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Results for “SELF STIMULATION”

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At least 307 records · Page 17Linked to original sources

PubMed1981

Self-stimulation of the habenular complex in the rat.

The rewarding effect of habenular stimulation was studied in 65 rats. The animals learned to bar press for electrical stimulation of the medial or lateral habenular nucleus or the fasciculus retroflexus, but not the surrounding thalamic nuclei. The response rates were moderate and steady and not influenced by food or water deprivation. Habenular self-stimulation was significantly facilitated by placing lesions in the ipsilateral anterior part of the medial forebrain bundle (MFB). Similarly, MFB self-stimulation was enhanced by ipsilateral habenular lesions. Lesions centered in the region of median raphe nucleus suppressed habenular self-stimulation for more than 4 wk. Self-stimulation of median raphe was not affected by habenular lesions. The results show that habenular stimulation can produce a rewarding effect by exciting neurons in the region of the raphe nuclei but apparently without requiring the participation of the well-known MFB reward system.

Animals↗

PubMed1993

Tolerance and sensitization to stimulant and depressant effects of nicotine in intracranial self-stimulation in the rat.

Nicotine is thought to be an important factor in addiction to tobacco but its psychopharmacological properties are still uncertain. In the present study, rats were trained to operate a pedal to obtain threshold-current, variable-interval hypothalmic stimulation. Response rates were printed out at 10min intervals to provide a continuous record of facilitatory or depressant effects by injected nicotine. Responding was enhanced in all rats but this depended on dose, time after injection, and previous exposure to the drug. In the first 10min after injection, responding by drug-naive rats was either unaffected (40-130mg/kg s.c., as base) or strongly depressed (400µg/kg). This phase was followed by prolonged (>50min) dose-dependent facilitation. Higher doses (1.3mg/kg) caused prostration. Chronic exposure to nicotine (400µg/kg x 10 at 2-5 day intervals) reduced the initial depressant effect; it also augmented subsequent responding, but only in the early minutes after injection; the latter finding indicates that apparent sensitization to chronic nicotine may depend primarily on tolerance to its depressant effects, rather than on receptor upregulation. Stimulant and depressant effects of nicotine were prevented by pretreatment with the centrally acting antagonist, mecamylamine (2.0mg/kg s.c.), but not by the peripheral antagonist, hexamethonium (1.0mg/kg s.c.) or by the muscarinic receptor antagonist, hyoscine (scopolamine; 100-300µg/kg s.c.). Self-stimulation was unaffected by mecamylamine alone. Thus the inhibitory action of nicotine is unlikely to be due to depolarization block, peripheral activity or muscarinic activity. Its facilitatory and depressant effects appear to be narrowly time- and dose-specific, thus accounting for divergent findings in many studies.

Journal Article↗

PubMed1990

Stressor induced variations of intracranial self-stimulation from the mesocortex in several strains of mice.

Intracranial self-stimulation (ICSS) from the mesocortex was assessed in BALB/cByJ, C57BL/6J and DBA/2J mice immediately, 24 h and again 168 h following stressor application. Stressor exposure failed to influence ICSS performance in C57BL/6J mice, while self-stimulation performance was reduced among BALB/cByJ mice only in the immediate post-stressor interval. In contrast, DBA/2J mice exhibited reduced rates of responding for brain stimulation at each of the post-stressor intervals. The potential contribution of DA alterations to the strain-dependent variations of ICSS performance induced by uncontrollable footshock are discussed.

Animals↗

PubMed1982

Apomorphine-induced facilitation of intracranial self-stimulation following dopamine denervation of the nucleus accumbens.

