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Results for “SELF STIMULATION”

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At least 217 records · Page 12Linked to original sources

PubMed1990

Self-stimulation behavior: consequences upon immunity?

A variety of behavioral and emotional factors can affect the immune response by changing the brain immunoregulatory mechanisms, resulting in immunosuppression or immunopotentiation. This experiment deals with the effect of chronic self-stimulation behavior on the immune response and lymphoid tissue. Male rats were stereotaxically implanted with bipolar electrodes into the lateral hypothalamus and 7 days after surgery were screened for self-stimulation behavior. Lateral hypothalamus self-stimulating rats (LH-SS) were allowed to self-stimulate for 60 min/day for a period of 9 consecutive days: 5 days before and 4 days after immunization with 5 x 10(9) sheep red blood cells (SRBC). The animals were sacrificed and plaque-forming cell assay (PFC), microhaemmagglutination reaction with SRBC, and differential blood leucocyte counts were performed. The thymus, spleen, and inguinal lymph nodes were weighed and processed for histological examination. In the LH-SS group, an enhanced PFC response and increased anti-SRBC antibody titer were observed when compared to controls. The thymus and spleen of LH-SS rats were smaller in size in comparison with controls, but only with moderate changes in splenic cellular make-up. The relative number of lymphocytes was increased in peripheral blood of LH-SS rats when compared to intact animals. The results obtained suggest that chronic self-stimulation behavior can modulate some parameters of humoral immune response and affect the relative weight of lymphoid organs in the rat.

Animals↗

PubMedDate not supplied

[The relationship between the frequency of self-stimulation and parameters of the stimulus].

The dependence of self-stimulation frequency on stimulation parameters (current intensity, stimulation frequency, pulse duration, duration of pulse bursts) was studied in fifteen rats with monopolar electrodes implanted in the lateral hypothalamus, using rectangular current pulses for brain stimulation. All the experiments revealed qualitatively similar response surfaces to the combined change of stimulation frequency and pulse duration Self-stimulation frequency is connected in a non-linear way with the "specific charge" per unit of time, and in an approximately linear way, with the duration of the pulse burst. Regression equations are determined which precisely enough described the kind of response surface (R =0.7 to 0.95).

Animals↗

PubMed1980

Post-amphetamine depression of self-stimulation responding from the substantia nigra: reversal by tricyclic antidepressants.

The effects of long-term amphetamine treatment were examined on self-stimulation responding from the substantia nigra. Rates of self-stimulation responding were substantially depressed among rats chronically treated with amphetamine and tested in the absence of the drug. When rats were subsequently retested after a two day hiatus in which they received imipramine or amitriptyline, the post-amphetamine depression of rates of self-stimulation responding was mitigated. The efficacy of imipramine and amitriptyline in reversing the post-amphetamine depression of self-stimulation responding was also evident during a continuation of the drug (imipramine or amitriptyline)/test sequence, for seven test sessions. The results of the present investigation were related to changes in dopamine and acetylcholine neurotransmission following long-term amphetamine treatement.

Amitriptyline↗

PubMed1998

Effect of adrenalectomy on cocaine facilitation of medial prefrontal cortex self-stimulation.

Adrenalectomy (ADX) is known to block the acquisition of intravenous cocaine self-administration. A previous study therefore examined whether ADX decreases sensitivity of the 'brain reward system' in general, or its response to cocaine in particular, by measuring thresholds for intracranial self-stimulation with and without concurrent cocaine administration. ADX had no effect on thresholds for lateral hypothalamic self-stimulation (LHSS) and did not alter the cocaine dose-response curve for lowering the LHSS threshold. This result suggested that ADX does not affect sensitivity of the brain reward system. However, medial prefrontal cortex (MPFC) appears to be an important site in the mediation of cocaine reinforcing effects, and MPFC self-stimulation (MPFCSS) is mediated by a neural substrate that is largely independent of that which mediates LHSS. The present study therefore assessed whether ADX diminishes cocaine facilitation of MPFCSS. It was found that the threshold-lowering effect of cocaine (5.0, 10.0 and 20.0 mg/kg, i.p. ) did not differ between ADX rats maintained on 0.7% saline, ADX rats maintained on corticosterone (50 microg/ml) in 0.7% saline, and sham-operated controls. However, there was a trend toward desensitization of MPFCSS, itself, following ADX in the group that did not receive corticosterone supplementation. Based on this observation, and the similar responses of MPFCSS and cocaine self-administration to noncontingent priming stimulation, stress, and NMDA receptor antagonism, it is speculated that acquisition of MPFCSS and cocaine self-administration may be dependent upon a common sensitization process that is regulated by corticosterone.

