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PubMed1992

Parametric manipulations and fixed-interval self-stimulation.

Three experiments investigated hypothalamic self-stimulation under a fixed-interval (FI) reinforcement schedule. An FI 20-s schedule was chosen to reduce stimulation density in order to minimize the influence of priming effects or stimulation aftereffects that can affect responding under other schedules of reinforcement. The first experiment showed that the influence of train duration is greatest at levels up to 1 s and thereafter level off over a wide range of train durations (1-32 s). The second experiment showed that altering frequency, current, or pulse width produced almost identical changes in FI responding. These findings show that the neutral network subserving hypothalamic self-stimulation simply integrates the amount of charge over time. It is relatively insensitive to the combination of stimulation parameters that make up a given waveform. In the third experiment, the chronaxies from the strength-duration curves indicate the neural substrate supporting self-stimulation has a great current-integrating capacity. Together, these experiments show that varying the amount of brain stimulation produce large and consistent changes in a number of FI response measures. These measures effectively describe different attributes of FI performance and include response rate, the postreinforcement pause, interresponse times of short duration and the temporal distribution of responses within the interval.

Animals↗

PubMed1987

Opposite effects of unilateral forebrain ablations on ipsilateral and contralateral hypothalamic self-stimulation.

Unilateral ablations of frontal cortex, rostral striatum, nucleus accumbens, septal area and olfactory tubercle decreased ipsilateral hypothalamic self-stimulation; the same ablations had the opposite effect on contralateral self-stimulation. The ablations shifted the function relating response rate to stimulation frequency (rate-frequency function) to the right for ipsilateral self-stimulation and to the left for contralateral self-stimulation, suggesting a reduction and an augmentation, respectively, of the rewarding impact of the stimulation. The inhibition of ipsilateral self-stimulation was neither total nor permanent; 20-30% shifts in threshold were seen at first, but behavior returned to near-normal levels over a period of several weeks. In contrast, the augmentation of contralateral self-stimulation showed no significant change over the same period; in this case the 20-30% shifts in threshold were immediate and permanent. The degree of change in ipsilateral threshold was positively correlated with lesion size; the degree of change in the contralateral threshold was not. Ablations restricted to cortical tissue caused a lesser degree of augmentation of contralateral self-stimulation and had no effect on ipsilateral self-stimulation. The small effects of large ablations on ipsilateral self-stimulation confirm similar observations of Huston and Stellar and their co-workers and raise questions for current theories regarding the role of dopamine in brain stimulation reward. The facilitation of contralateral self-stimulation indicates that brain stimulation reward does not involve a completely lateralized mechanism.

Animals↗

PubMed1991

Prefrontal cortex self-stimulation and energy balance.

The relation between sulcal prefrontal cortex (SPC) and medial prefrontal cortex (MPC) self-stimulation and energy balance was investigated in rats. SPC but not MPC self-stimulation induced feeding but not the gnawing of wooden blocks. SPC but not MPC self-stimulation enhanced weight gain over several weeks of exposure to stimulation. Food deprivation (48 hr but not 24 hr) increased SPC self-stimulation rates under a 5-s fixed-interval reinforcement schedule and decreased current thresholds for SPC self-stimulation. MPC self-stimulation was unaffected by food deprivation. Insulin (4 U/kg) and 2-deoxy-D-glucose (300 mg/kg) inhibited both SPC and MPC self-stimulation, probably through interfering with performance. Satiety induced by prolonged intake of a sweetened solution or deprivation-induced feeding moderately facilitated SPC self-stimulation. Overall, it appears that SPC but not MPC self-stimulation modulates, and is modulated by, energy balance.

Animals↗

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↗

PubMed1983

Bromocriptine promotes recovery of self-stimulation in 6-hydroxydopamine-lesioned rats.

Rats with stable self-stimulation response rate-current intensity functions were subjected to bilateral 6-hydroxydopamine injections into the substantia nigra. The effect of several drug treatments were evaluated on the 6-hydroxydopamine lesion self-stimulation deficit. d-Amphetamine (1.0, 2.0 and 3.0 mg/kg) and scopolamine (0.25, 0.5 and 1.0 mg/kg) had little or no effect on self-stimulation, but bromocriptine (2.0 and 4.0 mg/kg) produced a nearly complete recovery of self-stimulation performance. In contrast, scopolamine increased locomotor activity: whereas, bromocriptine did not increase activity. These results point up the efficacy of bromocriptine in reversing self-stimulation deficits induced by a dopamine deficiency, and indicate that self-stimulation may be a more useful behavior than locomotor activity for evaluating drugs which might alleviate Parkinsonism.

Animals↗

PubMed1992

Determinants of the slow acquisition of medical and sulcal prefrontal cortex self-stimulation: an individual differences approach.

