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Results for “SELF STIMULATION”

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At least 415 records · Page 23Linked to original sources

PubMed1991

Desmethylimipramine promotes recovery of self-stimulation from the prefrontal cortex following footshock.

Intracranial self-stimulation (ICSS) was assessed from the prefrontal cortex in CD-1 mice immediately (0 h), 24 h and 168 h following exposure to uncontrollable footshock. Marked reductions in ICSS rates were observed in all mice immediately following the stressor. Although the ICSS alterations were transient in some animals, ICSS rates were reduced in the majority of animals 24-h and 168-h poststressor. Mice of either the shock or no shock treatment groups were administered either saline or desmethylimipramine (DMI, 5 mg/kg x 2) for 20 consecutive days. Chronic DMI ameliorated the stressor-induced ICSS deficits from the prefrontal cortex. Potential explanations for the stressor-provoked variations in ICSS and the effects of DMI are discussed.

Animals↗

PubMed1990

[Role of noradrenaline of the dorsal hippocampus in the mechanism of self-stimulation reaction in rats].

In has been established that intrahippocampal bilateral injection of NA did not influence common frequency of lateral hypothalamic self stimulation. After the destruction of hippocampal NA - terminals of 6-OHDA increased the frequency of self stimulation and rearing. It is suggested that NA hippocampus inhibit the recall trace of the memory of sensory reinforcement stimuli in the course of stimulation "reward".

Animals↗

PubMed1982

[Effect of the "memory peptide" ACTH 5-10 on the self-stimulation reaction of rabbits].

Experiments on rabbits were made to study variation in the frequency of the self-stimulation reaction from the lateral hypothalamus under the effect of the corticotropin fragment ACTH5-10. Intraperitoneal administration of the peptide in a dose of 50 micrograms/kg that causes the improved training in different behavioral models produces no significant effect on the mechanism of intracranial positive reinforcement. Intraventricular injection of 5 microliters of 0.9% NaCl leads to a short-term suppression of the self-stimulation reaction. Administration of 50 pcM/kg ACTH5-10 in the same volume of physiological saline completely abolishes the inhibitory action of the intraventricular injection itself.

Adrenocorticotropic Hormone↗

PubMed1981

Intracranial self-stimulation: mapping against the lateral boundaries of the dopaminergic cells of the substantia nigra.

The lateral boundaries of the substantia nigra, zona compacta, were mapped for intracranial self-stimulation in rats. The boundaries of the positive region for self-stimulation were found to correspond to the boundaries of the dopaminergic cell layer. These data strengthen the view that rewarding stimulation in this system activates the tegmental dopaminergic cells or, more likely, their immediate afferents.

Animals↗

PubMed1991

Interactions between amygdaloid and hypothalamic self-stimulation: a re-examination.

The function relating bar-pressing rate to the frequency of cathodal pulses was obtained in rats self-stimulating with amygdaloid (AMY) and lateral hypothalamic (LH) electrodes. The maximum self-stimulation (SS) rates in the AMY was found to be very low, compared to the LH. Concurrent stimulation with pairs of AMY-LH pulses did not shift the rate-frequency functional laterally, indicating the absence of summation of the two rewarding effects. In a second experiment, concurrent AMY-LH stimulation (using sub-threshold intensity LH pulses) facilitated bar-pressing for AMY stimulation (it increased the slope of the AMY rate-frequency function) without shifting this function laterally. In a third experiment, subjects were given a choice between a pulse frequency yielding maximal AMY rate and a series of higher pulse frequencies. Subjects consistently preferred the higher frequency values, attesting that the maximum AMY rates were not constrained by a saturating reinforcing effect. In a fourth experiment, subjects were given a choice between AMY stimulation and concurrent AMY-LH stimulation, using low intensity LH pulses. Subjects showed no preference for either stimulation condition, although rates were higher for the latter condition. These findings suggest that the maximum rate for AMY stimulation was constrained by factors interfering with bar-pressing and that the effect of these factors was attenuated by co-activation of the LH. In a fifth experiment, pre-treatment with phenobarbital mimicked the rate-enhancing effect of concurrent AMY-LH stimulation for 2 of the 4 subjects tested. This finding suggests that the LH pulses contributed to attenuate seizure activity accompanying AMY SS. In a final experiment, AMY SS rates were also increased by co-activation of rewarding sites in the rostral MFB but not the dorsal raphe, suggesting an anatomical specificity of this effect.

Amygdala↗

PubMed1981

Effects of naloxone on the self-stimulation behavior of the postero-lateral area of the hypothalamus in rats--influence of procedural conditions.

Rats exhibiting self-stimulation behavior through chronic electrodes implanted in the posterolateral part of the hypothalamus were subcutaneously injected with low doses (0.003-0.3 mg/kg) of naloxone. The animals were allowed to self-regulate the duration of rewarding brain stimulation. It was found that naloxone increases the duration of self-stimulation in rats in which the brain stimulation has previously been associated with footshock. Vehicle injections or injections of naloxone in rats that had not received footshock prior to testing, did not modify self-stimulation behavior. It is suggested that naloxone may facilitate an aversive central component of the brain stimulation; the conditioned rats therefore increased the duration of brain stimulation to compensate for this negative process.

