The characteristics of the behavioral effects of 2,5-dimethoxy-4-methylamphetamine (DOM or STP) were compared with those of mescaline and methamphetamine in rats and mice. DOM significantly increased locomotor activity in an open-field situation at 0.5-1.0 mg/kg i.p., but at doses above 5 mg/kg i.p. caused biphasic changes, i.e. an initial decrease followed by an increase in motility and exploratory behavior. This hyperactivity was not accompanied by simultaneous increase in rearing. Besides, DOM induced head twitches in rats as well as in mice at doses above 0.1 mg/kg i.p., and marked backward locomotion only in rats at doses larger than 5 mg/kg i.p. The occurrence of backward locomotion might be attributable to the initial decrease in general activity. Behavioral effects of DOM were different from those of either mescaline or methamphetamine although they resembled those of mescaline in some respects.

DOM 2,5-Dimethoxy-4-Methylamphetamine↗

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Changes in acetylcholine content in rat brain after bilateral olfactory bulbectomy in relation to mouse-killing behavior.

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Acetylcholine↗

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Effects of midbrain raphe stimulation and lesion on EEG activity in rats.

In order to clarify whether the dorsal raphe (d-R) and medial raphe nuclei (m-R) of the midbrain play a different role in EEG activity, the effects of either electrical stimulation or lesion of each raphe nucleus were examined in rats. After m-R stimulation, EEG activity changed to a marked drowsy pattern. D-R stimulation, however, failed to produce such effects. M-R lesion elicited a significant arousal in EEG. The change in hippocampal EEG was the most characteristic, i.e., synchronized waves with an extreme increase in voltage. D-R lesion did not produce such a change. The hippocampal EEG arousal was easily abolished by L-5-hydroxytryptophan without any change in the cortical EEG or behavior. These results suggest that the m-R plays a more important role than the d-R in regulating the hippocampal EEG activity, especially in inhibiting the appearance of high voltage synchronized waves in the hippocampus.

5-Hydroxytryptophan↗

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Potentiation of pressor and behavioral responses to brain stimulation following bilateral olfactory bulbectomy in freely moving rats.

The effects of bilateral olfactory bulb (OB) ablation on pressor and behavioral responses to stimulation of the posterior hypothalamic area (PHA) and midbrain reticular formation (MRF) were investigated in unanesthetized and unrestrained rats with chronic electrodes and arterial cannula implants. Bilateral olfactory bulbectomy induced a marked increase in emotional responses to given stimuli. A high incidence of muricide was also observed after olfactory bulbectomy. The threshold for inducing behavioral arousal and pressor response to PHA and MRF stimulation were markedly enhanced. The enhancement in pressor response to MRF stimulation occurred immediately after olfactory bulbectomy and persisted throughout the experiment, while that to PHA stimulation appeared gradually and reached maximum at 10 days after olfactory bulbectomy. These results suggested that olfactory bulbectomy has a great influence not only on emotionality but also on the central neural mechanisms of autonomic regulation.

Aggression↗

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Bicarbonate stimulatory action of nizatidine, a histamine H(2)-receptor antagonist, in rat duodenums.

Nizatidine, a histamine H(2)-antagonist, is known to inhibit acetylcholinesterase (AChE) activity and is used clinically as a gastroprokinetic agent as well as the anti-ulcer agent. We examined whether or not nizatidine stimulates duodenal HCO(3)(-) secretion in rats through vagal-cholinergic mechanisms by inhibiting AChE activity. Under pentobarbital anesthesia, a proximal duodenal loop was perfused with saline, and the HCO(3)(-) secretion was measured at pH 7.0 using a pH-stat method and by adding 10 mM HCl. Nizatidine, neostigmine, carbachol, famotidine or ranitidine was administered i.v. as a single injection. Intravenous administration of nizatidine (3-30 mg/kg) dose-dependently increased the HCO(3)(-) secretion, and the effect at 10 mg/kg was equivalent to that obtained by carbachol at 0.01 mg/kg. The HCO(3)(-) stimulatory action of nizatidine was observed at the doses that inhibited the histamine-induced acid secretion and enhanced gastric motility. This effect was mimicked by neostigmine (0.03 mg/kg) and significantly attenuated by bilateral vagotomy and pretreatment with atropine but not indomethacin. The IC(50) of nizatidine for AChE of rat erythrocytes was 1.4 x 10(-6) M, about 12 times higher than that of neostigmine. Ranitidine showed the anti-AchE activity and increased duodenal HCO(3)(-) secretion, similar to nizatidine, whereas famotidine had any influence on neither AChE activity nor the HCO(3)(-) secretion. On the other hand, duodenal damage induced by acid perfusion (100 mM HCl for 4 h) in the presence of indomethacin was significantly prevented by nizatidine and neostigmine, at the doses that increased the HCO(3)(-) secretion. These results suggest that nizatidine increases HCO(3)(-) secretion in the rat duodenum, mediated by vagal-cholinergic mechanism, the action being associated with the anti-AChE activity of this agent.

