SEARCH · PubMed Health

Results for “SELF STIMULATION”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 487 records · Page 27Linked to original sources

PubMed1990

Failure of amygdaloid lesions to increase the threshold for self-stimulation of the lateral hypothalamus and ventral tegmental area.

It has been proposed that the directly stimulated axons underlying the rewarding effect of medial forebrain bundle (MFB) stimulation originate in the forebrain and descend at least as far as the ventral tegmentum. However, little is known about the location of the somata that give rise to these axons. Among the nuclei that contribute fibers to the descending component of the MFB and project past the lateral hypothalamus (LH) and ventral tegmental area (VTA) are cell groups within the amygdaloid complex. In this study, the rewarding effectiveness of stimulating the LH and VTA was measured before and after the amygdaloid complex was damaged by electrolytic lesions. Changes in rewarding effectiveness were inferred from shifts in the frequency required to sustain a half-maximal rate of lever-pressing at each of 3 currents. Following the lesions, there was no clear evidence of substantial, sustained decreases in rewarding effectiveness at the 14 stimulation sites, although one subject ceased to self-stimulate reliably. Given that the lesions damaged the principal amygdaloid sources of descending MFB fibers, these results suggest that the amygdaloid complex is not a major source of the directly activated fibers responsible for the rewarding effect of MFB stimulation.

Amygdala↗

PubMedDate not supplied

[Conditioned-reflex activation of electrical self-stimulation of the brain: a model of a situational craving for narcotics].

Rats with electrodes implanted into lateral hypothalamus were trained to press a lever to obtain electrical stimulation of the brain. After elaboration of self-stimulation (SS) conditioning of morphine-induced activation of SS-response was carried out. Five pairings were performed of morphine (3 mg/kg, i.p.) administration and SS in the box with distinct environmental cues (brightness, color, floor texture, background noise). After morphine withdrawal activation of SS was reproduced after simple placing of the animal in "conditioned" chamber. This effect was naloxone-sensitive. The observed effect is considered to be the adequate model of addictive substances craving.

Animals↗

PubMed1996

Increased ipsilateral expression of Fos following lateral hypothalamic self-stimulation.

Immunohistochemical labeling of Fos protein was used to visualize neurons activated by rewarding stimulation of the lateral hypothalamic level of the medial forebrain bundle (MFB). Following training and stabilization of performance, seven rats were allowed to self-stimulate for 1 h prior to anesthesia and perfusion. Brains were then processed for immunohistochemistry. Two control subjects were trained and tested in an identical manner except that the stimulator was disconnected during the final 1 h test. Among the structures showing a greater density of labeled neurons on the stimulated side of the brains of the experimental subjects were the septum, lateral preoptic area (LPO), medial preoptic area, bed nucleus of the stria terminalis, substantia innominata (SI), and the lateral hypothalamus (LH). Several of these structures, the LPO, SI, and LH, have been implicated in MFB self-stimulation by the results of psychophysical, electrophysiological, and lesion studies.

Animals↗

PubMedDate not supplied

[Effect of neuroleptics on foot-pedal self stimulation from the ventral tegmentum mesencephali in rats and its correlation with cataleptogenic action].

Experiments on rats have shown that droperidol, fluorophenazine, haloperidol, triphtazine, aminazin, thioridazin and clozapin are capable to reduce pedal self-stimulation from the ventral tegmen of the midbrain, which is not related to the cataleptogenic action of the neuroleptics or to their effect on the actuating motor mechanisms but is a consequence of the action on the emotional-positive reinforcement system. A significant positive correlation was disclosed between the ability of the neuroleptics given in effective doses to reduce pedal self-stimulation from the ventral tegmen and their cataleptogenic action.

Animals↗

PubMed1998

Development of osteoarthritis in the knee joints of Wistar rats after strenuous running exercise in a running wheel by intracranial self-stimulation.