Adrenalectomy↗

PubMedDate not supplied

[A comparison of the efficiency of stimulation of the right and left lateral hypothalamus during a self-stimulation reaction].

Higher rate of the right-side self-stimulation of the lateral hypothalamus than of the left-side was found in freely behaving (30 +/- 8 versus 16 +/- 5 pressings per minute) and fixed rabbits (15 +/- 3 versus 10 +/- 2 pressings per minute, accordingly) under conditions of optimal current (current strength was leveled about the thresholds of food motivational reactions).

Animals↗

PubMed1993

SCH 23390 decreases self-stimulation of the medial prefrontal cortex in the rat.

We studied the effects of peripheral and central administration of SCH 23390, a selective antagonist of dopamine D1 receptors, on intracranial self-stimulation of the medial prefrontal cortex of the rat. Intraperitoneal injections of SCH 23390 produced a dose-related decrease in self-stimulation. Unilateral microinjections of SCH 23390 into the medial prefrontal cortex also produced a dose-related decrease in self-stimulation in the ipsilateral medial prefrontal cortex. However, self-stimulation of the contralateral, noninjected prefrontal cortex, used as control, was not affected. Together with previous data, the present results suggest that the dopamine neurotransmission involved in self-stimulation of the prefrontal cortex of the rat is mediated by dopamine D1 receptors.

Animals↗

PubMed1986

The occurrence of autistic children's self-stimulation as a function of familiar versus unfamiliar stimulus conditions.

The present study was conducted to determine whether certain stimulus conditions were associated with high and low rates of autistic children's self-stimulation. Six autistic boys were assessed in situations varying along three dimensions: familiarity or unfamiliarity of setting, learning task, and therapist. Each child was observed in 10 10-min stimulus conditions, and trained observers recorded the occurrence of self-stimulation within each condition. The results of a 2 x 2 x 2 ANOVA indicated that self-stimulation occurred significantly more often with an unfamiliar than with a familiar therapist. Unfamiliar versus familiar setting and task were not significant effects, and there were no significant interactions. Also, significant differences were found within each condition, with self-stimulation increasing in frequency as the sessions progressed. Finally, there was a significant and negative correlation between the occurrence of self-stimulation and correct responding. These findings suggest several treatment strategies for facilitating a generalized suppression of autistic children's self-stimulation.

Autistic Disorder↗

PubMed1992

Behaviourally derived estimates of excitability in striatal and medial prefrontal cortical self-stimulation sites.

The refractory periods of the substrate underlying brain-stimulation reward were investigated in three rats with moveable electrodes implanted in the rostral caudate-putamen and the medial prefrontal cortex. Acquisition of caudate-putamen self-stimulation occurred within the first session, while self-stimulation for medial prefrontal cortex was observed only after three sessions of caudate-putamen stimulation. The currents required for self-stimulation ranged from 300 to 800 microA (0.1 ms pulse duration) across animals; the maximum response rates averaged roughly 40 bar presses per minute for both structures. Refractory period estimates were obtained from ten caudate-putamen and four medial prefrontal cortex sites. The time course of recovery had the following profile: the curves began to rise at 0.65 ms and 0.95 ms for caudate-putamen and medial prefrontal cortex stimulation, respectively, thereafter increasing to approach an asymptote at 6.00 ms for the caudate-putamen and 6.25 ms for the medial prefrontal cortex. The mean effectiveness value corresponding to the asymptotic portion of the curves was 73% for the caudate-putamen and 69% for the medial prefrontal cortex. Like other forebrain structures, the behaviourally derived refractory periods underlying caudate-putamen and medial prefrontal cortex stimulation, at least at these particular sites, are significantly longer than those observed in most medial forebrain bundle areas, both beginning and ending later. One interpretation for the similarity in their refractory period profiles and the apparent facilitating effect of caudate-putamen stimulation on acquisition of medial prefrontal cortex self-stimulation is that these two regions form part of the same reward substrate.

