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At least 109 records · Page 6Linked to original sources
PubMed1980

Apomorphine: selective inhibition of the aversive component of lateral hypothalamic self-stimulation.

The effects of dopamine agonists on self-stimulation are a matter of considerable dispute. Apomorphine has variously been reported to inhibit, have no effect on, or to facilitate lever-press self-stimulation. To investigate the possibility that these discrepancies may reflect peculiarities of the lever-press test situation, the present study investigated the effects of apomorphine on locomotor initiation of and escape from lateral hypothalamic stimulation in a shuttle-box. Apomorphine had relatively little effect on the initiation behavior, but it produced a large and dose-dependent inhibition of escape. These data suggest that apomorphine acts to inhibit the aversive component of lateral hypothalamic stimulation. The implications of these findings for the usefulness of the shuttle-box in investigating the pharmacology of self-stimulation are discussed.

Animals↗
PubMed1984

[Differentiation of the effects of diazepam on self-stimulation behavior as a function of the structure of the stimulated brain].

The effect of diazepam was tested on self-stimulation in 21 mice with a bipolar electrode in lateral hypothalamus (HL), dorsolateral hippocampus (HPC) or lateral entorninal cortex (CEL). Diazepam at 0.5, 1 and 2 mg/kg significantly increased self-stimulation rates in HL while 4 and 8 mg/kg had no significant effect. Similar increases were seen in CEL mice but high doses produced a significant suppression. HPC animals showed a drastic suppression of self-stimulation beginning at 2 mg/kg of diazepam, lower doses having no significant effect. The results demonstrate that entorhinal and hippocampal self-stimulation involve at least partly independent neuronal mechanisms and point to a possible inhibitory influence of HPC and CEL.

Animals↗
PubMed1980

Naloxone and shuttlebox self-stimulation in the rat.

Rats self timed electrical brain stimulation on and off periods in a shuttlebox. Electrodes for self-stimulation were located either in the lateral hypothalamic area (LHA) or the periaqueductal gray (PAG). Doses of the narcotic antagonist, naloxone, were administered intraperitoneally immediately prior to self-stimulation testing. Doses of 1.0, 5.0, 10.0 or 50.0 mg/kg failed to alter shuttlebox self-stimulation behavior. These results are inconsistent with one lever-press self-stimulation study employing PAG electrodes [3], but agree with other studies using LHA electrodes [9, 15, 21, 24). Possible reasons for the discrepancy are suggested.

Animals↗
PubMed1979

Hypothalamic self-stimulation and stimulation escape in relation to feeding and mating.

This review begins with James Olds' discovery that self-stimulation at various brain sites can be influenced by food intake or androgen treatment. It then describes our research designed to reveal the functional significance of self-stimulation. The evidence suggests that lateral hypothalamic self-stimulation is controlled by many of the same factors that control feeding. We believe this control is exerted by at least two neural mechanisms. One is the classical, medial hypothalamic satiety system. Another is an adrenergic system ascending from the midbrain to the lateral hypothalamus. Damage to either one can disinhibit self-stimulation and feeding, thus contributing to obesity. Some of our studies use rats with two electrodes, one that induces feeding and one that induces mating. There are two response levers in the test cage, one for self-stimulation and one for escape from automatic stimulation. With the feeding electrode, rats self-stimulated less and escaped more after a meal than before. The same shift occurred after an anorectic dose of insulin or the commercial appetite suppressant phenylpropanolamine. With the sex electrode the shift from reward to aversion occurred after ejaculation. The review ends with credit to James Olds for pioneering this line of research into the neuropsychology of reinforcement.

Animals↗
PubMed1990

Cocaine facilitates prefrontal cortex self-stimulation.

It has been demonstrated that cocaine HCl lowers thresholds for and increases rates of medial forebrain bundle intracranial self-stimulation. The influence of cocaine on prefrontal cortex self-stimulation was assessed in the present experiment. The prefrontal cortex was chosen because evidence indicates that the neuroanatomical and pharmacological substrate for intracranial self-stimulation at this site may differ from the substrate for medial forebrain bundle self-stimulation. Cocaine significantly decreased train-duration thresholds and increased the rate of prefrontal cortex self-stimulation. It was concluded that cocaine facilitates both prefrontal cortex and medial forebrain bundle self-stimulation, perhaps by influencing neural activity in the mesocorticolimbic dopamine system. However, the role of dopamine in cocaine's effects at both sites remains speculative.

Animals↗
PubMed1980

Facilitation of self-stimulation in rats by methadone.