Acetylcholinesterase↗

PubMedDate not supplied

Effects of chronic administration of haloperidol, methamphetamine or cocaine on "wet-dog shakes" elicited by stimulation of the rat hippocampus.

We investigated the effect of chronic administration of haloperidol, methamphetamine or cocaine on wet-dog shakes (WDS), as induced by hippocampal stimulation. Although haloperidol, in a dose of 0.5 mg/kg, led to a marked reduction in the number of WDS, a reversion to the control level occurred after administration of haloperidol for 2 weeks. A single administration of methamphetamine and cocaine had no effect on the WDS. The total number of WDS did not change when methamphetamine was administered for 2 weeks and the hippocampus was stimulated 30 min after the last administration. However, the number of WDS after the repeated administration of cocaine was significantly decreased. We tentatively conclude that the hippocampal stimulation-induced WDS may be closely related with dopaminergic functions.

Animals↗

PubMedDate not supplied

Changes in [3H]-imipramine binding sites in relation to muricide following olfactory bulbectomy and the effect of nomifensine in brain of rats.

The effects of olfactory bulbectomy (OB) and nomifensine (NOM) on the binding of [3H]-imipramine (3H-IMP) in brain of rat were investigated. Seventy-five per cent of OB rats exhibited muricide. Acute NOM suppressed muricide in 55% and chronic NOM suppressed it in 60 80% of OB rats. In killer rats, OB increased Bmax of high-affinity (HA) and low-affinity sites (LA) in cortex (Cx) and both Bmax and KD of HA in amygdala (AMG). In rats with muricide suppressed by acute NOM 10 mg.kg-1 i.p., Bmax and KD of HA in Cx and of both HA and LA in AMG were reduced. Injection of NOM for 10 days produced further reduction of Bmax, especially of HA binding in Cx. Neither OB nor NOM exerted any significant effect on binding constants in caudate-putamen and hypothalamus. The possible relation between the changes of 3H-IMP binding, exhibition of muricide by OB rats and the antimuricidal activity of NOM are discussed.

Aggression↗

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Inhibitory effect of apomorphine on hippocampal stimulation-induced "wet-dog shakes" in rats may be due to a stereotyped behavior.

The effect of apomorphine on "wet-dog shakes" (WDS) elicited by hippocampal stimulation was investigated. Apomorphine in doses of 1.0 and 2.0 mg/kg given to rats s.c. reduced the number of WDS. Haloperidol in doses of 0.2-1.0 mg/kg given i.p. also significantly and dose-dependently reduced the number of WDS. The inhibitory effect of apomorphine in doses of 1.0 and 2.0 mg/kg on WDS was completely inhibited by haloperidol given in a dose of 0.5 mg/kg. It is, therefore, conceivable that the inhibition of WDS produced by apomorphine in doses of 1.0 and 2.0 mg/kg may result from the occurrence of stereotyped behavior and that the dopaminergic blocking action may be crucial for the inhibition of WDS induced by hippocampal stimulation. Despite a 50% increase in stimulation intensity, as compared with the afterdischarge threshold, the number of WDS remained unchanged. We tentatively concluded that apomorphine fails to increase the number of WDS, as a result of the ceiling phenomenon.

Animals↗