Animals↗

PubMed1981

Interactions between intracranial electrical self-stimulation behavior and cardiovascular responses.

Interactions between electrical self-stimulating behavior, cardiovascular state and reactions were studied in a series of chronically prepared cats. Pressor responses were found to be the most common cardiovascular concomitants of intracranial electrical self-stimulating behavior in cats. The lever-pressing rate for brain stimulation decreased under the effect of both dibenzyline, an adrenergic blocking agent, and local anesthesia of the cervical vago-sympathetic trunk by procaine. Bilateral vagotomy resulted in an acceleration in lever-pressing responses. The depression and the acceleration in the lever-pressing for brain stimulation were associated with an increase and a decrease in pulse pressure, respectively. It is suggested that peripheral autonomic modifications exert a regulatory feedback effect on the rewarding property of brain stimulation.

Adrenergic Fibers↗

PubMed1987

Learnt tolerance to sedative effects of chlordiazepoxide on self-stimulation performance, but no tolerance to facilitatory effects after 80 days.

Sedative and facilitatory effects on variable-interval hypothalamic self-stimulation were monitored during chronic treatment with chlordiazepoxide (CDP; 7.5 mg/kg IP), given at 48-h intervals in two groups of rats. Group 1 was injected immediately before each of 40 1-h self-stimulation sessions ("drugged responding"); Group 2 was injected after self-stimulation for the first 20 sessions ("undrugged responding"), and before self-stimulation for a further 20 sessions ("drugged responding"). Significant sedation occurred in both groups in initial sessions of drugged responding, even though Group 2 had already received 20 injections of CDP (after undrugged sessions). Sedative effects showed very rapid tolerance, and disappeared after 1-3 sessions, but only in rats which had been responding while drugged (and which thus had had opportunities to develop coping strategies against the sedative effects). After further sessions of drugged responding, sedation was replaced by apparently stimulant effects. Stimulant effects showed no tolerance at all in either group even after 40 injections, thus differing from anti-conflict (and other) effects of BZDs, which generally show gradual tolerance. These results show that coping strategies acquired by instrumental learning can account for rapid and selective tolerance to sedative effects. Coping strategies do not account for the differing rates of tolerance to stimulant and to other effects of BZDs; these differences may indicate pharmacologically distinct brain systems downstream from the BZD receptor.

Adaptation, Psychological↗

PubMed2004

Differential effects of intra-midbrain raphe and systemic 8-OH-DPAT on VTA self-stimulation thresholds in rats.

RATIONALE: Intra-median raphe nucleus (MRN) administration of the 5-HT(1A) receptor agonist 8-OH-DPAT decreases lateral hypothalamic self-stimulation thresholds and is reported to have biphasic effects following systemic administration. These experiments attempted to extend the previous findings to mesolimbic pathway self-stimulation at ventral tegmental area (VTA) electrodes. OBJECTIVES: This study was conducted to provide comparative data for systemic and intra-dorsal raphe nucleus (DRN) and intra-MRN effects of 8-OH-DPAT on VTA self-stimulation. METHODS: Male Sprague-Dawley rats with VTA electrodes were trained to respond for electrical stimulation. Systemic and intra-midbrain raphe 8-OH-DPAT effects on rate-frequency thresholds were measured. Systemic administration of WAY 100635 was used to confirm 5-HT(1A) receptor mediation of 8-OH-DPAT effects. RESULTS: 8-OH-DPAT (0.003-0.3 mg kg(-1) SC) increased rate-frequency thresholds and decreased maximal response rates. WAY 100635 alone (0.0125-0.1 mg kg(-1) SC) did not alter these measures. Intra-DRN and intra-MRN 8-OH-DPAT (5.0 microg) decreased rate-frequency thresholds without altering maximal response rates. Intra-DRN 8-OH-DPAT (0.1-5.0 microg) induced a slight decrease and intra-MRN 8-OH-DPAT a slight increase in locomotor activity. WAY 100635 (0.1 mg kg(-1)) blocked effects of 8-OH-DPAT on VTA self-stimulation. CONCLUSION: These results confirm threshold-decreasing effects of intra-MRN 8-OH-DPAT and extend this to the DRN and to VTA thresholds. Monophasic dose dependent increases in VTA thresholds following systemic 8-OH-DPAT are not equivalent to reports for hypothalamic self-stimulation. Differences between studies may be attributable to stimulation site and/or differences in threshold measurement procedures. Effects of WAY 100635 in this study indicate 5-HT(1A) receptor mediation of these 8-OH-DPAT effects.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1978

