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PubMedDate not supplied

[The role of biological needs in the genesis of self stimulation].

It has been found in fifteen rats with monopolar electrodes implanted in the lateral hypothalamus that after stimulation of the brain with bursts of electrical pulses of fixed duration, with definite combinations of stimulation parameters, the histograms of the duration of pedal pressing have a polymodal appearance. As the combinations of stimulation parameters change, the number, position and magnitude of the modes undergo a corresponding change. With unchanged parameters of stimulation the form of pressing duration histogram does not change significantly. A conclusion has been drawn that the modal duration of pressing in the course of self-stimulation is apparently an effector manifestation of central integration of reinforcing excitation. In a state of hunger and thirst as well as under weak nembutal anaesthesia, the previously monomodal histograms of the pressing durations produce additional modes which diminish and disappear after satiation and discontinuation of the nembutal effect. It is assumed that at least some modes of the histograms of the pressing duration of self-stimulation may reflect an activation of the systems of biological needs.

Animals↗

PubMed1990

"Temporal summation decay" in hypothalamic self-stimulation: threshold changes at long intrapair intervals due to axonal subnormal periods.

Rats were trained to bar press for trains of conditioning (C) and test (T) pulses delivered via lateral hypothalamic electrodes. As intrapair (C-T) intervals increased from 10 ms to 100 ms, the frequency of pulses required for self-stimulation increased, similar to results of Smith and Coons (1970). This effect was observed only for electrode placements where self-stimulation was obtained at frequencies below 16 Hz and currents of 600 microA and higher. The effect was larger when the train duration was increased from 0.5 s to 2.0 s. The threshold increase was abolished when the T pulses were greater in current than the C pulses but not when C pulses were larger than T pulses. The larger T pulses also removed relative refractory period effects at a C-T interval of 1.0 ms. Therefore, the increase in required current or frequency at long C-T intervals appears to be due to a decline in axonal excitability (i.e., the subnormal period) rather than a decay in synaptic temporal summation. Possible flaws in other reports of paired-pulse "temporal summation decay" at long C-T intervals using 2 electrodes are discussed.

Animals↗

PubMed1984

Dissociation of limbic structures by pharmacological effects of diazepam on electrical self-stimulation in the mouse.

The effect of diazepam was tested on self-stimulation (SS) in 21 mice implanted with a bipolar electrode in the lateral hypothalamus (LH), the dorsolateral hippocampus (HPC) or the lateral entorhinal cortex (LEC). Diazepam, injected i.p. in doses of 0.5, 1 and 2 mg/kg, significantly increased SS rates with electrodes in LH while 4 and 8 mg/kg of diazepam had no significant effect. At low doses, similar increases were seen in mice with LEC electrodes but high doses produced a significant suppression. HPC animals showed an almost total suppression of SS beginning at 2 mg/kg of diazepam; lower doses had no significant effect. The results indicate that entorhinal and hippocampal SS are at least partly independent phenomena; in addition, the suppression of SS by moderate doses of diazepam remains specific to the HPC among the brain structures studied to date.

Animals↗

PubMedDate not supplied

Brain self-stimulation and immunity: effect on humoral and cell-mediated immune responses.

This study was designed to evaluate the effect of intracranial self-stimulation (ICSS) on specific immunological reactivity in the rat. Male Wistar rats were implanted with stimulating electrodes in the lateral hypothalamus (LH) and ventral tegmental area (VTA). After recovery from surgery and screening procedure, animals were allowed to self-stimulate 30 minutes daily during different periods of time before or after immunization with sheep red blood cells (SRBC) and bovine serum albumin (BSA). We report here on the in vivo immunoregulating effects of ICSS on plaque-forming cell (PFC) response, hemagglutinin production to SRBC, and antibody titer and hypersensitivity skin reactions to BSA. The effects produced were dependent on the brain area which was stimulated, time relationship of ICSS and immunization, type of immune reaction, and antigen used for immunization. Therefore, ICSS appears to be a significant tool in the regulation of the immune system function, and thus provides further evidence of the interconnections between the immune system and behavior.

Animals↗

PubMed1976

Restoration of self-stimulation inhibited by neuroleptics.

Pimozide-induced inhibition of lever-pressing for brain stimulation in the lateral hypothalamic area was differentially restored by the centrally acting anticholinergic, dexetimide and by different dopaminergic drugs. In addition, a differential antagonism towards chlorpromazine-induced inhibition of self-stimulation was shown. The results indicate that anticholinergis (non-competitive antagonism) or drugs which enhance endogenous neuro-transmission by increased release or by uptake blockade (competitive antagonism) are able to reserve the neuroleptic-induced inhibition of self-stimulation more effectively than are receptor agonists.