Two groups of rats were trained to lever press for intracranial self-stimulation (ICSS) from electrodes aimed at the posterior lateral hypothalamus or at the region of the locus coeruleus. Following stabilization of baseline responding using descending rate/intensity functions, bilateral 6-hydroxydopamine (6-OHDA) lesions to the nucleus accumbens (N.Acc.) were performed. Subsequent injections of apomorphine (SC) resulted in significant increases in self-stimulation in both lesion groups and significant decreases in self-stimulation in both groups of sham operated animals. These results indicate that the destruction of the dopaminergic terminals in the nucleus accumbens results in a "supersensitive" enhancement of the ICSS stimulating properties of apomorphine regardless of the electrode placement. Both lesion groups also showed a pronounced increase in locomotor activity in photocell cages following treatment with the same dose of apomorphine. These results complement previous work showing that dopamine destruction affects ICSS regardless of electrode placement and support the hypothesis that the midbrain dopamine systems have a general response enabling role in reinforced behavior.

Animals↗

PubMed1986

Self-stimulation behavior can be elicited from various 'aversive' brain structures.

Electrical stimulation applied to various brain regions of the negative motivational system: the dorsal part of the mesencephalic central gray area (CG) the medial hypothalamus (MH), the medial lemniscus (ML), the lateral tegmentum (LT) and the reticular formation (RF), produces vigorous escape responses in mice. In spite of their highly aversive consequences, stimulation of all these regions also elicits self-stimulation behavior. This paradoxical approach response was clearly observed when the animals were placed in a Y-maze where they could successively trigger and turn off continuous electrical stimulation. In effect, mice stimulated in 'aversive' structures, similarly to animals stimulated in the lateral hypothalamus (LH), were able to discriminate between the reinforced arm and the non-reinforced arm of the Y-maze in order to self-administer the stimulation. When the mice were placed in a lever press box which delivered 0.2 s of electrical stimulation, an evident self-stimulation behavior was observed in LH and in some animals implanted in RF or MH. On the other hand, the very low response rates recorded in CG, LT, ML and in other RF or MH implanted mice do not permit a description of the motivational properties of these different stimulation sites. These results show that stimulation of brain structures of the negative reinforcement system has an approach component which, however, shows up clearly only in certain experimental situations.

Animals↗

PubMed1989

Footshock stress facilitates self-stimulation of the medial prefrontal cortex but not the lateral hypothalamus in the rat.

The effects of stress on self-stimulation were investigated by exposing rats to either controllable, uncontrollable or no footshock. Both controllable and uncontrollable footshock increased medial prefrontal cortex self-stimulation rates immediately as well as 24 h following treatment. Controllable footshock produced a greater enhancement than uncontrollable footshock. In contrast, self-stimulation of the lateral hypothalamus was unaffected by either footshock treatment. These results are interpreted with reference to the neurochemical response of the mesocortical dopaminergic system to acute stress.

Animals↗

PubMed1978

[Hypothalamic self-stimulation during the abstinence syndrome in morphine-dependent rats].

Rats with lateral hypothalamic self-stimulation were treated chronically with morphine (30 injections in the course of 15 days) in doses increasing stepwise from 20 to 120 mg/kg per injection. Morphine facilitated self-stimulation from the 9th injection. Both short-term abstinence (16-18 hours) and cessation of the narcotic resulted in inhibition of the response. Full suppression of self-stimulation occurred under the administration of nalorphine, morphine antagonist, in a dose of 5 mg/kg.

Animals↗

PubMed1997

Serotonergic modulation of 3,4-methylenedioxymethamphetamine (MDMA)-elicited reduction of response rate but not rewarding threshold in accumbal self-stimulation.

In a fixed interval 5-s rate-frequency function paradigm with rats, 3,4-methylenedioxymethamphetamine (MDMA; 0.5, 2 and 4 mg/kg) dose-dependently decreased response rate for nucleus accumbens self-stimulation while both D-amphetamine (0.3 and 1 mg/kg) and cocaine (5 and 15 mg /kg) increased response rates. The highest doses of MDMA caused a cessation of responding in many of the rats tested, but in those rats that continued to respond a significant reduction in frequency threshold for self-stimulation was seen. Cocaine and amphetamine dose-dependently reduced frequency threshold in all rats tested. The non-specific serotonin antagonist, methysergide (5 mg/kg), reversed the inhibitory effects of MDMA on response rates and caused all rats to respond following MDMA (4 mg/kg). Methysergide did not affect MDMA's threshold-lowering properties and when administered alone methysergide had not effect on self-stimulation. These results suggest serotonergic involvement in the performance but not reinforcement-modulating effect of MDMA in the self-stimulation paradigm.

