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PubMed1975

The effects of dexetimide on pimozide-, haloperidol- and pipamperone-induced inhibition of brain self-stimulation in rats.

Pimozide (0.04, 0.16, 0.63 and 2.50 mg/kg), haloperidol (0.01, 0.04, 0.16 and 0.63 mg/kg) and pipamperone (2.50, 10.0, 40.0 and 160 mg/kg) were given subcutaneously to rats, pressing a lever for brain-stimulation through electrodes implanted in the lateral hypothalamic region of the medial forebrain bundle. The lowest dose of each neuroleptic did not affect self-stimulation; the second dose inhibited the response rate by approximately 50%, whereas the two highest doses completely suppressed self-stimulation behaviour. The centrally acting anticholinergic dexetimide (0.63 mg/kg, s.c.) completly antagonized the pimozide-induced inhibition; the haloperidol-induced inhibition was also completely antagonized except at its highest doses, whereas the effects of the sedative neuroleptic pipamperone were not antagonized. These data are consistent with a presumed dopaminergic cholinergic striatal interaction and show brain self-stimulation to be an effective measure of neuroleptic-anticholinergic interaction.

Animals↗
PubMed1988

[Self stimulation against a background of action of blockers of the synthesis of proteins and oligopeptides].

The experiments on rabbits have demonstrated that blockade of protein synthesis by the administration of cycloheximide and actinomycin D abolishes self-stimulation in the central nervous system. The treatment with ACTH fragment (ACTH4-10) restored the self-stimulation. Unlike ACTH, injections of pentagastrin, Met-enkephalin, Leu-enkephalin and cholecystokinin were ineffective. The present study shows that ACTH4-10 plays an important role in genetic determination of self-stimulation behaviour.

Adrenocorticotropic Hormone↗
PubMed1998

Self-stimulation of lateral hypothalamus and ventral tegmentum increases the levels of noradrenaline, dopamine, glutamate, and AChE activity, but not 5-hydroxytryptamine and GABA levels in hippocampus and motor cortex.

Self-stimulation (SS) rewarding experience induced structural changes have been demonstrated in the hippocampal and motor cortical pyramidal neurons. In the present study, we have evaluated whether these changes are accompanied by neurochemical alterations in the hippocampus and motor cortex in SS experienced rats. Self-stimulation experience was provided one hour daily over a period of 10 days through stereotaxically implanted bipolar stainless steel electrodes, bilaterally in lateral hypothalamus and substantia nigra-ventral tegmental area. Self-stimulation experience resulted in a significant (P < 0.001) increase in the levels of noradrenaline, dopamine, glutamate and AChE activity but not 5-hydroxytryptamine and GABA levels in hippocampus and motor cortex. Such alterations in the levels of neurotransmitters may enhance the cognitive functions in the SS experienced rats.

Acetylcholinesterase↗
PubMed1979

Facilitation of self-stimulation with high doses of amphetamine in the rat.

Rats were trained to self-stimulate by interrupting a photobeam and brain stimulation was maintained for as long as the beam of light was broken. d-Amphetamine sulphate was then administered and response rate and total duration of stimulation were recorded. Both response rate and total duration were elevated by 1.0, 2.0, and 5.0 mg/kg dosages. The 1.4 s/response duration observed with saline was elevated to 2.0 s/response with 2.0 and 5.0 mg/kg doses. It was concluded that amphetamine's effects on self-stimulation are at least partially determined by the response requirements of the task employed.

Animals↗
PubMedDate not supplied

[Effect of serotonin on self stimulation and conditioned avoidance reactions in rats].

It has been shown that serotonin influences self-stimulation and avoidance conditioned reactions in rats in a different way. Serotonin administration caused a reorganization of self-stimulation process and enhanced its frequency; the avoidance reaction grew weaker and was achieved with a longer latency. Alternation of stages of activation and inhibition was observed in the EEG of the neocortex, hypothalamus and hippocampus as well as shifts in the heart rate. These changes did not always correlate with the animals' behaviour. Unidirectional, yet different serotonin effects on various behavioral reactions, brain electrical activity and vegetative processes testify to a relative independence of their mechanisms.

Animals↗
PubMed1982

Effects of various catecholamine receptor antagonists, muscle relaxation and physical hindrance on shuttlebox self-stimulation.