Animals↗

PubMed1986

Distinct substrates influence the acquisition of self-stimulation of the hippocampus and the prefrontal cortex.

Self-stimulation (SS) of both the medial prefrontal cortex (MPFC) and the dorsolateral hippocampus (HPC) is known to develop slowly, over a period of days. In both cases, the acquisition of bar-pressing can be markedly hastened by delivery of noncontingent electrical stimulation for several days prior to SS training. The similarity of these effects suggests that there might be a common substrate mediating the acquisition process. However, in the present experiment, pre-training noncontingent electrical stimulation of the MPFC had no effect on how rapidly rats acquired the bar-pressing response for HPC stimulation, or vice versa. A further dissociation of the elements governing the acquisition process for these two SS sites was suggested by the observation that pre-training noncontingent stimulation of the entorhinal cortex facilitated the speed of acquisition of SS of the HPC but not of the MPFC. It seems that the HPC and entorhinal cortex can be excluded from the subset of neural structures which are known to influence the acquisition process governing MPFC SS. These and other data suggest that the development of SS of the MPFC and HPC can be regarded, at least in part, as involving a process rooted in distinct substrates.

Animals↗

PubMedDate not supplied

[The self-stimulation reaction of rabbits in a helium-oxygen environment under increased pressure].

Change of intensity of hypothalamic self-stimulation was determined in rabbits during their stay in normoxic helium-oxygen medium under the pressures of 10, 15 and 40 kgf/cm2 at various speeds of compression. The experiments conducted testify to depressive influence on the hypothalamus self-stimulation of helium-oxygen medium under increased pressure; the influence was more expressed at higher pressures and great speed of compression. It is supposed that the decrease in frequency of pedal pressures was connected with the appearance of nervous syndrome of high pressures.

Animals↗

PubMed1976

Alpha-noradrenergic modulation of hypothalamic self-stimulation: studies employing clonidine, 1-phenylephrine and alpha-methyl-p-tyrosine.

An alpha-noradrenergic substrate of rewarding intracranial stimulation (ICS) has been hypothesized based on the observation that the alpha-antagonist phentolamine produced an inhibition of self-stimulation. The present experiment investigated the effects on hypothalamic self-stimulation of the alpha agonist clonidine in normal and in catecholamine-depleted rats. Using a shuttle-box technique that provides a rate-independent index of the rewarding and aversive components of ICS, it was demonstrated that clonidine produces a dose-dependent inhibition of reward that is clearly dissociable from any non-specific effects of the drug. The ineffectiveness of the peripheral alpha-agonist 1-phenylephrine indicates that the inhibition of reward produced by clonidine is mediated centrally. Clonidine and the catecholamine synthesis inhibitor alpha-methyl-p-tyrosine act together in a synergistic manner to greatly increase the magnitude and prolong the duration of the inhibition of reward while leaving the aversive component unaffected. These data are interpreted as supporting an alpha-noradrenergic basis of ICS reward while indicating that the aversive component of ICS is essentially independent of noradrenergic transmission.

Animals↗

PubMed1976

Comparison of the effects of morphine, pentazocine, cyclazocine and amphetamine on intracranial self-stimulation in the rat.

Rats were trained to press a lever in order to stimulate their hypothalamus through a chronically implanted electrode. Dose-response curves were determined for the effects of morphine (0.3-10 mg/kg), pentazocine (1.0-30 mg/kg), cyclazocine (0.03-30 mg/kg) and d-amphetamine (0.1-3.0 mg/kg) on responding for intracranial stimulation, and then were redetermined in the presence of one or two doses of naloxone. The three analgesics produced only dose-related decreases in responding with the following relative potencies: cyclazocine greater than morphine greater than pentazocine. The well-documented rate-increasing effects of d-amphetamine on intracranial self-stimulation were observed at 0.3 and 1.0 mg/kg of the drug; decreases in responding at 3.0 mg/kg were associated with stereotyped behavior. Naloxone, which had no effect of its own on self-stimulation, increased the dose of the analgesics required to depress response rate in a manner consistent with a competitive antagonism. In contrast, response rates at all doses of d-amphetamine tested in the presence of naloxone. Thus, the interaction between naloxone and d-amphetamine is qualitatively different from the one between naloxone and the analgesics. This finding extends to intracranial self-stimulation the generality of a previous report of interactions between d-amphetamine and naloxone on behavior in the rat.

Animals↗

PubMedDate not supplied

[Neuronal activity in self-stimulation zones of the hypothalamus in motivational and emotional states induced by electrical and natural stimuli].

Study of neuronal activity in hypothalamus areas of self-stimulation in rats showed two types of neurones. Some of them had an increased frequency at food and water deprivation and they had maximum activation at current stimulation, eliciting motivational behaviour. Others had maximum activation at current level, eliciting self-stimulation effects, some of these neurones had positive activating relation to satisfaction of food requirements. The obtained data are considered as morphofunctional substrate of motivational and emotional states.

