Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Amphetamine (0.1 to 5.0 mg/kg, IV) altered frontal cortex stimulation evoked neostriatal potentials in rats. The amplitude of wave P1, which corresponds to an initial intracellular excitatory postsynaptic potential, was reduced, as was the latency to wave N3, which corresponds to the late rebound depolarization. Repetitive electric stimulation of the mesencephalic reticular formation at low currents (0.05 to 0.5 mA, 0.2-ms duration, 60 Hz square waves) produced similar effects. The peripherally acting sympathomimetics, norepinephrine (3 and 10 micrograms/kg, IV) and vasopressin (10 mU/kg, IV), increased blood pressure but did not alter the neostriatal evoked response. In rats with medial thalamic lesions induced by kainic acid, wave N3 was eliminated, and the effects of amphetamine and mesencephalic reticular formation stimulation on neostriatal evoked responses were reduced or eliminated. Thus many of the effects of systemic amphetamine on frontal cortex evoked neostriatal potentials may be mediated via extrastriatal sites, including the mesencephalic reticular formation and the medial thalamus.
 ...
PMID:Amphetamine alteration of amplitude and timing of cortical-neostriatal interactions. 350 69

Prior sodium restriction cross-sensitizes rats to the psychomotor effects of amphetamines and vice versa. Repeated central injections of vasopressin (VP) induce a psychomotor sensitization similar to amphetamine sensitization and repeated sodium deficiency. Thus brain VP signaling may be a common mechanism involved in mediating these two motivational systems. In experiment 1, we tested the hypothesis that rats previously sensitized to central VP would show enhanced psychomotor responses to amphetamine. Rats were administered saline, VP (50 ng), or amphetamine (1 mg/kg or 3 mg/kg) on days 1 and 2, and given saline or amphetamine on day 3. Amphetamine produced psychomotor arousal in all groups. However, amphetamine on day 3 elicited a significantly greater psychomotor response in rats that had prior injections of amphetamine or VP than in rats previously treated with saline. In experiment 2, the hypothesis that prior experience with central VP would cross-sensitize rats to drinking hypertonic sodium (NaCl) solutions was tested. Rats were administered VP (50 ng) or saline for 3 days. On the fourth day, nondeprived rats were given access to 0.3 M NaCl and water for 1 h. Control and saline-treated rats only drank 1 ml of 0.3 M NaCl, but rats previously exposed to central VP drank significantly more hypertonic saline (4 ml). These results show that prior experience with central VP cross-sensitizes rats to the psychomotor stimulant effects of amphetamine and the ingestion of concentrated NaCl solutions. This pattern of cross-sensitization links central VP signaling, amphetamine, and sodium deficiency, and therefore it may play a role in the cross-sensitization between sodium appetite and amphetamines.
 ...
PMID:Centrally administered vasopressin cross-sensitizes rats to amphetamine and drinking hypertonic NaCl. 1756 21

Wistar male rats were injected intraperitoneally for 4 days in elevated doses with: (1) physiological saline (control; 0.1 - 0.2 - 0.4 - 0.8 ml/rat), (2) amphetamine (0.5 - 1.0 - 2.0 - 4.0 mg/kg); (3) fentanyl (0.00625 - 0.0125 - 0.025 - 0.05 mg/kg), (4) 40% aqueous ethanol solution (0.5 - 1.0 - 2.0 - 4.0 g/kg), (5) ethaminal sodium (2.5 - 5 - 10 - 20 mg/kg), and (6) dexamethasone (0.5 - 1.0 - 2.0 - 4.0 mg/kg). The forced regime of drug administration led to gradual load of the organism and prevented drug tolerance development. This method is widely used for the formation of drug dependence (or its features) due to various narcotic agents. The maximum level of mRNA expression for corticoliberin was registered in amygdala after the administration of dexamethasone (0.46 units compared to beta-actin), and the minimum level was observed after treatment with sodium ethaminal (0.07) and fentanyl (0.037). In hypothalamus, sodium ethaminal produced elevated mRNA expression (0.8 units), followed by ethanol (0.37) and fentanyl (0.039). Amphetamine activated mRNA expression for corticoliberin neither in hypothalamus nor in amygdala for all of the drugs studied. The mRNA expression for vasopressin was also not registered for all drugs in hypothalamus and amygdala. Therefore, the reinforcing system of hypothalamus supports the typical reaction on the administration of narcotic agents, while the extended amygdala system includes both the proper reinforcement and the stress reactivity elements.
 ...
PMID:[Expression of mRNA for corticoliberin and vasopressin in hypothalamus and amygdala on the background of administration of psychoactive drugs in rats]. 1881 32

Male Wistar rats received intraperitoneal injections of physiological saline (control), phenamine, fentanyl, ethanol, sodium ethaminal, or dexamethasone in increasing concentrations for 4 days. Forced administration of these drugs provided gradual load of the organism and prevented the development of tolerance. Such approach is extensively used for the development of drug addiction or several manifestations of this state. Expression of corticotropin-releasing hormone mRNA in the amygdala was maximum after administration of dexamethasone (0.46 arb. units vs. beta-actin), but was much lower in experiments with sodium ethaminal and fentanyl (0.07 and 0.037 arb. units, respectively). In the hypothalamus, enhanced mRNA expression was observed after injection of sodium ethaminal, ethanol, and fentanyl (0.8, 0.37, and 0.039 arb. units, respectively). Phenamine did not increase mRNA expression in the amygdala and hypothalamus. Expression of vasopressin mRNA was not detectable in brain structures of animals from various groups. Our results indicate that the hypothalamic reinforcement system provides a similar response to narcogens, whereas the extended amygdala includes elements of both reinforcement and stress reactivity.
 ...
PMID:Expression of mRNA for corticotropin-releasing hormone and vasopressin in the hypothalamus and amygdala of rats after administration of narcogenic. 1924 Aug 49