The effects of morphine and its derivatives on self-stimulation behavior have been widely studied. In those experiments which have used multiple injections (over days) and multiple post-injection tests (within days), the typical findings includes a depression of responding after the initial injections followed by a facilitation of responding on subsequent days. There have been only a few reports which have tested the effects of methadone in this paradigm. Some investigators have observed only depression of self-stimulation while others have reported both the transient depression and the subsequent facilitation generally obtained with morphine. In the present experiment we administered either 5 mg/kg or 10 mg/kg methadone IP over a five day period and tested MFB-LH self-stimulation at 2, 4, 6, 8, 10 and 23 hours post-injection. Compared to saline controls, the 10 mg/kg dose produced the typical opiate-induced changes in self-stimulation, i.e., an initial depression which lasted for two hours on the first two days but was replaced by significant facilitation by hour 4 of day 3. This facilitation persisted for at least 10 hours on all 5 days of the experiment. Except for a transient (days 2-3) depression of self-stimulation, 5 mg/kg was without effects. The present experiment demonstrates that methadone does facilitate self-stimulation but that its ability to do so is highly dose-dependent.

Animals↗
PubMed1988

Improvement of shuttle-box learning with pre- and post-trial intracranial self-stimulation in rats.

The effects of intracranial self-stimulation (ICSS) in the lateral hypothalamus upon the acquisition and long-term retention (LTR) of shuttle box avoidance conditioning were studied in Wistar rats. Two groups of subjects learned the avoidance task in 5 daily training sessions and were allowed to self-stimulate either before (Pre-ICSS group), or after (Post-ICSS group) each training session. A control group received training but no ICSS. Ten days following the last training session, LTR of the task was determined in one avoidance session without ICSS. A fourth group was added post-hoc which was allowed to self-stimulate before the training sessions as well as before the LTR test. Both the Post-ICSS and Pre-ICSS groups improved in acquisition of the learned response over the successive training sessions, as compared with Controls. In the LTR test, the animals of the Post-ICSS group maintained the response level achieved in the last acquisition session. In contrast, the subjects of the Pre-ICSS group showed a significant decrease of the same response, unless they were given ICSS treatment prior to the LTR test. This may indicate a 'state-dependent learning' effect being responsible for the decrease in the LTR observed in Pre-ICSS group. Because both pre- and post-training ICSS treatments improved the acquisition and the LTR of the learned response, it is suggested that the contingency of the treatment with training (that is, ICSS treatment immediately after the training sessions) is not a necessary condition to facilitate the acquisition and the consolidation of two-way active avoidance learning.

Animals↗
PubMedDate not supplied

Toward a cellular analysis of intracranial self-stimulation: contributions of collision studies.

Since the discovery of brain stimulation reward by Olds and Milner, researchers have struggled to identify the underlying neural circuitry. This goal has proved surprisingly elusive. For example, the identity of the directly-activated neurons ("first stage" neurons) responsible for the rewarding effect of stimulating the numerous brain sites that support self-stimulation remains largely or entirely unknown. It was to address this problem that the collision test was adapted for use in experiments on intracranial self-stimulation. By estimating the trajectory, conduction velocity and axonal diameter of the first stage neurons, it was hoped that their identification would be facilitated. Indeed, the choice of candidate pathways has been tightly constrained by collision data. For example, such data suggest that the circuitry underlying brain stimulation reward includes myelinated fibers directly linking self-stimulation sites in the lateral hypothalamus and ventral tegmental area; the conduction velocity of these fibers has been estimated at 1-8 meters/sec. Additional collision data suggest direct axonal links between self-stimulation sites in the preoptic area and lateral hypothalamus, as well as between sites in the ventral tegmental area and periaqueductal gray matter. Although collision data constrain the choice of candidate pathways, they cannot prove that a given population of neurons is part of the first stage. No matter how closely the anatomical and physiological characteristics of a given population match the properties inferred from collision data, the possibility remains that the population in question plays no role in reward but happens to resemble neurons that do. This ambiguity can be reduced by assessing how collision effects are altered by lesions of the candidate pathway. Coupled with data from single-unit recording experiments, inferences drawn from such lesion-induced changes provide a powerful means of linking an identified population of neurons to the rewarding effect of electrical brain stimulation.

Action Potentials↗
PubMed1982

Unilateral 6-hydroxydopamine lesions of dopamine neurons produce bilateral self-stimulation deficits.

Sixteen rats, which had electrode implants in each hemisphere which generated comparable self-stimulation rate-intensity functions, were used in this study. Eight of the rats received unilateral 6-hydroxydopamine injections into the substantia nigra pars compacta, which produced severe unilateral losses of dopamine and were effective in generating apomorphine-induced turning away from the injected hemisphere. Of the remaining 8 rats, 5 received unilateral 6-hydroxydopamine lesions aimed at the ventral tegmental area and 3 were give vehicle injections. The vehicle injections were without effect on self-stimulation and the ventral tegmental injections had an overall transient facilitative effect on self-stimulation. The 6-hydroxydopamine lesions of the pars compacta, however, had variable effects. In some rats there was a marked bilateral reduction in self-stimulation over 8 weeks; whereas, there was little, if any, effect in other rats. The rats which sustained the bilateral deficits also sustained the greatest unilateral loss of dopamine. The unilateral 6-hydroxydopamine lesions of the pars compacta consistently blocked the facilitative influence of 0.5 mg/kg of D-amphetamine on self-stimulation bilaterally, and this effect persisted over 8 weeks of postoperative testing. These results were considered supportive of a response rather than reinforcement role for dopamine in the mediation of self-stimulation behavior.