Animals↗

PubMedDate not supplied

[Comparative study of the effects of amphetamine and dimethoxymethamphetamine on brain self-stimulation in rats after perinatal administration of 6-hydroxydopamine].

The effects of amphetamine and its analog dimethoxymethamphetamine (DMA) on self-stimulation of the lateral hypothalamus was studied in adult rats treated with the neurotoxin 6-hydroxydopamine in the prenatal and early postnatal periods. Both compounds administered in a dose of 1 mg/kg produced similar activation of the brain self-stimulation suppressed by 6-hydroxydopamine. DMA, in contrast to amphetamine, did not produce such activation in intact rats and in the animals treated with 6-hydroxydopamine in the prenatal period.

DOM 2,5-Dimethoxy-4-Methylamphetamine↗

PubMedDate not supplied

[Spike activity of dorsal hippocampus neurons of rabbits during self stimulation].

Responses of 47 neurones of the dorsal hippocampus were studied in a chronic experiment on free-behaving rabbits during self-stimulation behaviour. The achievement by the animals of the instrumental habit of pressing the lever produced stimulation of the lateral hippocampus. It was found that different hippocampal neurones change the frequency of their discharges at different stages of self-stimulation behaviour: some at the stage of the animal's approach to the lever, others during stimulation and still others in the poststimulation period. Inhibition and activation reactions in most of the neurones were of opposite direction at the moment of stimulation and in the poststimulation period. During the reinforcing stimulation the hippocampal theta-neurones were the most reactive.

Action Potentials↗

PubMed2004

Influence of nicotine on brain reward systems: study of intracranial self-stimulation.

We used the rate-frequency curve-shift procedure to evaluate the effects of nicotinic blockers, locally infused into the mesopontine tegmentum or ventral tegmentum, on the threshold of brain stimulation reward. Mecamylamine, the nicotinic acetylcholine receptor blocker, was infused one hour before the self-stimulation of the medial forebrain bundle. When injected into the mesopontine tegmentum, mecamylamine shifted rate-frequency curves to the right. Similar effects were also observed when the drug was injected into the ventral tegmentum. Thus, in both the mesopontine tegmentum and the ventral tegmentum, nicotinic receptors appear to facilitate the rewarding effect of the self-stimulation.

Animals↗

PubMed1994

[The role of the paraventricular hypothalamic nuclei in the development of chronic neurogenic hypertension and the formation of a self-stimulation reaction].

Effects of bilateral electric lesion of the hypothalamic paraventricular nuclei on cardiovascular components of the defense response and on the self-stimulation operant behaviour, were studied in rats. Overloading of the highest nervous activity induced no hypertension in these animals, though the self-stimulation frequency increased.

Animals↗

PubMed1994

Medullary-induced alterations in intracranial self-stimulation from the substantia nigra.

The intracranial electrical self-stimulation (ICSS) from the substantia nigra (SN) was reduced by simultaneous stimulation of the nucleus of the solitary tract (NTS) in cats. This effect varied with the current intensity and the sequence of NTS stimulation paired with the rewarding SN stimulation. Namely, NTS stimulation preceding the SN stimulation was more effective in lessening ICSS than that following the SN stimulation. Both SN and NTS stimulations produced significant cardiorespiratory effects, when they were applied separately. However, the cardiorespiratory responses to NTS stimulation have no substantial role in altering ICSS, because vagotomy abolished the heart rate effects of NTS stimulation but caused no change in its reducing effect on ICSS. Moreover, no statistically significant correlation was found between the blood pressure changes and the decrease in response rate. These data are interpreted as suggesting that the NTS stimulation may reduce centrally the rewarding value ordinarily derived from ICSS at the SN.

Animals↗

PubMed1982

A comparison of atropine, benztropine and diphenhydramine on the reversal of haloperidol induced suppression of self-stimulation.

Acute haloperidol administration (0.25, 0.5 mg/kg) produced a severe reduction in locomotor activity and operant responding for intracranial self-stimulation in rats. If the rats were also given 10 mg/kg of either diphenhydramine or benztropine, this behavioral inhibition was substantially reversed. Atropine (10 mg/kg), however, did not significantly alter the haloperidol inhibition. In a second study, the rats were tested 30 and 120 minutes after the haloperidol treatment (0.25 mg/kg). Again, diphenhydramine and benztropine but not atropine substantially reversed the haloperidol suppression after 30 minutes. When retested after 120 minutes, however, atropine and benztropine but not diphenhydramine partially reversed the haloperidol suppression. Thus, the present study provides support that diphenhydramine can be effective in reversing haloperidol induced suppression of self-stimulation but for a shorter duration than benztropine.

Animals↗

PubMed1986

Behavioral research in self-injury and self-stimulation.

This article reviews the behavioral literature on self-injury and self-stimulation. Studies investigating the causes of such pathologic behavior and methods of treatment are critiqued. New, promising treatment procedures, such as "sensory extinction," are described and discussed.

Autistic Disorder↗