently reported that the rise in VP in response to hyperosmotic stimulation was significantly lower in humans given sodium valproate, a GABAergic agent. Bisset et al [5] demonstrated that injection of GABA or muscimol, an analogue of GABA, into the lateral cerebral ventricle inhibited the release of VP and OT by an os motic stimulus in the rat.…”

Section: Discussionmentioning

confidence: 99%

Influence of Pentobarbital and Urethane on Release from Magnocellular Neurons

Cheng

North²

1991

Neuroendocrinology

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We examined the responses of vasopressin-neurons (VP-neurons) and oxytocin-neurons (OT-neurons) to acute salt-loading in a group of conscious rats (CON, n = 8) and rats under sodium pentobarbital (NEM, 50 mg/kg, i.p., n = 8) or urethane (URE, 1.6 g/kg, i.p. n = 8) anesthesia. Fifteen minutes following the induction of anesthesia, sodium pentobarbital produced an increase in basal plasma osmolality (Posm, 290 ± 2 to 296 ± 3 mosm/kg H₂O, p < 0.007) while urethane did not change basal Posm (287 ± 2 to 289 ± 2 mosm/kg H₂O). Neither anesthetic agent resulted in any significant changes in basal plasma levels of vasopressin-associated neurophysin (VP-RNP) and oxytocin-associated neurophysin (OT-RNP). In response to intravenous infusion of 18% saline, all three groups of rats had similar rises in Posm. The slopes of the relationship between the rise in plasma VP-RNP and the rise in Posm were markedly reduced in both groups of anesthetized animals compared to that observed for conscious animals (CON = 2.54 ± 0.5; NEM = 1.22 ± 0.18; URE = 1.17 ± 0.24 fmol · mH · mosm^–1 · kg H₂O^–1 p < 0.0126). The slopes of the relationship between the rise in plasma OT-RNP and the rise in Posm were not significantly (p < 0.4478) different between the CON group and the NEM group, while the slope for the URE group was significantly (p < 0.05) smaller than that for the CON group (CON = 10.9 ± 1.5; NEM = 9.3 ± 1.5; URE = 6.3 ± 0.7 fmol · ml^–1 · mosm^–1 · kg H₂O^–1). Our data suggest that anesthesia induced by either sodium pentobarbital or urethane significantly reduces the responsiveness of VP-neurons to acute salt loading, but the responsiveness of OT-neurons is lowered by urethane only. It implies that the action of urethane on OT-neurons, and perhaps also on VP-neurons, might be mediated by a mechanism different from that of sodium pentobarbital. Barbiturates are known to reduce the activity at glutamate receptors and also to enhance the activity at γ-aminobutyric acid (GABA) receptors. GABA reportedly is involved in the osmotic release of both OT-neurons and VP-neurons. Therefore, the absence of an effect by pentobarbital on OT-neurons, in addition to its inhibitory influence on VP-neurons, suggests that GABA receptors do not play a predominant role in the actions barbiturates have on the osmotic responsiveness of VP-neurons. Our data might also imply that there is a relative scarcity of glutamate receptors on OT-neurons.

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Effects of the Gabaergic Agent Sodium Valproate on the Arginine Vasopressin Responses to Hypertonic Stimulation and Upright Posture in Man

Cited by 18 publications

References 17 publications

Valproate treatment and cocaine cue reactivity in cocaine dependent individuals

Valproate treatment and cocaine cue reactivity in cocaine dependent individuals

Temazepam Triggers the Release of Vasopressin into the Rat Hypothalamic Paraventricular Nucleus: Novel Insight into Benzodiazepine Action on Hypothalamic–Pituitary–Adrenocortical System Activity During Stress

Influence of Pentobarbital and Urethane on Release from Magnocellular Neurons

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