Animals↗
PubMed1989

[Septal nuclei in the mechanisms of lateral hypothalamic self stimulation in rabbits].

Unilateral lesions of medial septal nucleus and lateral septal nuclei (dorsalis, intermedius, ventralis) decreased ipsilateral hypothalamic self-stimulation; the lesions of n. dorsalis, n. medialis and lateral septal nuclei (intermedius and ventralis) has the opposite effect on contralateral self-stimulation. The inhibition of ipsilateral self-stimulation was neither total nor permanent; 25-32% decrease in stimulation rate was seen, but behaviour returned to near-normal levels over a period of few days. In contrast, the augmentation of contralateral self-stimulation showed no significant change over the same period; in this case the 35-40% shift in stimulation rate was immediate and permanent. Bilateral lesions of septal nuclei had no effect if the initial level of self-stimulation rate was high and significantly increased self-stimulation.

Animals↗
PubMed1977

Presynaptic alpha-adenoceptors: the depression of self-stimulation by clonidine and its restoration by piperoxane but not by phentolamine or phenoxybenzamine.

Depression of self-stimulation by clonidine has been ascribed to continuous direct stimulation of alpha-adrenoceptors with consequent disruption of reinforcement signals thought to be conveyed by noradrenergic pathways. This suggestion was tested by administration of alpha-receptor blocking agents (piperoxane, phentolamine and phenoxybenzamine, PBZ) differing in their affinity for pre- and post-synaptic receptor sites. Piperoxane in low doses (0.55-5.0 mg/kg) previously reported to cause specific blockade of pre-synaptic receptors implicated in negative feedback circuits, caused a significant increase in self-stimulation rate and strongly antagonized the depression of self-stimulation by clonidine (0.15 mg/kg). A larger dose of piperoxane (45 mg/kg) and graded doses of phentolamine and PBZ, affecting both pre- and post-synaptic receptors, depressed self-stimulation, and did not antagonize clonidine-induced depression of self-stimulation. It is concluded that depression of self-stimulation by clonidine may depend on clonidine-induced inhibition of NA release exerted via presynaptic receptors, and that the effect of clonidine is not necessarily evidence that noncontingent adrenergic stimulation disrupts reinforcement.

Animals↗
PubMed2000

The effects of cholecystokinin on stimulation-induced feeding and self-stimulation.

Cholecystokinin (CCK) is a peptide hormone which controls a number of important functions during the process of digestion. It is present in the gut and the central nervous system, although its exact role in the latter is not yet clear. Our interest was in the effects of intraperitoneal and intracerebral injections of CCK on brain stimulation reward and stimulation-induced feeding. Period thresholds for rewarding stimulation were unaffected by either route of peptide administration, whereas stimulation-induced feeding thresholds were weakly increased by centrally injected CCK. In addition, we evaluated stimulation-induced feeding using a more resolved measure and found it to provide clearer results. By actually measuring the amount of food eaten during a stimulation-induced feeding session, and not only the occurrence of feeding, CCK was shown to systematically decrease the total intake as a function of dose in an inverse manner. The efficiency of food utilization was calculated for each animal during the different phases of the experiment in order to monitor the effects of CCK on the animals' overall health. Centrally administered CCK appeared to increase the animals' efficiency and, furthermore, this level was sustained for the entire post-injection phase, about 2 weeks, suggesting a relatively enduring increase in metabolic rate. While the functional role of central CCK and other gastric peptides requires clarification, analyses which exploit the stimulation-induced feeding paradigm need to make use of more clearly defined microstructural variables.

Animals↗
PubMed1976

A dose-response study of anorectic drug effects on food intake, self-stimulation, and stimulation-escape.

A comparison was made of the short-term effects in rats of 3 anorectic drugs (amphetamine, fenfluramine, and phenylpropanolamine) on food intake and responses to obtain brain stimulation and to escape from automatic brain stimulation. At a dose which decreased food intake, amphetamine increased self-stimulation, but not stimulation-escape. Fenfluramine decreased both self-stimulation and stimulation-escape. Phenylpropanolamine, on the other hand, decreased self-stimulation, but not stimulation-escape. Even though all 3 drugs decreased food intake, each of them had different effects on hypothalamic self-stimulation and stimulation-escape. Only the actions of phenylpropanolamine were in agreement with the hypothesis that lateral hypothalamic reward and aversion reflect the animal's tendency to eat, suggesting that other aspects of reinforcement are also involved in lateral hypothalamic stimulation and were affected differently by these drugs.