Animals↗

PubMed1980

Evidence for an involvement of acetylcholine in self-stimulation of the prefrontal cortex in the rat.

The effects of injections of antagonists of muscarinic and nicotinic receptors on self-stimulation of the prefrontal cortex in the rat were studied. The results of this investigation suggest that acetylcholine is involved in self-stimulation of the prefrontal cortex through activation of muscarinic receptors, and also suggest a possible interaction between acetylcholine and dopamine in mediating self-stimulation of this area of the brain.

Acetylcholine↗

PubMed1977

Self-stimulation of the MFB or VTA after microinjection of haloperidol into the prefrontal cortex of the rat.

Haloperidol, a dopamine receptor antagonist, was microinjected in doses of 12 or 24 microng into the prefrontal cortex of the rat. Its effects on self-stimulation of the ventral tegmental area (VTA) or the medial forebrain bundle (MFB) were examined. It was found that these injections failed to attenuate self-stimulation at either structure. However, when haloperidol was injected into the caudate-putamen complex, a decrease in self-stimulation occurred within these structures. These results suggest that dopamine in the medial prefrontal cortex is not necessarily a part of the neurochemical substrate underlying self-stimulation of the ventral tegmental area or medial forebrain bundle.

Animals↗

PubMed1976

Effect of intraventricular oxytocin and vasopressin on self-stimulation in rats.

Oxytocin (500 mu u) and vasopressin (50 mu u) were injected into the lateral ventricle and its effect on hypothalamic self-stimulation has been studied. Oxytocin increased, while vasopressin decreased the self-stimulation rate tested 10-20 min following application. The hypothalamic and mesencephalic serotonin content decreased slightly while plasma corticosterone content did not change 20 min after oxytocin and vasopressin administration compared to the injected control animals. The data suggest that vasopressin and oxytocin have an opposite effect on self-stimulation and this action is not mediated through the brain serotoninergic or pituitary-adrenocortical axis.

Animals↗

PubMedDate not supplied

[Effect of excitation summation during interaction of self-stimulation zones].

A study was made on rats with electrodes implanted in the lateral preoptic hypothalamic area, of the interaction between distant foci of "positive" excitation in a situation when one of the foci (conditioning one) was set up by the animal itself by self-stimulation with a rhythmic current, while the other (testing) was imposed through stimulation of a different positive point with rhythmic and direct currents. Imposed stimulation of the distant positive zones by rhythmic current within a sufficiently wide range of intensities intensifies the self-stimulation in the conditioning focus. Polarization of the testing positive zones by a DC cathode produces a two-phase reaction of the conditioning points of self-stimulation: initial inhibition at the action of relatively weak DC intensities attended with its subsequent intensification when intensity of the polarizing current increases. It is suggested that the motivation (low-threshold) and reinforcing (high-threshold) components may be involved in the mechanism of phasic interaction between excitation foci in the self-stimulation system.

Animals↗

PubMed1978

Cocaine: acute effects on reinforcement thresholds for self-stimulation behavior to the medial forebrain bundle.

Reinforcing thresholds for self-stimulation behavior to the medial forebrain bundle were determined in rats by means of rate-free psychophysical method. The acute administration of cocaine lowered the reinforcing thresholds independent of motor stimulatory effects. These results indicate that cocaine affects the sensitivity of the reward pathways in the brain, and further demonstrate the utility of rate-independent methods in the assessment of drug effects on self-stimulation behavior.

Animals↗

PubMedDate not supplied

[Correlation of dopamin- and GABA-ergic mechanisms in the depressive effect of neuroleptics on pedal self-stimulation of the ventral tegmentum of the mesencephalon].