Amphetamine↗

PubMedDate not supplied

[A comparison of the effects of dopamine agonists on self-stimulation of the hypothalamus with destruction of the mesolimbic brain structures in rats raised under conditions of social isolation].

In rats bred in groups or under conditions of social isolation, amphetamine administration did not change significantly the basic rate of hypothalamic self-stimulation. The unilateral lesions of ventral tegmental area and medial prefrontal cortex in the early ontogeny (on the 17th day after birth) increased the sensitivity to amphetamine only in isolated rats. Apomorphine, the dopamine receptor agonist, in the dose which mainly affected the presynaptic receptors (0.05 mg/kg) inhibited self-stimulation by 21-23% both in grouped and socially isolated rats. Destruction of the ventral tegmental area did not change, but that of the medial prefrontal cortex doubled the sensitivity of isolated rats to apomorphine. It is suggested that the hypersensitivity of presynaptic dopamine receptors in the mesocorticolimbic system develops as a result of partial sensory and full intraspecies isolation in rats.

Amphetamine↗

PubMed1983

Hypothalamic self-stimulation in rats with one hemisphere isolated anterior to the midbrain and the other hemisphere devoid of the telencephalon.

The telencephalon was removed unilaterally in rats. In addition, the forebrain of the other hemisphere was isolated from its brain stem by a precollicular transverse cut. This preparation was then tested for self-stimulation via electrodes implanted in the region of the lateral hypothalamus and medial forebrain bundle (LH-MFB) of either hemisphere. Self-stimulation was found to be intact in both hemispheres. Possible pathways connecting the LH-MFB region of one hemisphere to the contralateral diencephalon were also investigated in the bilaterally detelencephalized rat. The technique of retrograde transport of horseradish peroxidase was used for this purpose. Some fibers from the LH-MFB of one hemisphere were found to decussate to the other hemisphere by way of the thalamic commissure. The supraoptic decussation as well as diffusely organized interdiencephalic connections provide additional routes for interhemispheric LH-MFB projections.

Animals↗

PubMed1982

Fiber pathways associated with cerebellar self-stimulation in the rat: a retrograde and anterograde tracing study.

Intracranial self-stimulation (ICSS) was obtained from an area of cerebellum just rostro-ventral to the fastigial nucleus. The acquisition of cerebellar ICSS was slow, although this depended in part on the type of operant task required. The afferent and efferent fiber connections of the region of cerebellum supporting ICSS were identified using silver-degeneration and horseradish peroxidase tracing techniques. Two major pathways, one ascending to the ventromedial thalamus and one descending to the paramedian reticular formation and the region of the solitary nucleus, are discussed as possible substrates of ICSS at sites in the cerebellum as well as from other pontine and medullary regions.

Animals↗

PubMed1978

Pharmacological analysis of analgesia and self-stimulation elicited by electrical stimulation of catecholamine nuclei in the rat brain.

The relationship between intracranial self-stimulation (ICSS) and stimulation-produced analgesia (SPA) was investigated in that rat employing an operant bar-press response and a modification of the hot-plate test. ICSS and SPA were elicited through bipolar electrodes chronically implanted in two catecholamine nuclei; the nucleus locus coeruleus (LC) and the substantia nigra (SN). These sites have previously been shown to yield both phenomena. SPA was shown to be of a magnitude similar to that of morphine. In addition, SPA deriving from both LC and SN was significantly reversed by the specific opiate antagonist, naloxone. The intensity of the stimulating current sufficient to induce SPA was found to be higher than that required for ICSS. The pharmacological susceptibilities of the two phenomena were tested by administering a number of drugs: haloperidol, propranolol, pimozide and AMPT attenuated ICSS in both LC and SN, while leaving SPA unaffected. In contrast, methysergide and PCPA blocked SPA and simultaneously facilitated ICSS. The present results indicate a dissociation of ICSS and SPA from LC and SN at both physiological and neurochemical levels; ICSS rates appeared to be a function of catecholaminergic tone, while SPA depended upon the integrity of serotonin transmission.

Analgesia↗

PubMed1992

Bromocriptine reverses the elevation in intracranial self-stimulation thresholds observed in a rat model of cocaine withdrawal.