Amphetamine↗
PubMed1985

Dopaminergic agents including 3-PPP and its enantiomers on medial septal self-stimulation.

The effects of several dopamine agonists were determined on medial septal self-stimulation in rats and compared with selected dopamine antagonists and with the psychostimulants, d-amphetamine and nomifensine. Apomorphine, 3-PPP, TL-99, N,N-dipropyl-5,6-ADTN and N,N-dipropyl-6,7-ADTN inhibited self-stimulation at dose ranges selective for the dopamine autoreceptor as indicated by biochemical studies. Haloperidol and molindone produced dose-related inhibition but sulpiride increased self-stimulation. D-amphetamine and nomifensine also increased responding. The agonist-induced inhibition differed from neuroleptic-induced inhibition of self-stimulation. Both (+) and (-) 3-PPP inhibited responding by a similar amount over the dose range 0.25-1.0 mg/kg. At higher doses, (-) 3-PPP further decreased responding whereas the effects of (+) 3-PPP plateaued at approximately 55% of controls. These studies show that dopamine agonists, like neuroleptics, inhibit medial septal self-stimulation. This effect appears to be mediated via autoreceptor activation. Differences between neuroleptic- and agonist-induced inhibition and the 3-PPP stereoisomer data accord with the hypothesis that behavioural inhibitory effects caused by autoreceptor activation are less severe than those caused by dopamine postsynaptic blockade.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1962

Hypothalamic control of feeding and self-stimulation.

Hypothalamic sites which control feeding exert a corresponding control over lateral hypothalamic self-stimulation. This was demonstrated in rats bearing four, intrahypothalamic electrode-cannulas for electrical stimulation or chemical injection. Self-stimulation of the lateral hypothalamus was inhibited by ventromedial excitation or by excessive feeding. Both self-stimulation and feeding were accelerated (disinhibited) by ventromedial ablation or anesthetization. Thus food acts via the ventromedial hypothalamus to inhibit not only feeding, but also lateral hypothalamic self-stimulation.

Animals↗
PubMed1991

Cocaine's effects on rate of intracranial self-stimulation.

While some investigators have reported that cocaine increases response rates for brain stimulation reward, others have failed to demonstrate this effect. The present study was designed to evaluate the influence of stimulation parameters, dose of cocaine and operant-dependent response requirements on cocaine's ability to alter self-stimulation rates. Self-stimulation rates were collected on a minute by minute basis for 45 min following IP injections of 0, 5, 15 or 30 mg/kg cocaine HCI. All doses were tested using both nose-poking and lever-pressing operants. It was found that mean lever-pressing rates were significantly increased by 5 mg/kg cocaine, while nose-poking rates were significantly increased by 15 and 30 mg/kg cocaine. Further examination of the pattern of results indicated that the cocaine-induced increases in lever-pressing rate were mainly due to an increase in the time spent self-stimulating, whereas increases in nose-poking were mainly due to increases in nose-poking rate/min within self-stimulation bouts. It was hypothesized that 5 mg/kg cocaine increased lever-pressing by producing response perseveration, while the higher doses increased nose-poking mainly due to the compatibility of the nose-poking response topography with cocaine-induced stereotypies.

Animals↗
PubMed1987

Electrical self-stimulation in the parabrachial area is depressed after ibotenic acid lesion of the lateral hypothalamus.

The involvement of lateral hypothalamic intrinsic neurons on electrical self-stimulation of the parabrachial area was analyzed. Rats were bilaterally implanted in the parabrachial area and with a guide cannula located above each lateral hypothalamus. They were subsequently tested for intracranial self-stimulation. Then, the lateral hypothalamus on one side of the brain was injected with ibotenic acid. The effect of the induced lesion was tested 8 days later on self-stimulation of the ipsilateral and contralateral parabrachial areas. The intrinsic neurons of the non-lesioned lateral hypothalamus were then destroyed with ibotenic acid. Self-stimulation was then tested 8, 12 and 30 days later. The unilateral lesion produced a significant decrease of self-stimulation using the electrode ipsilateral to the lesion, without any modification of the stimulation using the contralateral electrode. After bilateral lesion, self-stimulation was greatly reduced bilaterally. The results suggest that the main effect of the lesion was to increase the self-stimulation threshold. Given that the parabrachial area is a relay station for the gustatory inputs and that the intrinsic neurons of the lateral hypothalamus project back to the parabrachial area, the present results are tentatively interpreted as an indication that self-stimulation in this pontine area results from the activation of feedback loops between the lateral hypothalamus and the parabrachial area.

Animals↗