Inhibition of self-stimulation of the ventral tegmentum in male rats with droperidol, haloperidol, trifluoroperazine and chlorpromazine is realized by dopamin- and GABA-ergic mechanisms of the emotional-positive reinforcement system. The GABA-ergic rather than dopaminergic mechanisms of the positive reinforcement systems realize the fluphenazine-induced reduction of self-stimulation of the midbrain ventral tegmentum. Analogous effects of clozapine and thioridazine are realized outside the dopamin- and GABA-ergic mechanisms of the reinforcement system.

Animals↗

PubMedDate not supplied

Differential effects produced by an anticholinergic on the neuroleptic inhibition of motor behaviour and self-stimulation of the prefrontal cortex in the rat.

A specific dopamine receptor blocker, spiroperidol (0.016, 0.032, 0.064 and 0.128 mg/kg) alone or in combined treatment with the centrally acting anticholinergic, dexetimide (0.5, 1.0 mg/kg) was given intraperitoneally to rats pressing a lever for brain self-stimulation through electrodes implanted in the medial prefrontal cortex. The same treatment was also given to rats in which the spontaneous motor behaviour was measured. Spiroperidol produced a dose-related inhibtion of both self-stimulation and spontaneous motor activity. Dexetimide, given to spiroperidol treated rats, was able to antagonize the motor impairment produced by spiroperidol, but prefrontal cortex self-stimulation remained decreased. These data support the suggested role for dopamine in self-stimulation of the prefrontal cortex in the rat.

Animals↗

PubMed1973

Histamine: effect on self-stimulation.

When injected discretely into the lateral hypothalamus of rats, histamine inhibited electrical self-stimulation at the injection site without affecting self-stimulation in the contralateral lateral hypothalamus. This effect was blocked by prior treatment with antihistaminics. Histidine, the amino acid precursor of histamine, produced a similar effect after a delay of 6 to 10 minutes.

Animals↗

PubMed1980

On the role of reduced auditory feedback and kinesic self-stimulation during Stroop Color-Word Performance.

Feedback from one's own voice provides important vocal-motor cues for effective cognitive processing. Reduction of such feedback is known to disturb such functioning. Work in our laboratory has shown that kinesic self-stimulation also plays an important role in cognition, and appears to regulate the focusing of attention under conditions of distraction. The present study investigated the effects of both auditory feedback and kinesic self-stimulation in the regulation of cognitive interference during performance of the Stroop Color-Word Task. Twelve subjects were tested on the Stroop task under conditions of normal and occluded hearing. Kinesic self-stimulation and response errors during color-word performance were recorded on video tape. The findings indicated that not only did self-stimulation increase when voice feedback was reduced, but that this increase was associated with a reduction in specific types of color-word performance errors. Individual differences revealed that high kinesic responders made significantly fewer errors in task performance than did low kinesic responders. Results were interpreted as revealing a kinesic feedback mechanism which has adaptive significance in regard to self-editing when auditory feedback is reduced.

Adolescent↗

PubMed1989

Naloxone suppression of self-stimulation is independent of response difficulty.

The action of the opiate antagonist naloxone on relatively easy (nose-poke) and relatively difficult (lever-press) self-stimulation behaviors was compared, in order to determine if opiate antagonists suppress self-stimulation by interfering with the ability of the animal to respond, or by reducing the reinforcement value of the stimulation. Naloxone (0.2, 2.0 and 20 mg/kg) significantly suppressed both nose-poking and lever-pressing self-stimulation rates, and the degree of suppression was virtually identical for both tasks at all doses examined. If naloxone had interfered with the ability of the animal to respond, then lever-pressing--which requires more motor output than nose-poking--should have been more suppressed than nose-poking. The results suggest that opiate antagonists do not interfere with the ability of the animal to respond, and are therefore consistent with the hypothesis that these drugs reduce the reinforcement value of the stimulation.

Animals↗