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 451 records · Page 25Linked to original sources

PubMed1984

Intracranial self-stimulation distinguishes between two benzodiazepine antagonists.

Low doses of Ro 15-1788 and CGS 8216 were without effect on variable-interval self-stimulation, but completely abolished the enhancement of responding produced by chlordiazepoxide (5 mg/kg). Higher doses of Ro 15-1788, unlike other benzodiazepine receptor antagonists, produced an increase in response rates similar to that found after chlordiazepoxide. This result is consistent with its suggested action as a partial agonist. The combination of a high (benzodiazepine-like) dose of Ro 15-1788 with chlordiazepoxide produced a depression of responding similar to that seen with high doses of benzodiazepines. High doses of CGS 8216 produced a depression of self-stimulation, which was not reversed by chlordiazepoxide (5 mg/kg). Thus, the present procedure is able to distinguish contrasting behavioural effects of benzodiazepine antagonists.

Animals↗

PubMed1989

Opioid-neuroleptic interaction in brainstem self-stimulation.

Injection of morphine into the ventral tegmental area (but not dorsal to it) induced a dose-dependent decrease in the frequency threshold for midline metencephalic brain stimulation reward. Facilitating doses of ventral tegmental morphine also reversed, in 4 of 6 animals, the threshold-increasing effects of pimozide (0.35 mg/kg, i.p.). This reversal was itself reversed by naloxone (2 mg/kg, i.p.), suggesting a direct action of morphine at ventral tegmental opiate receptors. These data fit with electrophysiological evidence that ventral tegmental morphine stimulates or disinhibits dopamine impulse flow, which would result in increased synaptic dopamine concentrations and decreased synaptic pimozide effectiveness. In the remaining two animals, the combined neuroleptic-opiate treatment resulted in a complete cessation of responding that was not reversed by a 5-fold increase in stimulation frequency. This finding suggested a complete inactivation of the reward mechanism, which might be expected from the interaction of high doses of two drugs that are each known to be capable of producing depolarization inactivation of dopaminergic neurons. These data confirm that brainstem self-stimulation, like medial forebrain bundle self-stimulation, depends critically on the function of the mesocorticolimbic dopamine system.

Animals↗

PubMedDate not supplied

[The behavior of rats with different regimes of cerebral self stimulation].

The behaviour of rats was studied during electrical self-stimulation (SS) of the brain in a chamber with a pedal: with a fixed duration of stimuli trains (fixed SS regime), and in a self-controlled regime, where the duration of trains was set by the rat itself. As the current intensity or the duration of the trains continues to increases, the SS frequency in the fixed regime rises no longer. The duration of pressing becomes shorter than that of the trains, and the number of short pauses drops down to 50% of its total number of pauses, if at the same current intensity the duration of the train is the same or greater than that set by the rats in the self-controlled SS regime. With weak current intensities, the rats could fail to press the pedal if they received 0.1 sec. trains. But at the same current intensities the rats began SS, if they received for pressing the pedal a succession of trains of 0.1 sec. each with intervals of 0.1 divided by 0.2 sec. SS discontinued if the interval in the trains succession increased up to 0.4 sec.

Animals↗

PubMed1988

The effect of chronic cocaine on self-stimulation train-duration thresholds.

The effect of chronic cocaine treatment on brain stimulation reward was assessed by examining self-stimulation train-duration thresholds. Following a predrug, saline injection period, cocaine hydrochloride (10 or 15 mg/kg) was injected (IP) across 18 consecutive days of testing. Cocaine lowered thresholds across the entire period of drug administration, with the magnitude of cocaine's effect remaining stable during this time. The subjects returned to predrug, saline levels during a postdrug test conducted immediately following chronic cocaine treatment. In a final attempt to modify cocaine's effects, the subjects received 25 mg/kg cocaine HCl three times/day for three consecutive days. Subsequent testing at the original dosage levels revealed no change in the magnitude of cocaine's effect. It was concluded that cocaine's effect on brain stimulation reward does not show tolerance or sensitization with chronic use. Similar effects have been reported for morphine and amphetamine's effect on brain stimulation reward.

Animals↗

PubMed1976

Hyperthermia following self-stimulation of the median raphe in the rat.

Electrical self-stimulation (SS) in the median raphé of the rat but not in the locus coeruleus resulted in a dramatic rise of body temperature. This hyperthermia was facilitated by pretreatment with a inhibitor of serotonin uptake. The functional significance of the hyperthermia elicited by stimulation of the media raphé was discussed on the basis of the relationship between SS and primary reinforcers.

Animals↗

PubMed1977

Blockade of intracranial self-stimulation by antipsychotic drugs: failure to correlate with central alpha-noradrenergic blockade.