The influence of excessive running load on the development of knee osteoarthritis (OA) was investigated in male Wistar rats. Running exercises were performed in a running wheel using intracranial self-stimulation to motivate Wistar rats to run daily distances of 500 m at 5 days/week. Hereby, ten rats ran a distance of 15 km within three weeks while a further ten rats run a total of 30 km within six weeks. Thirteen Wistar rats without running exercises served as controls. Complete knee joint sections of all rats were evaluated histologically using MANKINs grading system with categorization of the findings into non, mild moderate, and severe osteoarthritis. In addition, immunoreactivity of the chondrocytes to MMP-3 as an important cartilage degrading enzyme in OA was assessed by immunostaining with monoclonal MMP-3 IgG antibodies. Histological assessment of the knee joint sections revealed a significant increase in osteoarthritic changes with higher running load. While in rats with 15 km running all but two knee joints showed mild OA, moderate OA was the predominant finding in rats with 30 km running. In contrast, no OA was found in the controls. Immunostaining for MMP-3 revealed a significant increase in immunoreactivity of the chondrocytes to MMP-3 with higher running load, indicating a running load-depending production of this cartilage-degrading enzyme in the course of increasing OA. Compared to 47.4% immunoreactive chondrocytes to MMP-3 in the controls, this ratio rose to 70.4% in rats with 15 km running and even up to 89.9% in rats with 30 km running. In conclusion, in Wistar rats, excessive running load leads to marked, running distance-depending osteoarthritic changes which are caused, at least in part, by an increase in MMP-3 production rising with greater running distance. Within this exercise model of OA, intracranial self-stimulation is an effective method to motivate Wistar rats to extremely excessive running in a running wheel. This model offers a wide range of further approaches to studying different processes of the development of OA.

Animals↗

PubMed1982

Intracranial self-stimulation in the thalamus of the rat.

Rats were tested for intracranial self-stimulation (ICSS) via bipolar electrodes situated throughout the thalamus. Of 112 animals in the study, 55 met the criteria for ICSS, with scores ranging from 55 to 921 bar-presses in a 15 minute session. A map of both positive and neutral placements is presented. Positive sites for ICSS were found in all aspects of the mediodorsal nucleus, except for the central segment. The ventromedial nuclear complex was also a positive area of ICSS, with the exception of the submedial nucleus (nucleus gelatinosus). Each of the intralaminar nuclei (central medial, parafascicular, paracentral, and central lateral) supported ICSS, as did each of the midline nuclei (rhomboid, paratenial and paraventricular). No placements were found in the nucleus reuniens. Both "major" relay nuclei, the ventrobasal and ventrolateral, supported ICSS; but neither the laterodorsal nor the lateral posterior nuclei had positive caudal thalamus. As a general rule, ICSS scores appeared to be higher as the electrode placements approached the midline. Sites in which no positive placements were seen included the reticular nucleus, as well as the stria medularis, the mammillothalamic tract, and the fasciculus retroflexus.

Animals↗

PubMed1993

Ventral tegmental self-stimulation selectively induces opioid peptide release in rat CNS.

Intracranial self-stimulation (ICS) is thought to activate neuronal systems involved in processing natural reinforcing agents. Metabolic mapping studies have previously demonstrated a subset of CNS structures specifically engaged by ICS in animals receiving stimulation actively vs. passively. Since opiates are known to enhance ICS behavior and presumably its reinforcing properties, the current study addressed the question of the role of opioid peptides as mediators of ICS. Rats were trained on a fixed ration (FR) 20 schedule of responding maintained by ICS. Following response stabilization, rats were assigned either to an active or a corresponding yoked stimulation group at 1 of 2 schedules of reinforcement (i.e., FR1-YFR1, FR20-YFR20, or sedentary control), and opioid peptide release was inferred from in vivo receptor occupancy. Autoradiographic analyses identified 3 groups of structures. Treatment-induced alterations in occupancy were seen in the medial dorsal nucleus of the thalamus, basolateral amygdala, ventral pallidum, medial habenula, dorsal raphe, posterior hypothalamus, substantia nigra pars compacta, agranular preinsular cortex, and zona incerta. Depending upon the structure, peptide release was dependent upon stimulus contingency (active vs. yoked) and/or schedule (FR1 vs. FR20). Evidence for ICS-induced inhibition of peptide release was found in the habenula and preinsular cortex. Nine additional structures, all components of, or receiving projections from, the limbic system, revealed complex interactions between ICS treatment and the electrode side. Finally, a widespread ipsilateral increase in receptor binding was seen rostrally from the cingulate, olfactory tubercle, and nucleus accumbens, along the lateral hypothalamus and hippocampus, and extending caudally to the substantia nigra and ventral tegmentum. These later effects appear to be related to stimulation-induced changes in blood flow and subsequent ligant presentation increases. Collectively, these data point towards the ability of rewarding brain stimulation to activate discrete neuronal opioid systems contingent upon specific behavioral as well as stimulus conditions.

Amygdala↗

PubMed1992

Effects of acute and chronic fenfluramine on self-stimulation and its facilitation by amphetamine.