Certain drugs, particularly clozapine and clonidine, have been reported to increase selectively the latency to initiate brain stimulation (the ON latency) in a shuttlebox test of self-stimulation, suggesting a preferential attenuation of the "reward" component. The pharmacological selectivity of this reported effect was systematically evaluated. At doses that blocked bar-pressing self-stimulation, metoclopramide (3 mg/kg), prazosin (3 mg/kg) clonidine (0.1mg/kg), clozapine (3 mg/kg)and haloperidol (0.3 mg/kg), all elevated the ON latency to a greater extent than the OFF latency. Methocarbamol (200 mg/kg), and a muscle relaxant, also elevated the ON latency preferentially but the magnitude of this preferential effect was smaller than that produced by the other drugs. A hurdle in the center of the shuttlebox increased the ON and OFF latencies nonselectively. The shuttlebox procedure does not clearly discriminate among various substances that interfere with noradrenergic or dopaminergic neurotransmission, but the common profile produced by the these substances is distinguishable to some degree from simple motor disruption.

Adrenergic alpha-Antagonists↗
PubMed1978

Effect of pimozide on the improvement in learning produced by self-stimulation and by water reinforcement.

When rats self-stimulate immediately after the training trial of an appetitive task their performance on a retention test is improved the next day. In the present study, this improvement was blocked by pretraining injections of pimozide, a dopaminergic blocker. In a second experiment, injections of pimozide retarded learning on the same task when the learning was reinforced by drinking water, but had no effect on learning which occurred in the absence of a reinforcer. The data made the hypotheses that the animal's behavior was a result of an action of primozide on sensory or motor mechanisms, or that the drug produced state-dependent effects, highly unlikely. We concluded that neural systems involving dopamine mediate an effect of reinforcing events on behavior.

Animals↗
PubMed1997

Nicotine-induced decreases in VTA electrical self-stimulation thresholds: blockade by haloperidol and mecamylamine but not scopolamine or ondansetron.

The effects of repeated daily injections of (-)-nicotine (+) hydrogen tartrate (mg kg-1 s.c.) on electrical self-stimulation of the ventral tegmental area were investigated. Nicotine reduced the frequency required to maintain half-maximal response rates with animals responding in rate-frequency threshold tests. Under these conditions, nicotine induced an increase in the total number of self-stimulation responses per session, but had no statistically significant effects on the maximal response rate. These effects of nicotine were observed by the second day of administration of this drug. Acute injections of the D2-like dopamine receptor antagonist haloperidol (0.03 mg kg-1 s.c.) and of the nicotinic acetylcholine receptor antagonist mecamylamine (1 mg kg-1 s.c.) attenuated the effects of nicotine, indicating that the observed effects involve stimulation of D2-like dopamine receptors as a result of nicotinic receptor activation. The muscarinic acetylcholine receptor antagonist scopolamine (3 mg kg-1 s.c.) and the serotonin 5-HT3 receptor antagonist ondansetron (0.01 and 0.1 mg kg-1 s.c.) did not alter the effects of nicotine. The results of this study indicate that repeated daily administration of (-)-nicotine increases the rewarding effects of electrical self-stimulation of the ventral tegmental area. These data are consistent with the proposal that repeated daily injections of nicotine positively effect a mesolimbic dopaminergic substrate of reward.

Animals↗
PubMedDate not supplied

Effects of excitotoxic lesions of the basal forebrain on MFB self-stimulation.

Electrolytic lesions of the anterior medial forebrain bundle (MFB) have been shown to attenuate the rewarding impact of stimulating more caudal MFB sites. In the present study, excitotoxic lesions were employed to determine the relative contribution of somata or fibers of passage contributing to that effect. Changes in reward efficacy were inferred, at three currents, from lateral displacements of the curve relating the rate of responding to the number of stimulation pulses per train. After baseline data were collected from stimulation sites in the lateral hypothalamus (LH) and the ventral tegmental area (VTA), 70 nmol of N-methyl-D-aspartic acid was injected via cannulae aimed at basal forebrain sites. Three subjects were injected with vehicle and served as controls. In 5 out of 15 cases, lesions encompassing the lateral preoptic area, anterior LH, and substantia innominata resulted in long-lasting, large increases (0.2-0.47 log10 units) in the number of pulses required to maintain half-maximal rates of self-stimulation for low currents delivered via the LH electrode; smaller increases (0.08-0.33 log10 units) were noted at moderate and high currents. Seven rats with similar or more dorsally located damage showed moderate or transient increases in the number of pulses required to maintain half-maximal rates of LH or VTA self-stimulation. Vehicle injections did not affect behaviour. Varying degrees of demyelination were seen, mostly removed from the electrode tip, and in locations that varied substantially across subjects manifesting similar changes in self-stimulation. These results support the notion that somata in the basal forebrain give rise to some of the directly activated fibers subserving self-stimulation of the MFB.