The involvement of central alpha-noradrenergic receptors in intracranial self-stimulation (ICSS) was studied. Dose-response curves were established for the blockade of ICSS by the antipsychotic drugs chlorpromazine, thioridazine, clozapine, and pimozide and the alpha-antagonist phenoxybenzamine. Antagonism of the facilitation, produced by the central alpha-agonist clonidine, of flexor withdrawal reflexes in the reserpinized spinal rat was used to assess the central alpha-blocking potency of the same drugs, and dose-response curves were established. No correlation was found between central alpha-blockade, as reflected by the ED50 for blockade of clonidine-facilated spinal reflexes, and the ED50 for blockade of ICSS. Pimozide blocked ICSS at doses virtually devoid of central alpha-blocking activity, while phenoxybenzamine was a potent alpha-antagonist and a weak blocker of ICSS. The lack of correlation between central alpha-blockade and decreased ICSS suggests that alpha-receptors are not critically involved in self-stimulation behavior.

Animals↗

PubMed1983

Effects of agonists and antagonists of D1 and D2 dopamine receptors on self-stimulation of the medial prefrontal cortex in the rat.

The possible participation of D1 versus D2 dopamine receptors in mediating dopaminergic neurotransmission of self-stimulation (SS) in the medial prefrontal cortex (MPC) of the rat was studied neuropharmacologically. Intracerebral as well as intraperitoneal injections of agonists and antagonists of dopamine receptors were used in this study. In all experiments performed with systemic injections, spontaneous motor activity (SM) was measured parallel to self-stimulation behavior as control for non specific effects of the drugs. Intracranial injections were done unilaterally serving SS of the contralateral side (not injected or injected with 0.9% NaCl) as control in the same animals. Spiroperidol and pimozide were used as D1-D2 dopamine antagonists, while sulpiride was used as a specific D2 antagonist. Apomorphine was used as D1-D2 agonist, while bromocriptine and lergotrile were used at doses in which these ergot drugs are considered predominantly D2 agonists. Sulpiride, intraperitoneally or intracerebrally injected at the same locus at which the stimulating electrode was located produced no effect on SS. On the contrary, the D1-D2 antagonists, spiroperidol and pimozide intraperitoneally or intracerebrally injected produced a dose-dependent decrease on SS. On the basis of these data it is suggested, that the dopamine neurotransmission involved in SS of the MPC is mediated via D1 dopamine receptors. This suggestion is further emphasized by the results obtained with the agonists, apomorphine, bromocriptine and lergotrile. Apomorphine produced a dose-related decrease on SS and a decrease at lower doses and an increase at higher doses on SM. Bromocriptine and lergotrile had, on the contrary, no effect on SS and a dose-related decrease on SM.

Animals↗

PubMed1984

Electrical self-stimulation of dentate gyrus granule cells.

Male albino rats implanted with a chronic stimulating electrode electrophysiologically guided into the granule cell layer of the dorsal dentate gyrus were tested in a self-stimulation paradigm. It was found that subjects self-administer electrical stimulation to the granule cells at low, steady rates. Consistent with the presence of opioid-like immunoreactivity in the granule cell mossy fiber pathway, intraperitoneal injection of the opiate antagonist naloxone diminishes granule cell self-stimulation in a dose-related fashion. The results suggest that a granule cell opioid synapse participates in expression of reward at this site.

Animals↗

PubMedDate not supplied

A dual approach to self-stimulation and locomotor trace affected by chronic methamphetamine treatment for an animal model of schizophrenia.

The effect of long-term methamphetamine (MAP) treatment on intracranial self-stimulation of the lateral hypotholamus and locomotor traces was assessed. An attempt was made to provide a useful animal model for understanding anhedonia, stereotypy, and reoccurrence of liability, which are analogous to symptoms of schizophrenia. The frequency of intracranial self-stimulation (ICSS) as used as a measure of the animals' "hedonic-anhedonic" state. Following long-term MAP treatment (3 mg/kg), rats gradually showed stereotyped behavior, and became inactive and unresponsive to ICSS. These behavioral changes and decreased ICSS lasted several weeks after cessation of chronic MAP treatment and seemed to suggest post-MAP chronic psychosis and (or) anhedonia, two of the negative symptoms of schizophrenia. The traces of rat behavior affected by chronic MAP treatment were classified into three types, peripheral, mixed, and fixed, occurring in a dose-dependent manner. Reverse tolerance, similar to the reoccurrence of schizophrenic symptoms, was observed as a fixed stereotypy associated with loss of ICSS. These abnormal phenomena were suppressed by pretreatment with haloperidol. In the present study, the combination of ICSS and locomotor trace affected by chronic MAP treatment was proposed as an animal model of schizophrenia and as a useful technique for gauging the effect of neuroleptics.