DL-Fenfluramine (20 mg/kg) releasing serotonin and amphetamine (2 mg/kg) releasing dopamine were given to adult rats trained to bar press for electrical stimulation to the medial forebrain bundle. Amphetamine treatment enhanced lever-pressing for 1-2 h. A single fenfluramine treatment rapidly suppressed self-stimulation with slow recovery in 5-7 days to a rate below the initial basal rate. A second treatment a week later again suppressed response rate and rates returned to a still lower baseline. Combined fenfluramine-amphetamine treatment at this time transiently abolished lever pressing for 1-3 h followed by 9-11 h of enhanced responding. The serotonin antagonist, ketanserine (0.1 mg/kg), but not cyproheptadine (0.1 mg/kg i.p.), partially protected against the effects of fenfluramine. The serotonin agonist, quipazine (0.5 mg/kg), but not dimethoxyiodophenylisopropylamine (DOI) (2.2 mg/kg), partially substituted for fenfluramine in the combined treatment. Fenfluramine markedly depleted serotonin and 5-hydroxyindoleacetic acid in frontal cortex, hippocampus, and caudate putamen. Ventral and midline midbrain regions were less affected. Combined fenfluramine and amphetamine treatment elevated dopamine levels in frontal cortex, hippocampus and caudate-putamen, but not in midbrain. These findings support a serotonin-dopamine interaction in self-stimulation behavior and suggest that repeated fenfluramine treatment results in chronic low level serotonergic stimulation and diminished serotonin storage capacity.

Amphetamine↗

PubMed1976

Intracranial self-stimulation in rats as a function of various stimulus parameters. VI. Influence of fentanyl, piritramide, and morphine on medial forebrain bundle stimulation with monopolar electrodes.

The effects of different subcutaneous doses of fentanyl (0.02, 0.04, 0.08, and 0.16 mg/kg), piritramide (0.63, 2.50, 10.0 and 40.0 mg/kg), and morphine (2.50, 5.00, 10.0 and 20.0 mg/kg) on self-stimulation in rats were studied. Different stimulus parameter combinations (SPC) inducing low, high or intermediate control response rates (CRR) were applied during the same experimental sessions. The three narcotic analgesics induced response depression (RD) and response stimulation (RS). RS was mostly observed at low dose levels; RD was dose-related. SPC's inducing low CRR were more sensitive than those inducing high CRR. Fentanyl was more potent than piritramide and than morphine. The RD is related to motor incapacitation, as the doses needed to effectively reduce self-stimulation also induced obvious catatonia. The RS probably is a more specific effect reflecting sensitization of structures involved in reinforcement of behavior.

Analgesics, Opioid↗

PubMed1996

Comparison of intracranial self-stimulation evoked from lateral hypothalamus and ventral tegmentum: analysis based on stimulation parameters and behavioural response characteristics.

The comparison of intracranial self-stimulation (ICSS) derived across the anteroposterior axis of medial forebrain bundle (MFB) from the anterior border of lateral hypothalamus (LH) to the ventral mesencephalon including ventral tegmental area-substantia nigra (VTA-SN) in Wistar rats was assessed through stimulation parameters and behavioural response characteristics. The interpretation of response rate/charge consumption (muC/min) with respect to rectangular wave and sine wave electrical stimulation parameters suggests that the rectangular wave parameters are better in order to get the maximum responding rates. The most vigorous and robust responding was observed in the VTA or VTA-SN boundary placements, followed by placements in medial sector of LH. The acquisition of ICSS was fastest in the case of VTA-stimulation. The next site with respect to rapidity of ICSS was posterio-ventral LH. The extinction curves indicated that it is faster and exponential in case of VTA-SN, but it is slower with longer duration in case of LH-MFB. ICSS of SN were accompanied by exploratory locomotion and head bobbing. Thirty-one percent subjects with SN/VTA stimulation showed rotational behaviour. Seventy-eight percent of subjects with LH stimulations showed stimulus-bound ejaculations. Thirty-two percent of subjects with posterior LH stimulations showed biting of pedal edges. LH stimulations were accompanied by induced seizures and increased grooming in 18% and 13% of subjects, respectively. There was lateralisation of cerebral hemispheric function as right paw preference was noted in majority of rats, whether sites of stimulation were in the left or right cerebral hemisphere. The various other modes of pedal pressing operants like use of paw and mouth, alternate paw dribbling, use of head electrode assembly to manipulate the pedal were also recorded and analysed.

Animals↗

PubMed1990

Interactions of naloxone with morphine, amphetamine and phencyclidine on fixed interval responding for intracranial self-stimulation in rats.

