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At least 145 records · Page 8Linked to original sources

PubMed1993

Chronic food restriction and weight loss produce opioid facilitation of perifornical hypothalamic self-stimulation.

Electrical stimulation frequency thresholds for lateral hypothalamic (LH) self-stimulation were monitored throughout a 3 week period of food restriction and a subsequent 3 week period of re-feeding. Rats with electrodes placed in the perifornical LH were sensitive to this dietary manipulation as evidenced by a high positive correlation between body weight and self-stimulation threshold. Rats with electrodes in the zona incerta/subincertal region or ventral hypothalamus displayed little or no change in threshold. Lateral ventricular injection of naltrexone (200.0 nM) reversed the decline in threshold that was otherwise present during food restriction in rats with perifornical placements. Naltrexone had no effect on thresholds of rats with placements outside the perifornical region. These findings suggest that food restriction and weight loss activate an opioid mechanism that facilitates perifornical LH self-stimulation. The documented association of perifornical LH with the phenomenon of stimulation-induced feeding, and the reciprocal connections between this region and gustatory structures, supports the hypothesis that facilitation of self-stimulation by food restriction is related to the natural phenomenon of positive alliesthesia (i.e. the hunger-dependency of food reward).

Animals↗

PubMed1978

Effects of catecholamine manipulations on three different self-stimulation behaviors.

Rats with self-stimulation electrodes in the medial part of lateral hypothalamus (LH) or in the lateral part of LH were trained to bar press, to run in a continuous, square-shaped runway, and to move their tails from side to side while otherwise restrained, all using LH stimulation on an FI 2 sec schedule as the reinforcement. At low doses of pimozide (a dopaminergic blocker) or of FLA-57 (a dopamine beta-hydroxylase inhibitor) different effects on rates of responding were observed on each of the three tasks at the two electrode placements, indicating that the rate reductions were not the results of specific performance effects of the drugs. The patterns of rate changes suggested that the effects of LH stimulation on behavior in the runway were primarily, but not exclusively mediated by a dopaminergic system; that the effects of LH stimulation on tail movement were primarily, but not exclusively mediated by a noradrenergic system; and that the effect of LH stimulation on bar pressing was mediated by both, or either of these substrates. These results suggest that the reinforcement of behavior by LH stimulation is flexibly mediated by at least two different neural systems.

Animals↗

PubMed1978

Morphine and self-stimulation: evidence for action on a common neural substrate.

Recent studies have demonstrated that the self-stimulation phenomenon may provide a useful technique for investigating the rewarding properties of potentially addictive drugs such as morphine. The present study attempted to examine the nature of morphine's effects on self-stimulation by observing changes in rate-intensity functions following morphine administration. The results indicate that morphine markedly enhanced bar pressing for low intensity stimulation when the intensities were presented in an ascending sequence but morphine produced only slight changes in self-stimulation rates when a descending series was used. The failure of morphine to facilitate responding in the descending series suggests that adaptation of the self-stimulation system can block morphine's effects on this system. These findings appear to support the hypothesis that morphine affects the excitability of the neural system which mediates self-stimulation.

Animals↗

PubMed1982

Rate dependent inhibition of self-stimulation by apomorphine.

The effect of three doses of apomorphine 0.125, 0.25 and 0.5 were studied on self-stimulation generated by three levels of current intensity. Eight rats exhibited overall dose dependent decreases in self-stimulation obtained at the two lowest current intensities. Self-stimulation at the highest current intensity, however, was unaffected by even the highest dose level of apomorphine (0.5 mg/kg) despite typical signs of stereotypy exhibited by the rats in their home cages. Additionally, self-stimulation obtained under the 0.5 mg/kg dose of apomorphine under went extinction when reinforcement was discontinued. Thus, brain stimulation can be an effective reinforcement when an animal is given a stereotypy inducing dose of apomorphine if the current intensity is of sufficient magnitude and if the response manipulandum is not compatible with stereotypic responses. These observations appear consistent with a dopaminergic involvement in the response rather than reinforcement aspect of self-stimulation.