Animals↗

PubMed1997

Fos-like immunoreactivity in forebrain regions following self-stimulation of the lateral hypothalamus and the ventral tegmental area.

According to the descending-path hypothesis, the direct excitation of descending fibers linking the lateral hypothalamus (LH) and ventral tegmental area (VTA) contributes to the rewarding effect produced by electrical stimulation of the medial forebrain bundle (MFB). To visualize forebrain neurons activated by stimulation of both the LH and VTA, Fos-like immunoreactivity (FLIR) in forebrain regions was assessed following self-stimulation of these two sites in male rats. Among the regions where FLIR was greater in the stimulated hemisphere following either LH or VTA stimulation were the anterior LH, the substantia innominata, and the bed nucleus of the stria terminalis, and olfactory tubercle. These findings are analyzed with reference to the effects of forebrain lesions on self-stimulation of the MFB. Advantages and limitations of using FLIR to identify neurons activated by rewarding stimulation are discussed.

Animals↗

PubMed1990

Effects of antibodies to dynorphin A and beta-endorphin on lateral hypothalamic self-stimulation in ad libitum fed and food-deprived rats.

Many laboratories have reported that systemically administered naloxone has little or no effect on lateral hypothalamic self-stimulation (LH ICSS). In the present study, lateral ventricular infusion of beta-endorphin antiserum and a high dose of naloxone (100 micrograms) produced small but significant increases in stimulation frequency threshold for LH ICSS. beta-Endorphin activity, mediated by a non-mu (e.g. delta or epsilon) receptor, may therefore be involved in the reinforcement of self-stimulation behavior. When rats are deprived of food for 24 h, LH ICSS thresholds decline. Under this condition, systemic naloxone elevates the LH ICSS threshold, often returning it to the pre-deprivation level. In the present study, lateral ventricular infusion of dynorphin A(1-13) antiserum similarly reversed the threshold-lowering effect of food deprivation. The effects of systemic naloxone and intraventricular dynorphin A antiserum on LH ICSS, which are specific to food-deprived animals, may be related to previous findings that these two treatments elevate LH stimulation threshold for eliciting feeding behavior. Results of the ICSS and stimulation-induced feeding studies suggest a model for the mediation of incentive stimuli by dynorphin A activity that is afferent to LH 'reward' neurons and positively gated by 'hunger'. An hypothesized role for 'hunger'-gated dynorphin A release in potentiating the hedonic response to alimentary stimuli and drugs of abuse is discussed.

Animals↗

PubMed1984

Sensitization to the effects of repeated amphetamine administration on intracranial self-stimulation: evidence for changes in reward processes.

The effects of daily administration of 1.0 mg/kg of D-amphetamine for 20 consecutive days on self-stimulation responding from the substantia nigra, and nucleus accumbens were evaluated at several current intensities. Raising current intensity increased rates of responding when electrodes were situated in these areas, and amphetamine significantly enhanced rates of responding from both brain regions. Moreover, the drug-induced response enhancements were facilitated further after repeated drug/test pairings. Although response sensitization was observed at several current intensities, it developed sooner at the lower current levels indicating that the sensitizing effect of repeated drug administration on self stimulation responding was not due to variations in locomotor activity or arousal levels induced by amphetamine treatment. Furthermore, sensitization was observed at current levels that engendered both high and low levels of responding, suggesting that the sensitization was unrelated to the rate dependent effects of the drug. Rather, it was argued that repeated amphetamine treatment sensitized animals to the rewarding properties of electrical brain stimulation. Possible neurochemical and behavioral mechanisms that may be involved in the development of reverse tolerance after repeated amphetamine treatment were discussed.

Animals↗

PubMed1981

[Comparative characteristics of the self-stimulation response in rabbits following administration of angiotensin II into the cerebral ventricles and application to the conjunctiva].

Experiments on rabbits have shown that intraventricular administration of angiotensin II induces the dose-dependent suppression of the self-stimulation reaction after varying intervals. The same suppression of the self-stimulation in rabbits but after a greater interval is produced by the application of angiotensin aqueous solution to the eye conjunctiva. In both cases the amount of drinking reactions in the animals significantly rises after the oligopeptide administration as compared with controls. Examination of the time course of arterial pressure, respiration and ECG has shown that only intravenous injection of angiotensin II in doses of 500 ng provokes a temporary increase in arterial pressure, marked bradycardia and changes in respiration, whereas other routes of administration produce no changes in the characteristics studied.

Administration, Topical↗

PubMed1983

Self-stimulation and task-related responding: the role of sensory reinforcement in maintaining and extending treatment effects.