Rats were implanted with stimulating electrodes aimed at the medial forebrain bundle-lateral hypothalamus (MFB-LH) and were trained to lever-press for brain self-stimulation on a fixed interval: 60 s schedule of reinforcement. The effects of graded doses of naloxone (0.1-30 mg/kg), morphine (0.3-5.6 mg/kg), naloxone plus morphine, d-amphetamine (0.03-1.0 mg/kg), naloxone plus d-amphetamine, phencyclidine (0.3-5.6 mg/kg), and naloxone plus phencyclidine were tested. Naloxone produced a significant decrease in rates at 30 mg/kg. Naloxone (0.1-1.0 mg/kg) plus morphine blocked the dose-dependent decrease produced by morphine alone. In contrast, naloxone (1.0-10 mg/kg) plus d-amphetamine attenuated the graded increase in response rates produced by d-amphetamine. Naloxone (1.0-10 mg/kg) plus phencyclidine did not reliably change the increase in response rates produced by phencyclidine alone. The use of the fixed interval schedule of brain self-stimulation to study these drug interactions is novel, and further demonstrates that the highly reinforcing aspects of brain stimulation, known to be influenced by dopamine, may also be modulated by the endogenous opiate system.

Amphetamine↗

PubMed1997

Rapid recovery of self-stimulation from depression produced by the atypical neuroleptic risperidone is not prevented by 5-HT2 receptor stimulation.

Behavioral effects of the antipsychotic drug risperidone were tested in rats responding for variable-interval stimulation of the ventral tegmental area (VTA). Risperidone (0-0.9 mg/kg) produced a dose-dependent depression of responding in the 60 min after injection. Self-stimulation tests delayed for 30 or 120 min after injection showed that inhibition of responding by risperidone was limited in duration, with response rates recovering to pre-injection levels in a time-dependent manner. Recovery occurred regardless of opportunity to engage in self-stimulation, and was virtually complete at a time when receptor occupancy has been shown to be almost undiminished. The atypical properties of risperidone have been ascribed to its potent antagonist activity at 5-HT2 receptors; however, spontaneous recovery from the effects of risperidone was not prevented by simultaneous administration of a selective 5-HT2 agonist (DOI), even though DOI when given alone produced a 50-70% reduction in response rates. These results show that the inhibitory effect of risperidone on operant performance may be self-limiting in a manner that is not accounted for by its pharmacokinetic properties nor by its antagonist activity at central 5-HT2 receptors.

Amphetamines↗

PubMed1985

Unilateral lesion of the intrinsic cells in the medial forebrain bundle depresses self-stimulation but not stimulus-bound locomotor activity.

The intrinsic neurons of the medial forebrain bundle were unilaterally destroyed, in rats, through local injection of ibotenic acid (4 micrograms in 0.5 microliter). Ten days later, electrodes were bilaterally implanted, one in the lesioned lateral hypothalamus, the other into the contralateral hypothalamus. Firstly, self-stimulation was studied with stimulation of each electrode separately. Later on, the effect of non-contingent electrical stimulation on evoked locomotor activity in the open-field was analysed for each electrode. While self-stimulation of the lesion area was greatly depressed in comparison with the unlesioned lateral hypothalamus, the increase in locomotor activity produced by stimulation, at the intensity applied, was the same whether the stimulated hypothalamus was lesioned or not.

Animals↗

PubMed1991

Self-stimulation: a rewarding decade.

In the past decade, there has been considerable emphasis on developing and refining the measurement instruments used to assess the rewarding effect of brain stimulation. These efforts have given rise to quantitative methods aimed at revealing the underlying neurophysiology and neuroanatomy by tracing the trajectories of the relevant neurons. In this paper, we summarize some of the quantitative findings that have resulted from research at the University of Ottawa in the neurobiology of motivated behavior. These include studies using markers to reveal which structures are metabolically activated by rewarding brain stimulation, comprehensive mapping of brain areas for self-stimulation and other stimulation-induced behaviors, and examination of the effects of benzodiazepines on feeding and reward.

Animals↗

PubMedDate not supplied

Effects of NMDA lesions of the medial basal forebrain on LH and VTA self-stimulation.

Rewarding stimulation of the medial forebrain bundle (MFB) increases Fos-like immunoreactivity in many brain areas, including an ipsilateral, basal forebrain region extending from the medial preoptic area (MPO) to the lateral preoptic area, and substantia innominata. Excitotoxic lesions of the lateral portion of this region have been found to produce large sustained or transient increases in the number of pulses required to maintain half-maximal lever-pressing (required number of pulses) for MFB stimulation. In the present study, changes in self-stimulation of the lateral hypothalamus and ventral tegmental area were assessed following excitotoxic lesions of more medial structures, including the MPO and bed nucleus of the stria terminalis. Increases in the required number of pulses (up to 0.16 log10 units) were seen in only 2 of 10 subjects. In two other rats, the reward effectiveness of the stimulation was moderately increased after the lesion as manifested in decreases of up to 0.14 log10 units in the required number. No appreciable change from baseline was seen in the remaining six subjects. The simplest interpretation of these results is that neurons with cell bodies in the medial portion of the basal forebrain may make a smaller contribution to the rewarding effect of MFB stimulation than neurons in the lateral portion.