Animals↗

PubMed1988

Catecholamines and endogenous opioids in ventral tegmental self-stimulation reward.

Midbrain dopaminergic pathways and opioid receptor systems have been implicated in the reward experienced in electrical intracranial self-stimulation behavior. In the present experiment, the influence of graded doses of the dopamine antagonist haloperidol and of the agonist cocaine were investigated on electrical self-stimulation reward, elicited by electrodes located in the ventral tegmental area. A threshold method, which is rather insensitive for aspecific motor effects, was applied to determine the reward of self-stimulation. The method allowed to determine simultaneously the rate of lever pressing for self-stimulation. All doses of haloperidol and cocaine were administered with and without the opioid antagonist naloxone, in order to investigate the interaction between dopaminergic and opioid modulation of reward. Haloperidol lowered and cocaine tended to increase the response rate, whereas cocaine but also haloperidol lowered the self-stimulation threshold. The effects appear to be dose-dependent. Naloxone did not interact with the effect of the drugs on threshold and it lowered the response rate, but in the haloperidol-treated rats only. It is concluded that dopamine is involved in the reward of electrical self-stimulation elicited from the ventral tegmental area and that this involvement is independent of endorphin systems, suggesting the existence of separate catecholamine and opioid mechanisms modulating brain reward.

Animals↗

PubMed1978

Effects of catecholamine depleting drugs and d-amphetamine on self-stimulation of the substantia nigra and locus coeruleus.

6-Hydroxydopamine treatments which preferentially depleted either norepinephrine or dopamine were used to define the importance of these transmitter systems in the behavioral alterations produced by catecholamine synthesis inhibitors and d-amphetamine on self-stimulation of the locus coeruleus and substantia nigra. After chronic reduction of brain dopamine, an acute depression of self-stimulation of both the locus coeruleus and substantia nigra occurred. Preferential depletion of norepinephrine with 6-hydroxydopamine did not result in a significant decrease in self-stimulation of locus coeruleus or substantia nigra. However, a dose of alpha-methyltyrosine wihch had no effect in control rats or in rats with brain norepinephrine depleted caused a significant reduction in responding at both electrode placements in animals depleted of brain dopamine. Administration of U-14,624 affected neither substantia nigra nor locus coeruleus self-stimulation, even though it produced an additional 70% depletion of norepinephrine. When d-amphetamine sulfate was given to 6-hydroxydopamine-treated rats, the facilitation of self-stimulation produced by this compound was significantly attenuated in rats with prior depletion of brain dopamine. Depletion of brain norepinephrine did not affect the actions of d-amphetamine on self-stimulation. In other experiments, the actions of d-amphetamine to increase self-stimulation of animals pretreated with reserpine was found to be antagonized by alpha-methyltyrosine but not by U-14,624. Results suggest that drugs can alter self-stimulation of a site in brain anatomically associated with noradrenergic neural pathways and self-stimulation of a site primarily associated with dopaminergic pathways in a similar manner. These data also provided evidence for the involvement of dopamine fibers in the pharmacological actions of d-amphetamine, reserpine and alpha-methyltyrosine.

Animals↗

PubMed1989

The role of the lateral cortico-cortical prefrontal pathway in self-stimulation of the medial prefrontal cortex in the rat.

