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At least 19 recordsLinked to original sources
PubMed1975

Interactions of adrenergic stimulants and blockers on self-stimulation behavior in rats.

Self-stimulation behavior in rats was facilitated by two adrenergic stimulants, amphetamine (0.5 or 1 mg/kg, intraperitoneal, i.p., or 100 mug, intracerebroventricular, i.c.v.) and cocaine (5 mg/kg, i.p.). Three alpha-adrenergic blockers (phenoxybenzamine, dibenamine, phentolamine) and a beta-adrenergic blocker (propranolol) decreased self-stimulation responding at 100 mug i.c.v. doses, but showed very little effect at small i.p. doses. Pretreatment with alpha- and beta-adrenergic blockers (i.c.v.) also decreased amphetamine-facilitated responding. The effects of amphetamine or cocaine (i.p.) were not significantly altered by these blockers at the doses used. The depressant effects of the alpha- and beta-adrenergic blockers on self-stimulation behavior appear to be nonspecific with respect to the type of adrenergic receptors.

Adrenergic alpha-Agonists↗
PubMed1976

Separation of inhibiting and stimulating effects of morphine on self-stimulation behaviour by intracerebral microinjections.

The effects on self-stimulation behaviour of 5 mug morphine HCl applied into the ventricular system and into different areas throughout the brain were studied. Injections into the ventricular system and in areas intermediate between the posterior hypothalamus and the periaqueductal grey matter had biphasic effects: an inhibition followed by an excitation. Injections into the posterior hypothalamus resulted in increased self-stimulation whereas injections into the periaqueductal grey matter and into the locus coeruleus were only inhibiting.

Animals↗
PubMed1975

A role for dopamine in the psychopharmacology of electrical self-stimulation.

The psychopharmacology of electrical self-stimulation of the lateral hypothalamus was studied using 6-hydroxydopamine, alpha-methyltyrosine, U-14, 624, and d-amphetamine. Reduction of brain dopamine, but not norepinephrine, with 6-hydroxydopamine produced an acute depression of responding which eventually recovered to pretreatment levels. A low dose of alpha-methyltyrosine, which did not affect responding in control rats, significantly depressed responding in the rats with brain dopamine reduced. This treatment did not alter responding of rats with norepinephrine reduced by 6-hydroxydopamine. A dopamine-beta-hydroxylase inhibitor, U-14, 624, depleted norepinephrine an additional 70% yet failed to alter self-stimulation in any of the groups. In other experiments, the 6-hydroxydopamine treatment which reduced brain dopamine was found to block the facilitation of self-stimulation produced by d-amphetamine. This facilitation of lateral hypothalmic self-stimulation was not influenced by treatments which reduced brain norepinephrine. An experiment suggesting that dopamine is of importance to locus coeruleus self-stimulation is also described. Implications of these data indicating a role for dopamine in self-stimulation responding are discussed in relation to the "catecholamine hypothesis of self-stimulation".

Animals↗
PubMed1976

Hyperthermia and inhibition of feeding produced by self-stimulation in the septum and preoptic area in dogs.

Dogs bearing electrodes implanted in the anterior part of the basal forebrain were tested for their response to food upon electric stimulation of rewarding sites, and for self-stimulation-produced hyperthermia. Self-stimulation and forced (experimenter-induced) stimulation of 12 out of 16 loci evoked a negative reaction to food the strength of which was determined according to occurrence and persistence of three effects: ignoring food (the dog performing self-stimulation in the presence of readily available meat), food rejection (the dog's failure to take meat offered together with passive stimulation of the rewarding site), and food ejection (throwing meat out of the mouth upon passive stimulation). The rise in body temperature during self-stimulation was positively correlated with the rate of responding. Hyperthermia was significantly higher during self-stimulation in sites where stimulation produced a strong negative reaction to food, as compared with those where stimulation failed to stop the animal from eating. The stimulus-contingent negative reaction to food may reflect a short-term satiety which is supposed to play an essential role in the mechanism of reinforcement. Hyperthermia, and particularly stabilization of hypothalamic temperature on an elevated but fairly constant level, argues for a shift of the set-point for temperature regulation. Occurrence of the two effects supports the claim that self-stimulation produces some complex activation of neural processes controlling energy homeostasis.

Animals↗
PubMed1975

[Effects of various psychotropic drugs on self-stimulation behavior in the rat].