Stimulation-naive rats were tested for motor activity during noncontingent electrical stimulation of the medial prefrontal cortex (MPC) or sulcal prefrontal cortex (SPC). Defecation during stimulation was also measured. The rats were then tested using a conditioned taste aversion paradigm for aversion to a novel flavor (0.1% saccharin) paired with stimulation. Finally, the rats were trained to acquire self-stimulation over 26 days of training. Large individual differences were seen in motor activity, defecation, and conditioned taste aversion to initial stimulation and in the subsequent speed of self-stimulation acquisition. In the MPC-stimulated group, acquisition speed was positively correlated with motor activity to initial stimulation and negatively correlated with defecation to this stimulation. In the SPC-stimulated group, the same correlations were evident, but only when rats suffering seizures prior to self-stimulation acquisition were excluded from the analysis. Such preacquisition seizures, which were only found in the SPC-stimulated group, retarded self-stimulation acquisition. In most rats, MPC or SPC stimulation failed to condition a taste aversion to saccharin. These results suggest that the slow acquisition of MPC and SPC self-stimulation may be partly related to the motor suppressive, aversive, and convulsive properties of initial stimulation.

Animals↗

PubMed1990

Enhanced dopamine receptor activation in accumbens and frontal cortex has opposite effects on medial forebrain bundle self-stimulation.

This study was undertaken to investigate the effects of activating dopamine receptors in accumbens and prefrontal cortex on self-stimulation behavior in the medial forebrain bundle. The experiments were carried out in rats chronically implanted with one stimulating electrode in medial forebrain bundle and two bilaterally-placed cannulas for giving injections into accumbens or prefrontal cortex. After completion of training, animals classified as responders and non-responders were given drug tests. The non-responders were tested to determine the effects of the treatment on motor activity. The self-stimulation task involved the depression of a lever to obtain a stimulus of 0.25 s duration, 60 Hz sine waves applied to the medial forebrain bundle. Dopamine receptor activation in accumbens or prefrontal cortex was induced with bilateral injections in these structures of a mixture containing 5 mg dopamine, 10 mg d-amphetamine sulfate and 5 mg pargyline mixed in 0.5 ml saline containing 0.1% ascorbic acid (dopamine + d-amphetamine sulfate + pargyline, the cocktail). Each injection was of 2 microliters/side, yielding a concentration of 20 micrograms of dopamine, 40 micrograms of d-amphetamine sulfate and 20 micrograms of pargyline/injection. The bilateral injections were given immediately before the self-stimulation session which lasted 12 h, starting in late afternoon. The effects of saline containing the ascorbate were determined in control sessions. Saline injected bilaterally in accumbens or prefrontal cortex of self-stimulators or non-self-stimulators had no effects on the response-rate of self-stimulators or on the gross motor activity of non-responders. In contrast, the cocktail of dopamine + d-amphetamine sulfate + pargyline injected in accumbens of self-stimulators induced a complex response which included first a facilitation, then a prolonged suppression and then again one or two episodes of facilitation interspersed with periods of suppression of self-stimulation and then a return to baseline rats. The same cocktail of dopamine + d-amphetamine sulfate + pargyline injected bilaterally in accumbens of non-self-stimulators resulted also in a complex response including as a first component a facilitation of responding, but the complex effect was of shorter duration and lower magnitude, never raising the rate of lever-pressing to levels meeting self-stimulation criteria. The same cocktail of dopamine + d-amphetamine sulfate + pargyline injected in prefrontal cortex of self-stimulators simply attenuated or suppressed responding, and the effect lasted for most of the session. The same effect was seen in non-self-stimulators indicating a decrease in gross motor activity.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMedDate not supplied

[The effect of isradipine on the morphine-activated self-stimulation reaction in rats].

Lateral hypothalamic self-stimulation in rats was studied using two schedules of reinforcement: continuous reinforcement and fixed-ratio schedule. Isradipine, the blocker of calcium channels (1, 2, 4 mg/kg, subcutaneously) dose-dependently decreased self-stimulation rate and increased the threshold intensity in continuous reinforcement schedule, as well as suppressed self-stimulation under fixed-ratio schedule. The data obtained count in favour of common dihydropyridine-sensitive mechanism of the reinforcing effect of both electrical and pharmacological activation of the brain reward system.

Animals↗

PubMed1982

Effects of parenteral morphine and oral methadone on self-stimulation in the rat.

Facilitation of self-stimulation has been reported following the administration of various opiates. Methadone, a synthetic narcotic used in the treatment of narcotic addiction, has recently been demonstrated to facilitate self-stimulation when administered parenterally. The present study examined the effects of orally administered methadone (20 and 30 mg/kg), the route of administration used clinically, on MFB-LH self-stimulation at 2.5, 5, 8, 12, 17, and 24 hours post-administration. Reliable facilitation was observed at 2.5 hours post-administration. However, the effect of methadone was less pronounced than that observed with a dose of parenteral morphine which was approximately equivalent in terms of analgesic potency.