Effects of electrolytic and kainic acid lesions at several stereotaxic planes of the lateral cortico-cortical prefrontal efferent pathway on self-stimulation of the medial prefrontal cortex were investigated. Electrolytic bilateral lesion of the sulcal prefrontal cortex, the first terminal area of this pathway, produced no effects on self-stimulation of the medial prefrontal cortex. However, bilateral electrolytic lesion of this pathway at the rostral part of the external capsule produced a permanent abolition of self-stimulation of the medial prefrontal cortex. These effects seemed selective since operant behaviour to obtain water, similar to that performed for self-stimulation and used as a control, was not affected by the lesion except on the 1st, 3rd (P less than 0.01) and 5th (P less than 0.05) days postlesion. Interestingly, bilateral microinjections of kainic acid (10 nmol in 0.8 microliters) at the same stereotaxic planes of the external capsule where electrolytic lesion was produced, had no effects on self-stimulation. These results suggest that fibres-of-passage through the external capsule are responsible for the abolition of self-stimulation. Bilateral electrolytic lesion of the entorhinal cortex, one of the caudal terminal areas of this descending set of fibres, produced a short transient decrease of self-stimulation of the medial prefrontal cortex. These results are discussed on the basis that complex, rather than single circuits are involved in maintaining self-stimulation in this neocortical area.

Animals↗

PubMed2001

Intracranial self-stimulation induces Fos expression in GABAergic neurons in the rat mesopontine tegmentum.

The cholinergic neurons which originate in the mesopontine tegmentum and innervate the midbrain ventral tegmental area have been proposed to play a key role in intracranial self-stimulation reward. This mesopontine area also contains GABA neurons. Detailed information is still lacking, however, about the relationship of cholinergic and GABAergic neurons in this region to self-stimulation reward. Therefore, using double immunostaining for Fos as a marker of neuronal activity and choline acetyltransferase as a marker of cholinergic neurons, or for Fos and GABA, we investigated whether self-stimulation of the medial forebrain bundle induces Fos expression within cholinergic and GABAergic neurons in two regions of the mesopontine tegmentum, i.e., pedunculopontine tegmental nucleus and laterodorsal tegmental nucleus. Self-stimulation of the medial forebrain bundle for 1 h induced a large increase in the number of cells expressing Fos in both the pedunculopontine tegmental nucleus and laterodorsal tegmental nucleus, when compared to control brains. However, the self-stimulation-induced expression of Fos was restricted mostly to GABA-, but not choline acetyltransferase-, immunostained cells. We also examined, using microdialysis, whether self-stimulation increases acetylcholine efflux in the ventral tegmental area, a terminal region of the mesopontine tegmentum cholinergic pathway. One hour of self-stimulation significantly increased acetylcholine efflux from this terminal area. These results indicate that intracranial self-stimulation of the medial forebrain bundle may increase acetylcholine release without affecting expression of Fos in cholinergic neurons, while the same stimulation may induce Fos expression in GABAergic neurons of the mesopontine tegmentum. GABAergic as well as cholinergic neurons in this area appear to be activated by self-stimulation reward in the medial forebrain bundle.

Acetylcholine↗

PubMed1984

[Effect of amantadine on intracranial self-stimulation behavior and cerebral glucose utilization in rats].

Effect of amantadine, an adamantane derivative, was investigated on intracranial self-stimulation behavior and cerebral glucose utilization (CGU) in rats. The experiments were performed on Wistar strain male rats. The low rate responses induced by low current brain stimulation on lateral hypothalamic self-stimulation behavior in a Skinner box were increased by p.o. administration of amantadine at doses of 5 and 10 mg/kg, but were decreased at doses of over 50 mg/kg. Amantadine at doses of 5 and 10 mg/kg, p.o., increased the running speed in run-way performance of animals rewarded with electric stimulation of the medial forebrain bundle in the lateral hypothalamus. On a "conflict" situation induced by combining the hypothalamic self-stimulation with midbrain dorsal central gray stimulation in a Skinner box, amantadine at doses of 5 and 10 mg/kg, p.o. caused an increase of lever pressing in the unpunished period without affecting the punished responses. The CGU measured by [14C] 2-deoxyglucose autoradiography was increased by i.p. administration of 5 mg/kg. In addition, amantadine at a dose of 5 mg/kg, i.p., decreased the high optic density in bilateral habenulae induced by pimozide at 0.75 mg/kg, i.p. These results indicate that amantadine facilitates the intracranial self-stimulation behavior related to a dopaminergic mechanism at low doses, and inhibits the high local CGU of bilateral habenulae induced by pimozide.