Effects of various psychotropic drugs on tegmental and hypothalamic self-stimulation behavior in rats with chronically implanted electrodes in the brain were studied. Effects of elecrtical stimulation in several brain structures on self-stimulation behavior and influences of drugs on the stimulation effect were also investigated. The hypothalamic self-stimulation behavior was more markedly inhibited by chlorpromazine than the tegmental self-stimulation, whereas the latter was more strongly inhibited by diazepam. The effects of pentobarbital on the self-stimulation behavior were similar to those of diazepam. Methamphetamine facilitated both the tegmental and hypothalamic self-stimulation behavior. Suppressive effect of hypothalamic stimulation on the tegmental self-stimulation behavior was inhibed by chlorpromazine, while those of amygdaloid and septal stimulation were augmented. All the effects of hypothalamic, amygdaloid and septal stimulating on the tegmental self-stimulation behavior were inhibed by diazepam and pentobarbital, while these were facilitated by methamphetamine. Suppressive effects of tegmental, amygdaloid and septal stimulation on the hypothalamic self-stimulation behavior were all facilitated by both chlorpromazine and methamphetamine. The effects of amygdaloid and septal stimulation on this behavior were inhibed by diazepam and pentobarbital, while those of tegmental stimulation were enhanced. The effects of imipramine, in all experiments, were variable in each rat and not significant.

Animals↗
PubMed1977

Concurrent intracranial self-stimulation and amphetamine self-administration in rats.

In a two-lever testing chamber, rats had concurrent access to intravenous amphetamine and brain stimulation reinforcers. Responding for each reinforcer was generally increased above baseline rates taken when only one reinforcer was available. Amphetamine stereotypy was observed, but did not interfere with rapid lever-pressing for brain stimulation.

Amphetamine↗
PubMedDate not supplied

In vivo neurochemical analysis, by push-pull perfusion, of the mesocortical dopaminergic system of the rat during self-stimulation.

The region immediately adjacent to a self-stimulation site in the medial prefrontal cortex of the unanesthetized rat was prelabeled with 0.5 mu Ci 14C-dopamine (DA) injected through an indwelling guide cannula. Then successive 5 min push-pull perfusions of the site with an artificial CSF were carried out at a rate of 25 microliter/min so that a washout curve of declining radioactivity was generated under control conditions. When square wave 100 Hz pulses were delivered to the contiguous self-stimulation site, the release of 14C-DA was enhanced either during the actual interval of electrical stimulation or in the perfusion sample collected immediately thereafter. In parallel experiments, however, self-stimulation by the rat of its ventral tegmental area failed to alter the kinetics of 14C-DA release from the cortex when homologous loci were perfused. Analyses by thin-layer chromatography of the perfusates for their content of catechol metabolities revealed that the homovanillic acid fraction declined during stimulation, whereas the level of DOPAC remained relatively elevated. Evidence was also obtained for the new synthesis and subsequent release of norepinephrine during the stimulation of the cortex of the rat. These results suggest that endogenous dopamine, because of the notable alterations in its release and metabolism, plays an important synaptic role in the mediation of self-stimulation behavior at the level of the cerebral cortex.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1979

Facilitation of self-stimulation of the prefrontal cortex in rats following chronic administration of spiroperidol or amphetamine.

The effect of chronic administration of spiroperidol, a dopaminergic antagonist, on self-stimulation of the prefrontal cortex was investigated. When spiroperidol was administered either before or after daily self-stimulation tests for 9 days, self-stimulation rates were significantly elevated for several weeks following withdrawal of the drug. Self-stimulation of the nucleus accumbens, supracallosal bundle, and other forebrain sites was not altered, suggesting that the increased self-stimulation of the prefrontal cortex was not due to increased motor activity. Self-stimulation of the prefrontal cortex was also facilitated by chronic administration of d-amphetamine whereas self-stimulation of the supracallosal bundle was suppressed and self stimulation of the nucleus accumbens was unchanged. The results suggest that dopamine modulates self-stimulation of the prefrontal cortex. Additionally, the effects of chronic spiroperidol on self-stimulation of this structure may model the therapeutic effects of neuroleptics in humans.

Amphetamine↗
PubMed1978

Using self-stimulation as reinforcement for autistic children.

This experiment examined the effects of using self-stimulatory behavior as reinforcement for spontaneous appropriate sentences in two autistic children. The children were put on a token system and always received one token for every spontaneous appropriate sentence they made. An ABABA design was employed. In condition A, the opportunity to self-stimulate was contingent on the payment of tokens (two tokens for 2 minutes of self-stimulation). In condition B, no tokens were required for self-stimulation. The results showed that both subjects exhibited a much higher rate of spontaneous appropriate sentences during the contingent self-stimulation (A) condition, demonstrating that self-stimulation functioned as an effective reinforcement. The possibility of using self-stimulation as reinforcement in the treatment of autistic children is discussed.

Autistic Disorder↗
PubMed1979

Dopamine--acetylcholine "balance" in nucleus accumbens and corpus striatum and its effect on hypothalamic self-stimulation.