Response-dependent effects of morphine on reinforcing lateral hypothalamic self-stimulation.

The effects of morphine (10mg/kg) on intracranial self-stimulation were studied in three separate test situations, each requiring rats to perform different types of responses. Self-stimulation was depressed in a test of rate of bar-pressing, to a lesser extent in a test of rate of wall-pressing in which a wider range of movements were reinforced, but not in a shuttle-box, with brain stimulation continuously available on one side of box. This resonse dependency suggests that the depressive effect of morphine on bar-pressing for lateral hypothalamic stimulation reflects a performance deficit rather than an effect on the reinforcing value of the stimulation.

Animals↗

PubMed1987

Effects of knife-cut lesions of the medial forebrain bundle in self-stimulating rats.

Unilateral frontal-plane knife-cut lesions were made in the anterior medial forebrain bundle ipsilateral to a lateral hypothalamic self-stimulation electrode. Behavioral effects of the knife cut on self-stimulation reward and operant performance capacity were measured via the reward summation function method. Knife cuts placed at the level of the anterior commissure were ineffective in altering reward or motor/performance capacity, whereas knife cuts just posterior in the caudal lateral preoptic area degraded reward and sometimes impaired motor/performance capacity. In a second experiment, knife cuts placed posterior to the ventral tegmental area were ineffective unless they intruded on the ventral tegmental area itself. Several small knife cuts placed just anterior to the ventral tegmental were effective in reducing self-stimulation reward. The results are discussed in terms of the anatomical substrate of lateral hypothalamic self-stimulation reward and as a first step in a larger mapping study.

Animals↗

PubMed1990

Differences in sensitivity to neuroleptic blockade: medial forebrain bundle versus frontal cortex self-stimulation.

The effects of systemic injections of the dopamine receptor antagonist, cis-flupenthixol were tested on intracranial self-stimulation at electrode sites in the medial forebrain bundle and the medial prefrontal cortex. Changes in the reward effectiveness of the brain stimulation were assessed using a curve-shift paradigm. Low to moderate doses of cis-flupenthixol (0.05, 0.1 and 0.15 mg/kg) consistently produced larger upward shifts in the rate-frequency function for medial forebrain bundle than for medial prefrontal self-stimulation. At the highest doses of cis-flupenthixol (0.15 and 0.2 mg/kg), some of the medial forebrain bundle rats failed to respond, whereas all medial prefrontal rats responded at these doses. These results demonstrate that medial forebrain bundle self-stimulation is much more dependent on dopamine systems than is prefrontal cortex self-stimulation.

Animals↗

PubMed1989

Kelatorphan, a potent enkephalinases inhibitor, and opioid receptor agonists DAGO and DTLET, differentially modulate self-stimulation behaviour depending on the site of administration.