Amantadine↗

PubMed1979

Intracranial self-stimulation in orbitofrontal cortex and caudate nucleus of rhesus monkey: effects of apomorphine, pimozide, and spiroperidol.

Rhesus monkeys were prepared with stimulating electrodes implanted into the orbitofrontal cortex and head of the caudate nucleus under stereotaxic control. These regions of the brain contain high levels of dopamine, and intracranial self-stimulation was readily elicited from these loci in all animals tested using licking behavior as the operant response. Self-stimulation at both sites was significantly attenuated following peripheral injections of the dopamine receptor blocker spiroperidol (0.02 mg/kg). Similarly, pimozide (0.15 and 0.20 mg/kg) significantly reduced self-stimulation in the orbitofrontal cortex, but the suppression observed at caudate placements did not reach statistical significance. Licking for a reward of blackcurrant juice was unaffected by either drug. Apomorphine (0.2, 0.4 mg/kg) had a differential effect on self-stimulation. This drug significantly attenuated self-stimulation in the orbitofrontal cortex, while the same treatment tended to facilitate self-stimulation in the caudate. Apomorphine did not significantly affect responding for the fruit juice reward. The parallels between the effects of dopamine agonists and antagonists on self-stimulation in the monkey and rat suggest that dopamine influences self-stimulation of some sites in both the primate and the rat.

Animals↗

PubMed1978

Effects of catecholamine manipulations on three different self-stimulation behaviors.

Rats with self-stimulation electrodes in the medial part of lateral hypothalamus (LH) or in the lateral part of LH were trained to bar press, to run in a continuous, square-shaped runway, and to move their tails from side to side while otherwise restrained, all using LH stimulation on an FI 2 sec schedule as the reinforcement. At low doses of pimozide (a dopaminergic blocker) or of FLA-57 (a dopamine beta-hydroxylase inhibitor) different effects on rates of responding were observed on each of the 3 tasks at the 2 electrode placements, indicating that the rate reductions were not the results of specific performance effects of the drugs. The patterns of rate changes suggested that the effects of LH stimulation on behavior in the runway were primarily, but not exclusively mediated by a dopaminergic system; that the effects of LH stimulation on tail movement were primarily, but not exclusively mediated by a noradrenergic system; and that the effect of LH stimulation on bar pressing was mediated by both, or either of these substrates. These results suggest that the reinforcement of behavior by LH stimulation is flexibly mediated by at least 2 different neural systems.

Animals↗

PubMed1987

Refractoriness of neurons mediating intracranial self-stimulation in the anterior basal forebrain.

The post-stimulation excitability of neurons mediating electrical self-stimulation of the anterior basal forebrain was evaluated psychophysically in the rat. Rats with electrodes in the nucleus accumbens, caudate nucleus, lateral preoptic area, diagonal band, or anterior medial forebrain bundle pressed a lever to earn 0.5-s trains of conditioning (C) and test (T) pulse pairs. The C-T interval was systematically varied and the effectiveness of the T-pulse was estimated by measuring the frequency of pulse pairs required to sustain criterion responding. All sites tested demonstrated similar recovery; T-pulse effectiveness, normalized against the effect of the C-pulse, was lowest at delays of 0.4-0.8 ms and it rose monotonically until 5 ms when it achieved an effectiveness plateau of one. Increasing the current of the T-pulse by 50 or 60% failed to hasten recovery, suggesting that the recovery profiles primarily reflect the activation of neurons very soon after emergence from absolute refractoriness. Compared to lateral hypothalamic and ventral tegmental self-stimulation, the neurons that support self-stimulation in the ventral basal forebrain recover more slowly; recovery here is only about half done by the time lateral hypothalamic placements demonstrate complete recovery.

Animals↗

PubMedDate not supplied

[Lysergic acid diethylamide blockade of the brain serotoninergic receptors prevents the facilitating effect of phenamine on self-stimulation in rats with destruction of the medial prefrontal cortex].