Animals↗
PubMed1979

Actions and interactions of amphetamine on self-stimulation in rats.

The dose-response relationship for d-amphetamine (0.125-2 mg/kg, IP) and its l-isomer (0.125-3 mg/kg, IP) was studied in self-stimulation behavior of rats each with an electrode at posterior hypothalamus (PH, mainly monoaminergic) or area ventralis tegmentum (A10, dopaminergic). The drug effects increased with the dose reaching a peak (at 0.5 mg/kg with d-amphetamine and at 1.0 mg/kg with 1-amphetamine) and then decreased. The d-isomer was approximately twice as potent as the l-isomer in enhancing intracranial self-stimulation (ICSS) rate with electrodes at either site. Azaperone (mainly an alpha-adrenergic blocker) and haloperidol (an antidopaminergic neuroleptic) used in small doses (0.05 and 0.008 mg/kg respectively) which did not affect the baseline responding, blocked amphetamine-induced enhancement of ICSS in both groups of rats. Thus, amphetamine-induced facilitation of ICSS at both PH and A10 areas and its blockade by an alpha-adrenergic blocker as well as an antidopaminergic neuroleptic show the involvement of both noradrenergic and dopaminergic mechanisms in self-stimulation behavior.

Amphetamine↗
PubMedDate not supplied

[Role of serotoninergic mechanisms in realizing the influence of diazepam on the effect of self-stimulation].

It has been shown in experiments on rats that diazepam (I mg/kg) abolishes an inhibitory action of cytalopram, the serotonine reverse uptake inhibitor (10 mg/kg) on the self-stimulation effect. Activation of self-stimulation was observed during diazepam action and in the presence of a decrease in the activity of serotoninergic processes, that was achieved by parachloramphetamine administration in doses of 5 and 15 mg/kg. It is concluded that the activating effect of diazepam is not mediated through the serotoninergic systems of the brain.

Animals↗
PubMedDate not supplied

Influence of new ACTH fragments on self-stimulation, avoidance, and grooming behavior in rabbits.

The effects of new cyclic analogs of ACTH fragments, EHFRWGKPVG-NH2 and KHFRWG-NH2, which have specific and nonspecific active centers in their structure, in the self-stimulation, avoidance, and grooming behavior of rabbits were investigated in this study. The intraventricular administration of EHFRWGKPVG-NH2 in doses of 0.1-2.5 micrograms increased the frequency of self-stimulation (SS), while in doses of 4-5 micrograms, it decreased the frequency of self-stimulation. The administration of KHFRWG-NH2 in doses of 0.1-5.o micrograms, induced a decrease in the frequency of SS by 25-30% in the first 15 min following the injections; this indicator returned to the baseline level thereafter, and decreased again. SS was more intense after 24-48 h, 5-8% higher than the baseline level, and remained practically unchanged over the course of a two-hour experiment. The administration of the EHFRWGKPVG-NH2 fragment in doses of 0.5-2.0 micrograms increased the latent period of the avoidance reaction, decreased the time of the anxiety state, and increased the time of the comfort state. In addition to these changes, both ACTH fragments induced intense grooming, increased the duration of grooming by 200-400% as compared with the control animals which were administered physiological solution.

Adrenocorticotropic Hormone↗
PubMed1983

Intrinsic neurons are involved in lateral hypothalamic self-stimulation.