Endogenous enkephalins have been found in the perikaryon of the mesolimbic dopaminergic ventral tegmental area and in axonal terminals in the nucleus accumbens. To examine whether endogenous opioid peptides may modulate this mesolimbic system, injections of dopamine receptor agonists and antagonist, the mu-opioid receptor agonists DAGO and morphine, the delta-opioid receptor agonist DTLET and kelatorphan, a new potent inhibitor of multiple enkephalin-degrading enzymes, were performed into the lateral ventricle and into the nucleus accumbens. Intracranial self-stimulation behaviour, obtained through electrodes chronically implanted into the medial forebrain bundle in the posterolateral hypothalamus of the rat, was used as behavioural paradigm. Injections of kelatorphan and DTLET into the lateral ventricle both induced an ICI 174,864-reversible increased self-stimulation behaviour, a similar increase was observed after injection of d-amphetamine, while morphine and DAGO reduced the rate of self-stimulation. In contrast, the administration of kelatorphan or dopamine receptor agonists into the nucleus accumbens reduced the rate of intracranial self-stimulation, while DTLET was without effect, when injected into the same structure. Finally, intra-accumbens injections of DAGO produced a similar behavioural profile to that produced by intraventricular injections of the drugs. Opioids may thus differentially affect intracranial self-stimulation behaviour, as a function of the neuroanatomical locus of administration. Furthermore, these results suggest that kelatorphan may increase self-stimulation behaviour through an action at delta-opioid receptor, while DAGO and morphine may reduce self-stimulation behaviour through an action at mu-opioid receptors.

Animals↗

PubMed1976

Is the release of noradrenaline necessary for self-stimulation of the brain?

The hypothesis that a quantity of noradrenaline released contingently on every response made to obtain brain stimulation mediates the reward produced by the stimulation was tested. An alternative hypothesis is that reward is mediated by a different system, but that a steady activation of post-synaptic receptors by noradrenaline is necessary for normal behavior. The synthesis of noradrenaline was inhibited by disulfiran, and when lateral hypothalamic self-stimulation in the rat had ceased, alpha-adrenergic stimulants were injected intraventricularly (IC) or intraperitoneally (IP). The directly acting receptor stimulants oxymetazoline (0.9-250 mug IC), naphazoline (20-250 mug IC), and clonidine (0.75-3 mug IC, 0.037-3 mg/kg IP) did not restore self-stimulation, but the indirectly acting stimulants amphetamine (2 mg/kg IP), methylphenidate (3 mg/kg IP) and phenylephrine (15 mug IC) did not restore self-stimulation. In Experiments 2 and 3, in which either the functional noradrenaline pool was depleted with disulfiram and amphetamine, or the reserve noradrenaline pool was depleted with reserpine, the action of phenylephrine in restoring self-stimulation was shown to be indirect, probably by mobilizing a reserve pool of noradrenaline. Because only indirectly acting noradrenergic stimulants which facilitate the release of noradrenaline restores self-stimulation, it is concluded that noradrenaline must be released contingent on every response for self-stimulation to occur. Whether this released noradrenaline mediates the reward or has some other function associated with bar-pressing behavior remains to be shown.

Amphetamine↗

PubMed1977

[Influence of psychotropic substances on the self stimulation response].

D-amphetamine and cocaine were found to facilitate septal self-stimulation. In low doses morphine, imipramine, benactyzine, meprobamat, diazepam, chlordiazepoxide, phenobarbital, LSD-25 failed to influence this index, but in high doses they depressed the self-stimulation. It is supposed that d-amphetamine and cocaine exerted a direct stimulating action of the positive reinforcement system of the septum. Inefficiency of the other above-mentioned agents was due to the absence of the nervous substrate of negative reinforcement at the septum level. A comparative study of the above results and the influence of neurotropic agents on the hypothalamic self-stimulation (literature data) indicated that the activating effect of psychotropic agents on the systems of positive reinforcement depended upon their influence on the emotiogenic brain structures and not on the structures responsible for the formation of motivations.

Amphetamine↗

PubMed1973

Effects of -methyl-p-tyrosine and L-DOPA on brain self-stimulation and motor activity in rats.

Rats with electrodes implanted in the posterior lateral hypothalamus and ventromedial tegmentum were trained to self-stimulate. Animals were treated (i.p.) first with alpha-methyl-p-tyrosine (alpha-MPT) and then L-DOPA; their self-stimulation rates and spontaneous behaviour were recorded. alpha-MPT (100 mg/kg) had an immediate and long lasting suppressive effect on self-stimulation, within the first half hour. L-DOPA administration failed to reinstate self-stimulation. Hypoactivity also followed alpha-MPT injections. While the behavioural changes were minimal after L-DOPA 50 mg/kg, a decrease of spontaneous activity and moderate hyper-reactivity were observed following L-DOPA at a dose of 200 mg/kg. Theoretical implications are discussed.

Animals↗