Amphetamine (1 mg/kg) increased the rate of pedal self-stimulation of the lateral hypothalamus of Wistar rats in Skinner box by 37%. Lesion of the medial prefrontal cortex with kainic acid (16 mcg/kg in 8 mcl) 10-14 days prior to the experiment did not prevent facilitating effect of amphetamine on self-stimulation. Lysergic acid diethylamid (10 mcg/kg) did not influence self-stimulation response in rats with damaged medial prefrontal cortex, but after its preliminary administration prevented the stimulating effect of amphetamine on self-stimulation of the lateral hypothalamus. The findings are discussed from two points of view: 1) the phenomenon observed is associated with the existence of hypothalamic autoregulatory dopaminergic system which provides realization of self-stimulation; 2) modulating influence of the medial prefrontal cortex on the lateral hypothalamus is mediated not only by dopaminergic but also by serotoninergic axons. It is suggested that both mechanisms may underlie the phenomenon under study.

Amphetamine↗

PubMed2001

Dopamine and glutamate release in the nucleus accumbens and ventral tegmental area of rat following lateral hypothalamic self-stimulation.

Rewarding hypothalamic brain stimulation is thought to depend on trans-synaptic activation of high-threshold (and thus rarely directly depolarized by rewarding stimulation) dopaminergic fibers of the medial forebrain bundle. We used in vivo microdialysis and high-performance liquid chromatography coupled with electrochemical or fluorometric detection to investigate the concurrent release of dopamine and glutamate in the nucleus accumbens septi and in the ventral tegmental area, as a function of lateral hypothalamic self-stimulation.Self-stimulation at a variety of stimulation frequencies and pulse widths increased levels of dopamine and its primary metabolites, dihydroxyphenylacetic acid and homovanillic acid in the nucleus accumbens. Lateral hypothalamic self-stimulation also induced significant increases in ventral tegmental area dopamine and metabolite levels, and the percentage increase of dopamine was higher in this region than in the nucleus accumbens. Local perfusion with the dopamine uptake inhibitor nomifensine (10 microM) increased dopamine levels in the nucleus accumbens about three-fold and potentiated the increase of dopamine levels induced by self-stimulation. Nomifensine perfusion also induced a delayed decrease in nucleus accumbens glutamate levels, and self-stimulation did not modify this effect of the drug. Local perfusion with the D2-type dopamine receptor antagonist raclopride significantly increased both basal and self-stimulation induced dopamine release in the nucleus accumbens. Neither nomifensine nor raclopride perfusion significantly affected the maximal rates of self-stimulation. Perfusion with tetrodotoxin (2 microM) into nucleus accumbens significantly decreased basal and prevented stimulation-induced increases in accumbens dopamine levels but only slightly decreased the rate of self-stimulation. In contrast, perfusion of tetrodotoxin (0.5 microM) into the ventral tegmental area decreased basal and blocked stimulation-induced increases in both nucleus accumbens and ventral tegmental area dopamine levels; this treatment also blocked or strongly inhibited self-stimulation. While it had no effect on glutamate levels in the nucleus accumbens, lateral hypothalamic self-stimulation induced a significant and tetrodotoxin-sensitive increase in glutamate levels in the ventral tegmental area. Taken together, the present results indicate that, across a broad range of stimulation parameters, rewarding lateral hypothalamus stimulation causes major and persistent activation of the mesolimbic dopamine system, and suggest descending glutamatergic fibers in the medial forebrain bundle as a candidate for the directly activated descending pathway in lateral hypothalamus brain stimulation reward.

3,4-Dihydroxyphenylacetic Acid↗

PubMedDate not supplied

[Autonomic correlates of the formation of a functional self-stimulation system].