The present study was aimed at (a) eliminating self-stimulation and increasing task-related responding in severely handicapped children, and (b) assessing maintenance and carry-over of treatment effects following the use of sensory reinforcement. The results showed that applying sensory or edible-liquid reinforcement, contingent on low rates of task-related responses, did not increase these responses nor decrease self-stimulation. These behavior changes were obtained with the combination of reinforcement and punishment. Sensory reinforcement was effective in maintaining and extending the treatment results, while edible-liquid contingencies were not.

Attention↗

PubMed1977

Effects of apomorphine on self-stimulation behaviour in dorsal and ventral area of lateral hypothalamus in mice.

Intraperitoneal injections of low doses of apomorphine, a dopaminergic receptor agonist, depressed briefly, and then enhanced self-stimulation behaviour in the dorsal area of lateral hypothalamus. In contrast, only depressant effects were observed in the ventral area. These differential effects suggest the presence of a dopaminergic componant in the dorsal hypothalamic self-stimulation system.

Animals↗

PubMed1963

TEST OF DEUTSCH'S DRIVE-DECAY THEORY OF REWARDING SELF-STIMULATION OF THE BRAIN.

Deutsch's theory of intracranial self-stimulation generates experimental predictions regarding the effects of both free stimulation of the brain and the pre-extinction training procedure on extinction behavior after rewarding stimulation of the brain. The results of one experiment confirmed the prediction regarding free stimulation; the other experiment did not provide the expected result. We concluded that Deutsch's theory, in its present form, is of restricted enerality.

Brain↗

PubMedDate not supplied

Brain (PET) responses to vaginal-cervical self-stimulation in women with complete spinal cord injury: preliminary findings.

Our recent research provides evidence that women with complete spinal cord injury (SCI) at the midthoracic level show perceptual responses to vaginal and/or cervical self-stimulation (for example, pain suppression and sexual response, including orgasm). On the basis of studies in laboratory rats, we hypothesized that the vagus nerves provide a sensory pathway from the vagina, cervix, and uterus directly to the brain in women. To test this hypothesis, we performed a PET-MRI study on two women with complete SCI and 1 woman with no injuries. Whereas control foot stimulation of the women with SCI did not activate the somatosensory thalamus, cervical self-stimulation increased activity in the region of the nucleus of the solitary tract, which is the brainstem nucleus to which the vagus nerves project. These preliminary findings suggest that the vagus nerves can convey genital sensory input directly to the brain in women, completely bypassing SCI at any level.

Adult↗

PubMed1990

Behavioral characterization of intracranial self-stimulation from mesolimbic, mesocortical, nigrostriatal, hypothalamic and extra-hypothalamic sites in the non-inbred CD-1 mouse strain.

A behavioral analysis of intracranial self-stimulation (ICSS) was provided for mesolimbic/mesocortical, nigrostriatal, hypothalamic and extrahypothalamic sites in the CD-1 mouse. Robust responding and rapid acquisition of mesocortical ICSS appeared dorsally along notably fluorescent sites in rostral and caudal planes. ICSS was diminished demonstrably in medial and ventral positions in posterior planes. Mesolimbic ICSS from the medial and ventral nucleus accumbens (Nas), was accompanied by significant elevations in locomotor activity, corresponding to regions of dopamine (DA) and cholecystokinin co-localization. Stimulation-induced seizures appeared from both the Nas as well as the mesocortex. ICSS from the ventral tegmental field (VTA) was evident along its medial, lateral and dorsal borders with longer pulse durations more likely to elicit responding. Seizure activity was absent from the VTA. Striatal ICSS was conspicuously poor in dorsal and medial locations; regions presumably devoid of tegmental innervation. ICSS emerged from both the ventrocaudal and anteromedial striatum; regions linked to innervation by the dorsolateral and ventromedial VTA. The red nucleus, a previously neglected self-stimulation site supported marked responding for ICSS. Regions supporting rubral ICSS were correlated with thalamic innervation sites; notably the ventrolateral thalamic nucleus and the parafascicular nucleus, regions found to support ICSS. The substantia nigra supported high rates of responding for ICSS when electrode placement was restricted to the dorsomedial portion of the pars compacta. Electrode deviations lateral and dorsal to the substantia nigra pars medialis induced a progressive decline in responding. Hypothalamic sites were found to support significant responding for ICSS, although such performance was frequently associated with seizure induction. Taken together these data (1) provide the first behavioral analysis of ICSS in mice responding from previously unexamined DA sites in the mesolimbic (e.g. VTA, Nas) and nigrostriatal systems (e.g. caudate, red nucleus) (2) suggest an anatomical reconsideration of the assumptions underlying the elicitation of ICSS from the frontal cortex (3) suggest that the neural circuitry underlying thalamic, caudate, rubral and frontal cortical ICSS are interrelated and (4) suggest that the Nas and the frontal cortex, like the hypothalamus, in the mouse appear to be particularly sensitive to stimulation-induced seizures.

Animals↗