Administration, Oral↗

PubMed1994

Plasticity of hippocampal and motor cortical pyramidal neurons induced by self-stimulation experience.

The self-stimulation (SS) induced neuronal plasticity was observed in CA3 hippocampal and layer V motor cortical pyramidal neurons. SS experience was allowed daily for a total of 1 hour for 10 days through four bipolar electrodes implanted bilaterally in lateral hypothalamus (LH) and substantia nigra-ventral tegmental area (SN-VTA) in adult male Wistar rats. Examination of pyramidal neurons stained by rapid Golgi technique was made in a total of 1,600 neurons out of 80 rats consisting of 4 groups. The dendritic intersections were quantified upto 200 and 120 microns radial distances in apical and basal dendrites respectively. The CA3 hippocampal and layer V motor cortical pyramidal neurons of SS group revealed significant increase (P < 0.001, two-way ANOVA) in dendritic intersections in both apical and basal dendrites, compared to normal control (NC), sham control (SH) and experimenter-administered (EA) group of animals. These results demonstrate that SS experience promotes increase in dendritic length in hippocampal and motor cortical pyramidal neurons.

Animals↗

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↗

PubMed1985

Evidence for a role of the preoptic area in lateral hypothalamic self-stimulation.

We examined the effects of unilateral radiofrequency lesions in the preoptic area on lateral hypothalamic self-stimulation in 15 rats. The animals were tested for self-stimulation in the lateral hypothalamus at 3 different current intensities from electrodes placed in both hemispheres, and then received a unilateral lesion in the preoptic area. Four hours later they were again tested for self-stimulation at the 3 current intensities and then daily over the following 14 days, or until they recovered their presurgical rates of self-stimulation. Rate of self-stimulation decreased in the damaged hemisphere, and recovered to prelesion levels within 2 weeks in 6 of 9 rats. In the intact hemisphere rate of self-stimulation increased above the prelesion level during a period from 1 to 2 weeks after the lesion. These results suggest that the preoptic area is involved in lateral hypothalamic self-stimulation. The effects of D-amphetamine (1 mg/kg) and apomorphine (2 mg/kg) injections on turning behavior were also studied in an open field and in a rotometer. Apomorphine induced contraversive turning to the lesion side in the open field and D-amphetamine induced ipsiversive turning in the rotometer.

Animals↗

PubMed2006

Classical as well as novel antipsychotic drugs increase self-stimulation threshold in the rat--similar mechanism of action?

Antipsychotic drugs given acutely increase the threshold for intracranial self-stimulation elicited from the ventral tegmental area. As all the antipsychotic drugs share the dopamine D2-receptor antagonism it is reasonable to believe that this is the cause for suppression of intracranial self-stimulation behaviour. The objective of this investigation was to examine the effect of classical (haloperidol) as well as novel antipsychotic drugs (clozapine, olanzapine and sertindole) on intracranial self-stimulation behaviour. Furthermore, the effects of different specific receptor antagonists on intracranial self-stimulation behaviour were examined. Our results showed that both the classical (haloperidol) and the three novel antipsychotic drugs increase the threshold for intracranial self-stimulation. The results obtained with the receptor specific antagonists showed that dopamine D2, alpha1-adrenoceptor and serotonin 5-HT2A receptor antagonisms inhibit intracranial self-stimulation behaviour and that muscarinic receptor antagonism is without effect. Even though all the tested antipsychotic drugs inhibited intracranial self-stimulation behaviour, there seems to be a difference in their ratio between doses that inhibits intracranial self-stimulation behaviour and those that produce antipsychotic effect in a preclinical model (amphetamine hyperactivity). Sertindole was the only antipsychotic drug able to produce antipsychotic effect without significant inhibition of intracranial self-stimulation behaviour at a narrow dose interval. The remaining antipsychotic drugs all inhibited intracranial self-stimulation behaviour at equal or lower doses than those producing antipsychotic effect.

Animals↗

PubMed1988

Opposite effects of ibotenic acid and 6-hydroxydopamine lesions of the lateral hypothalamus on intracranial self-stimulation and stimulation-induced locomotion.