Three experiments investigated the suppression of hypothalamic self-stimulation in rats by neuroleptics and its restoration by centrally acting anticholinergic agents. Scopolamine (0.1--1.0 mg/kg i.p.) and benztropine (1.0--10.0 mg/kg i.p.) each enhanced self-stimulation when administered alone, and partially restored performance suppressed by spiroperidol (0.05--0.15 mg/kg i.p.). Benztropine strongly inhibits transmitter reuptake at DA synapses but scopolamine does not, thus inhibition of DA reuptake cannot fully account for the stimulant or antineuroleptic action of anticholinergic drugs. Neuroleptic and anticholinergic effects on self-stimulation rate were mutually subtractive, and statistical evidence of interaction was not obtained. Scopolamine was shown also to restore performance extinguished by discontinuation of the stimulating current. Smaller doses of scopolamine (50 nmol; 19 microgram) injected directly into the nucleus accumbens septi partially restored responding suppressed by spiroperidol, though similar doses of scopolamine injected bilaterally into the caudate-putamen were ineffective. These findings suggest that hypothalamic self-stimulation may be influenced by ACh-and DA-containing systems which exert independent effects on a third system controlling performance. These effects appear to reflect the level of arousal or motivation rather than the reinforcement process itself.

Acetylcholine↗
PubMed1975

Differential effects of amphetamine and food deprivation of self-stimulation of the lateral hypothalamus and medial frontal cortex.

Intracranial self-stimulation of the lateral hypothalamus of the rat was markedly increased by d-amphetamine administration and by food deprivation. In contrast, similar self-stimulation response rates obtained in the same animals from the medial frontal cortex were unaffected by food deprivation and only slightly increased by d-amphetamine administration. Furthermore, a large difference between d- vs. l-amphetamine on response rate was obtained for lateral hypothalamic but not for medial frontal cortex self-stimulation. The results of this study were consistent with a noradrenergic self-stimulation system for the lateral hypothalamus. Medial frontal cortex self-stimulation, however, appears to be mediated by a neuroanatomical and neurochemical system different from that of the lateral hypothalamus.

Amphetamine↗
PubMed1975

Autonomic effects of hypothalamic self-stimulation in the cat.

Respiration, heart rate and arterial blood pressure were recorded continuously during self-stimulation with systematically varied stimulus parameters. Conspicuous autonomic effects were induced by self-stimulation. Acceleration in the respiration and heart rate, and rise in the arterial blood pressure were generally obtained as direct effects of the stimulus train, which were followed by remarkable rebound-like aftereffects. A close relationship was found between the lever-pressing behaviour and the peripheral autonomic effects of self-stimulation. The frequency of self-stimulation increased in parellel with the amplitude of the autonomic responses to a certain level, and the animal stopped self-stimulation whenever the amplitude of the autonomic effects exceeded this level. The results are consistent with the idea that the periopheral autonomic changes can modulate self-stimulation.

Animals↗
PubMed1976

Catecholamines and self-stimulation: evidence suggesting a reinforcing role for noradrenaline and a motivating role for dopamine.

Investigation of the role of noradrenaline (NA) and dopamine (DA) in self-stimulation showed that d-amphetamine (which releases more DA than does l-amphetamine, but not more NA) was much more effective than l-amphetamine in enhancing self-stimulation of NA sites in the locus coeruleus and near-lateral hypothalamus. In DA sites in the substantia nigra and far-lateral hypothalamus the effects of the 2 isomers were confirmed to be more nearly equal. Thymoxamine HCl (10 mg/kg IP), a specific alpha-adrenergic receptor blocker, depressed self-stimulation at all sites, but significantly more severely at DA sites. Thus the drugs most effective in influencing self-stimulation at a particular site were those acting predominantly on the unstimulated system. These findings were interpreted in terms of a hypothesis that DA and NA play complementary roles in self-stimulation and that both are essential; or, more specifically, that DA pathways, implicated in other motivational activites, contribute to a state of drive or arousal necessary for self-stimulation; while response-contingent noradrenergic activity (elicited by the electrodes directly via a transsynaptic route) mediates reinforcement. Further predictions from this hypothesis were tested as follows: (1) Direct pharmacological stimulants of adrenergic alpha-receptors should disrupt self-stimulation by acting randomly on the reinforcement system and disrupting response-reward contingencies; this was confirmed by the finding that the alpha-receptor stimulant clonidine HCl (0.05 mg/kg) depressed self-stimulation at all sites tested. (2) Drect stimulants of DA receptors should enhance self-stimulation of NA sites by augmenting dopaminergic motivational activity; but in rats with DA electrodes, noncontingent stimulation of DA receptors would also impose similar noncontingent activity on the transsynaptic noradrenergic reinforcement pathways and thus depress self-stimulation; this was confirmed by the finding that apomorphine (0.3-1.0 mg/kg) was strongly stimulant for NA electrodes but strongly depressant for DA electrodes, and that the degree and direction of these effects was highly correlated with the differential effects of d- l-amphetamine (rho = .65, p less than 0.01). Neither effect of apomorphine depended on the occurrence of motor stereotypy. These results can be interpreted in terms of 2-component models for self-stimulation, with the predominant transmitter of the drive component being identified as DA and that g the reinforcing component as NA.

Amphetamine↗