The recent technique of using ibotenic acid to lesion selectively local neurons while sparing fibers of passage permitted us to answer a long-standing question: is lateral hypothalamic self-stimulation supported by fibers of passage or are the intrinsic hypothalamic neurons involved? Three groups of adult male Sprague-Dawley rats were used. In a normal group, electrodes were bilaterally implanted in the lateral hypothalamus and self-stimulation (ICSS) was obtained separately with the right and left electrodes, at various current intensities, using a nose-poke response. In the experimental group, the intrinsic neurons of the lateral hypothalamus were destroyed unilaterally by local injection of ibotenic acid (4 or 6 micrograms in 0.5 microliter); the other side served as the sham-lesion control. Ten days later ICSS electrodes were implanted bilaterally, one in the lesioned area, the other in the contralateral hypothalamus. As in the case of the normal animals, the rate of nose-poking (ICSS) was then determined separately for each electrode. In the normal rats, ICSS rates were the same with stimulation on either side and the increase in ICSS rate as a function of the increase in current intensity was the same on each side. In the experimental rats, ICSS of the lesioned side was decreased in all cases; moreover, after lesion with the 6 micrograms dose, ICSS was totally suppressed. Self-stimulation of the sham-lesioned side was not significantly different from that observed in the normal rats. In 6 rats sampled from the lesioned groups as well as in 3 additional unimplanted animals, biochemical assays compared dopamine and serotonin contents of the two striata and noradrenaline and serotonin contents of the two hippocampi. No difference was observed for these two structures between the side ipsilateral to the lesion and the contralateral side. Moreover, none of these monoamine levels differed from those seen in the unimplanted rats. These results, taken together, suggest that intrinsic lateral hypothalamic neurons are involved in ICSS.

Animals↗
PubMed1987

Effect of inhalation of xylene on intracranial self-stimulation behavior in rat.

The effect of the inhalation of xylene on intracranial self-stimulation behavior was studied in rats in a flow-through (dynamic) inhalational behavioral chamber. Rats were exposed successively to four graded concentrations (102, 192, 419 and 623 ppm) of xylene vapor during 2-hr sessions on different days. The rate of lever-pressing showed a dose-dependent decrease during exposure to 192, 419 and 623 ppm of xylene. The 4-hr exposure to the smallest concentration (106 ppm) of xylene failed to show any effect on self-stimulation behavior. During a 5-day 2 hr/day exposure, the decrease in response observed on the 1st day was further accentuated with a nadir on the 3rd day; from the 4th day onwards, the depressant effect was attenuated showing the development of tolerance.

Administration, Inhalation↗
PubMed1980

Response sensitization and depression following long-term amphetamine treatment in a self-stimulation paradigm.

The effects of long-term amphetamine treatment were evaluated on responding supported by self-stimulation of the substantia nigra. Rats repeatedly treated with d-amphetamine, and tested with a low dose of the drug that ordinarily has no behavioral effect, showed higher response rates than animals repeatedly treated with saline and tested with the same dose of amphetamine. In contrast, a depression in responding was observed among animals that received long-term amphetamine administration and were tested with saline. The effects of long-term amphetamine treatment on self-stimulation could not be explained by the intrusion of drug-induced competitive behaviors such as locomotor activity and stereotypy. The results were attributed to changes in dopamine neurotransmission following prolonged exposure to amphetamine and were also discussed in terms of an animal model for 'amphetamine psychosis' and 'postamphetamine depression' in man.

Amphetamine↗
PubMed1990

Pontine lesions attenuate physostigmine suppression of self-stimulation in the rat.

In male Wistar albino rats with chronically implanted electrodes, self-stimulation behavior was compared before and after making bilateral pontine lesions involving the subcoeruleus area and adjacent tegmental field. Before lesioning, slight suppression of bar pressing after subcutaneous injection of 0.05 mg/kg physostigmine, marked stable suppression after 0.1 mg/kg, and very strong suppression after 0.2 mg/kg were observed. After making pontine lesions, the suppressive effects of physostigmine were clearly attenuated. With 0.05 and 0.1 mg/kg, no effect or only occasional slight suppression was observed in most cases. With 0.2 mg/kg, total suppression was induced in association with some peripheral effects, but the duration was obviously less than in the prelesion controls. Control saline injection did not produce a suppressive effect. From these findings, it is suggested that suppression of self-stimulation by physostigmine up to 0.1 mg/kg is due to the inhibition of motor activity through the cholinoceptive dorso-lateral pontine tegmental area and not due to a direct effect on the forebrain cholinergic process, presumably involving reinforcement or motivation.

Animals↗