The purpose of the present study was to test the respective roles of the intrinsic neurons and of the catecholaminergic fibers in two behaviors elicited by electrical stimulation of the lateral hypothalamus, intracranial self-stimulation and the increase in locomotor activity produced by noncontingent stimulation. One group of rats was unilaterally injected in the middle lateral hypothalamus with a dose of ibotenic acid known to significantly decrease self-stimulation (4 micrograms/0.5 microliter). Two other groups received, in the same area, an injection of a small dose of 6-hydroxydopamine (2 micrograms/0.5 microliter). The rats of one of these groups were pre-treated with desmethylimipramine. Two other groups of rats were respectively injected with the vehicle of each neurotoxin. Eight days later all rats were bilaterally implanted with stimulation electrodes, one in the lesioned area, the other in the contralateral region. Each electrode of each animal was tested first for self-stimulation, then for locomotor activation measured in the open field produced by non-contingent stimulation. Whatever the lesion or the behavior tested, the response of the lateral hypothalamus contralateral to the lesioned area was normal. Self-stimulation was disturbed only with stimulation of the lateral hypothalamus lesioned by ibotenic acid. Self-stimulation in the lateral hypothalamus lesioned by 6-hydroxydopamine was normal. However, a significant loss of noradrenaline in the hippocampus and of dopamine in the striatum was observed. Furthermore, the brains of two rats unilaterally injected with the usual dose of 6-hydroxydopamine were processed for tyrosine hydroxylase immunocytochemistry.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1999

Regional differences in desensitization of c-Fos expression following repeated self-stimulation of the medial forebrain bundle in the rat.

The acute self-stimulation of the medial forebrain bundle was reported to induce the expression of c-Fos, the protein product of c-fos, an immediate early gene, in the central nervous system. In the present study, we examined regional changes in c-Fos expression in several reward-related areas of rat brain in response to short- and long-term exposure to self-stimulation of the medial forebrain bundle. Short-term one-hour stimulation of the medial forebrain bundle for one day after training, which evoked steady self-stimulation behavior, significantly increased the number of c-Fos-positive neurons bilaterally in all of 15 brain structures assayed, as compared to the non-stimulation control. Among them, structures showing a larger number of the stained neurons on the stimulated side were the anterior olfactory nucleus, amygdala, medial caudate-putamen complex, lateral septum, bed nucleus of the stria terminals, ventral pallidum, substantia innominata, lateral preoptic area, medial preoptic area, lateral hypothalamus rostral to the stimulating electrodes, and substantia nigra. Long-term stimulation of the medial forebrain bundle once daily for five successive days, which maintained consistently stable self-stimulation behavior, also increased the number of c-Fos-positive neurons in the aforementioned structures, as compared to the control. However, the long-term rewarding stimulation diminished the increased number of labeled neurons, as compared to the short-term rewarding stimulation. Seven areas, medial caudate-putamen complex, ventral pallidum, substantia innominata, lateral preoptic area, medial preoptic area, rostral lateral hypothalamus and substantia nigra, showed asymmetrical, ipsilateral predominance after the short- and long-term stimulation. However, the stained neuron count in those areas after the long-term stimulation was reduced to less than 50% of that found after the short-term stimulation with the exception of lateral preoptic area and rostral lateral hypothalamus. The results suggest that the development of desensitization of c-Fos response may differ among the reward-relevant brain regions as a consequence of repeated self-stimulation. They also indicate that a larger portion of neurons in the lateral preoptic area and rostral lateral hypothalamus may be implicated in both short- and long-term self-stimulations of the medial forebrain bundle.

Animals↗

PubMed1983

Learning and self-stimulation in mute and echolalic autistic children.

The effects of self-stimulation on task acquisition were studied in three mute low-functioning autistic and three echolalic higher-functioning autistic children in multiple-baseline designs. The study found that (a) the echolalic children were able to learn the task without external suppression of their self-stimulation and (b) the mute children were unable to learn the task until their self-stimulation was externally suppressed. It was suggested that the echolalic children may have acquired the ability to discriminate when to self-stimulate, so that their self-stimulation does not interfere with correct responding.

Adolescent↗

PubMed1999

Intracranial self-stimulation in the parafascicular nucleus of the rat.

A behavioral analysis of intracranial self-stimulation was provided for parafascicular nucleus. To evaluate whether intracranial self-stimulation in this nucleus could be site-specific and to determine if the positive sites are the same parafascicular areas that facilitate learning when stimulated, rats were tested via monopolar electrodes situated throughout the parafascicular nucleus. Animals were trained to self-stimulate by pressing a lever in a conventional Skinner box (1-5 sessions). Twenty-two of the 42 animals included in the study, had the electrode at the parafascicular nucleus. Only two of them showed intracranial self-stimulation. Histological analyses indicated that the latter rats had the electrode implanted at the anterior area of the medial parafascicular. Other two animals also showed intracranial self-stimulation but they had the electrode in a more posterior brain region, between the Dark-schewitsch nucleus and the red nucleus. The animals implanted at the parafascicular showed higher response rates than the other two rats. These results confirm that: (a) the anterior region of the medial parafascicular is a positive site for stable and regular intracranial self-stimulation behavior, and (b) these positive sites do not coincide with the parafascicular regions related to learning improvement.

Animals↗