Animals↗

PubMed1992

Dorsal diencephalic self-stimulation: a movable electrode mapping study.

The function relating electrical self-stimulation (ESS) bar-pressing rate to the frequency of cathodal pulses (0.2 mA and 0.1 ms) was obtained for several positions of a movable electrode in the dorsal diencephalon of the rat. The rate-frequency functions were fitted to a sigmoid model to obtain the asymptotic rate and threshold frequency. ESS was found along the epithalamic route (stria medullaris, habenula, and fasciculus retroflexus) and in the following thalamic nuclei: mediodorsal, paratenial, interanteromedial, centromedial, reuniens, and rhomboid. The lowest threshold (approximately 5 pulses/train), which was found in the stria medullaris and the junction of the paratenial and centromedial nuclei, was comparable to that usually obtained for the brain areas where the ESS is most effectively rewarding (medial forebrain bundle, dorsal raphe, and amygdala). However, most of threshold estimates were 4 to 8 times higher. In most brain sites, ESS was accompanied by epileptiform, motor, or aversive reactions (or a combination of these). These reactions may explain the fact that the maximum rates were generally very low. Nevertheless, no correlation was found between maximum rates and threshold frequencies.

Amygdala↗

PubMed1981

Intracranial self-stimulation from the sulcal prefrontal cortex in the rat: the effect of 6-hydroxydopamine or kainic acid lesions at the site of stimulation.

An electrode cannula system was used to elicit intracranial self-stimulation (ICSS) from the sulcal prefrontal cortex in rats to test the behavioral effects of local infusions of 6-hydroxydopamine (6-OHDA) or kainic acid (KA) into the brain area surrounding the electrode tip. In experiment I sulcal ICSS animals received injections of 6-OHDA with or without desipramine (DMI) pretreatment to block 6-OHDA uptake into noradrenergic (NA) terminals. Those animals that received DMI pretreatment were subsequently shown to have sustained sulcal cortical dopaminergic (DA) denervation while sulcal molecular layer NA systems were spared as revealed with glyoxylic acid-induced catecholamine histofluorescence. Those animals not receiving DMI pretreatment sustained near-complete denervation of both NA and DA sulcal cortical systems. Neither treatment had a lasting effect on sulcal ICSS suggesting that sulcal ICSS is not dependent on the presynaptic release or DA of NA into that brain area. In experiment II KA injections that lesioned neurons in sulcal cortical layers V and VI resulted in the abolition of sulcal ICSS for the duration of a 21 day postlesion trial period. These results suggest that activation of a descending corticofugal system originating in the sulcal cortex is responsible for the mediation of sulcal prefrontal cortical ICSS. This system was mapped by the selective silver impregnation of degenerating neural elements resulting from effective lesions.

Animals↗

PubMed1995

Ventral pallidum self-stimulation: a moveable electrode mapping study.

The distribution of electrical self-stimulation (ESS) foci within the ventral pallidum (VP) was mapped using moveable electrodes in rats. The function relating ESS bar-pressing rate to the frequency of cathodal rectangular pulses (0.4 mA and 0.1 ms) was obtained for several positions of a moveable electrode in the VP and in the various adjacent to VP nuclei. The rate-frequency functions were fitted to a sigmoid model to obtain the asymptotic rate and threshold frequency. ESS was found in almost all (98%) VP sites tested and to a lesser degree (66%) in the surrounding areas (namely globus pallidus and caudate). Depending on the VP site, maximum rates varied from 14 to 85 bar presses/min, whereas threshold frequencies varied from 10.2 to 36.4 pulses/train; no correlation between these two aspects of ESS was found. Extra-pallidal areas contained less low-frequency threshold sites compared to VP. The lowest threshold found in the VP was slightly higher than that usually obtained for the most rewarding brain areas (VTA, dorsal raphé, LH, amygdala), which suggests that the VP represents an important structure for reward. Furthermore the threshold frequencies were found to decline along the rostrocaudal axis of the VP which supports the view that the VP is heterogeneous in regard to reward related functions.

Amygdala↗