Capability of intracerebral electrostimulation to serve as an unconditioned reinforcing stimulus in classical conditioning was studied in rabbits. Changes of such vegetative characteristics as respiration frequency and ECG were taken as criterion of conditioned response (CR) elaboration. In preliminary experiments, optimal parameters of stimulation maintaining the highest level of instrumental self-stimulation behaviour were found for each of the animals. Isolated presentation of the unconditioned reinforcing stimulus led to the increase of respiratory rate. Such kind of stimulation induced tachicardia in 5 animals, bradicardia in 3 ones, and in the remaining 6 rabbits a biphasic reaction was observed with initial tachicardia changing for bradicardia. Reactions were taken as CRs if they were similar to those to the unconditioned stimulus and appeared at the moment of omitted reinforcement. After 10 pairings of conditioned sound stimulus with positive reinforcement, CR changes of the two vegetative parameters were observed in 21,4 per cent of cases. After 40 pairings CRs were observed in 87,5 per cent of trials for cardiac and in 78,5 per cent cases for respiratory components. The results obtained confirm the idea of validity and efficiency of intracerebral stimulation of self-stimulation zones as a factor of positive reinforcement.

Animals↗

PubMed1980

Intracranial self-stimulation in relation to the ascending dopaminergic systems of the midbrain: a moveable electrode mapping study.

Chronically implanted moveable electrodes were used to map the midbrain and caudal diencephalon for intracranial self-stimulation in relation to the ascendindg dopamine systems as revealed by fluorescence histochemistry. In the diencephalon the lowest self-stimulation thresholds and the highest response rates were in the areas traversed by the dopamine fiber bundles. In the midbrain, self-stimulation was restricted to the layer of dopamine containing cell bodies. Self-stimulation current thresholds and responses rates were proportional to the density of dopaminergic elements surrounding the electrode tip; the lowest thresholds and highest response rates were associated with the densest packing of dopaminergic neurons. However, not all portions of the dopamine cell groups supported self-stimulation. Self-stimulation was not obtained from the caudal poles of the A9 and A10 groups, nor from the A8 cell group. These findings suggest that a certain population of dopaminergic neurons directly participates in what is probably a multiple-link circuitry subserving positive reinforcement.

Animals↗

PubMed1985

Electrical self-stimulation deficits in the anterior and posterior parts of the medial forebrain bundle after ibotenic acid lesion of the middle lateral hypothalamus.

The aim of the present study was to analyse the involvement of the intrinsic neurons located in the middle lateral hypothalamus in electrical self-stimulation measured with electrodes in the anterior and posterior parts of the medial forebrain bundle. In rats without hypothalamic lesions, self-stimulation rates from both anterior and posterior electrodes were similar on either side of the brain. For all rats with ibotenic acid-induced lesions in the lateral hypothalamus, self-stimulation rates were lower with electrodes in the area of the lesion, while self-stimulation on the contralateral side was normal. In rats with electrodes in the anterior hypothalamus, the lesion produced a large deficit when stimulation was applied to the anterior electrode ipsilateral to the lesion. Only three rats showed a decrease in self-stimulation with stimulation of the posterior hypothalamic electrode ipsilateral to the lesion; self-stimulation of the other three rats was normal. These results suggest that self-stimulation in the anterior part of the medial forebrain bundle is supported by long fibers originating in the middle part of the lateral hypothalamus, while self-stimulation in the posterior part of the lateral hypothalamus can be influenced by another system not involved in reward processes observed in the rostral part of the medial forebrain bundle.

Animals↗

PubMed1980

The recombinant inbred strains: a tool for the genetic analysis of differences observed in the self-stimulation behaviour of the mouse.

The self-stimulation behaviour (ICSS) in the lateral hypothalamus of mice was studied using 5 recombinant inbred strains having the DBA/2 and BLAB/c lines for their parental origin. Two of these recombinant inbred strains behave like the recessive parental line (BALB/c) while the three others have a performance level similar to that of the dominant (DBA/2) parent. This division suggests that there is a major gene which determines the difference in performance between the two parental lines. The mean value for the self-stimulation threshold is negatively correlated with the value of the performance. The sensitivity to convulsions, which interrupt ICSS behaviour above certain current intensities, is under the control of a genetic determinant independent, but more complex, than the one which controls the level of performance.

Animals↗