Cocaine use frequently occurs in episodic prolonged binges. Following such a cocaine binge, the user suffers from severe depression mixed with irritability, anxiety, anergia and anhedonia. These symptoms constitute the cocaine withdrawal syndrome. Since cocaine's rewarding effects are mediated by enhanced dopaminergic neurotransmission in the mesocorticolimbic system, it is possible that a long-acting dopamine agonist might block the withdrawal effects associated with the termination of a prolonged bout of cocaine self-administration. An animal model of post-cocaine anhedonia was developed using the elevation in intracranial self-stimulation (ICSS) thresholds following the termination of prolonged periods of cocaine self-administration as a measure of an animal's "anhedonic" state. In the present study, an attempt was made to reverse the postcocaine elevation in ICSS thresholds with acute administration of a dopaminergic agonist, bromocriptine. Rats were allowed to self-administer cocaine for 24 hours continuously. Four hours after the termination of the self-administration session, animals were injected with either vehicle or bromocriptine (1, 2, or 4 mg/kg, IP). Two hours later (6 hours post cocaine), the animals' self-stimulation thresholds were assessed. Confirming previous work, treatment with the vehicle following a cocaine "binge" resulted in elevated ICSS thresholds compared to predrug baseline levels or to control rats' thresholds. Bromocriptine, at doses that had no effect on ICSS thresholds in control rats, reversed the postcocaine anhedonia in a dose-related manner. These results indicate that bromocriptine-like drugs (pharmacological agents that enhance dopaminergic neurotransmission) may be able to ameliorate some of the effects of cocaine withdrawal on mood and motivational state. In addition, the results of the present study indicate that the proposed animal model of cocaine withdrawal could be useful in the discovery and development of new pharmacotherapies for cocaine withdrawal.

Analysis of Variance↗

PubMed1991

Effects of continuous naloxone administration on ventral tegmental self-stimulation.

Continuous subcutaneous administration of naloxone (3 mg/kg/h), shifted ventral tegmental self-stimulation rate-frequency curves to the right, without suppressing behavioral performance. In addition this chronic blockade of opioid receptors altered mu binding parameters in the hippocampus and olfactory tubercle of naloxone-treated animals. These findings speak to the role opioid peptides paly in the mediation of brain stimulation reward.

Animals↗

PubMed1985

Chronic naltrexone treatment increases the heroin-produced facilitation of self-stimulation.

The facilitatory effects of heroin HCl (0.25 mg/kg, SC) on self-stimulation (SS) of the lateral hypothalamus before and after chronic treatment of naltrexone (10 mg/kg, SC, for 20 days) or vehicle were compared. The group that received chronic naltrexone had a larger heroin-induced facilitation of SS than the group that received vehicle. These data suggest that the sensitivity to the facilitatory effect of heroin on SS may be related to the amount of opiate receptor binding which is increased following chronic antagonist treatment. However, neither acute nor chronic treatment with naltrexone produced any significant changes in SS thresholds, suggesting that the directly stimulated substrate for the rewarding effect of brain stimulation is unlikely to be endorphinergic but is apparently modulated by the endogenous opioid system.

Animals↗

PubMed1990

Stressor-like effects of FG-7142 on medial prefrontal cortex self-stimulation.

The effects of uncontrollable stress and the anxiogenic beta-carboline FG-7142 were compared on rats bar-pressing for electrical stimulation of the medial prefrontal cortex (MPC). One minute of restraint stress produced an immediate 20% increase in response rates. A significant facilitation was also evident 24 and 48 h later. Similarly, FG-7142 (10 mg/kg) produced an immediate 20% elevation of self-stimulation rates and a significant facilitation 24 and 48 h following administration. Lower (3 mg/kg) and higher (20 mg/kg) doses of FG-7142 caused immediate decreases in MPC self-stimulation and no significant long-term effects. These results agree with previous findings that FG-7142, administered at certain doses, may mimic the effects of exposure to uncontrollable stress.

Animals↗

PubMed1977

Morphine and shuttle-box self-stimulation in the rat: a model for euphoria.

In a shuttle-box self-stimulation paradigm, analgesic doses of morphine increase the amount of time a rat leaves rewarding brain stimulation on, without altering average OFF times. This paradigm may serve as a model for the euphoria induced by narcotic drugs and as a useful tool for evaluating the reinforcing effects of drugs.

Animals↗

PubMed1982

Saccharin preferences in prepubertal male and female rats: relationship to self-stimulation.

Saccharin preferences were studied in 48 male and female prepubertal rats (22-23 days old at the beginning of the experiment) of four genetic lines (LC1-low, LC1-high, LC2-low, and LC2-high) which differed in their inherent tendencies to self-stimulate. Sodium saccharin solutions of 0.1, 0.3, 0.5, 1, 3, 10, and 30 mM concentrations were used against water in two-bottle tests. It was found that (a) prepubertal rats prefer saccharin solutions to water, with the range of favored concentrations similar to that of adults; (b) male and female prepubertal rats do not differ as to saccharin preferences; (c) within the LC2 population, animals of the genetically high self-stimulating line prefer saccharin more than do their LC2-low counterparts; no such differentiation of the LC1 high and low lines was observed.

Animals↗

PubMed1999

[Therapeutic intervention in infantile autism and generalized developmental disorders: self-injury and self-stimulation].

INTRODUCTION: In this article we present a review of the aetiology and treatment of self-injury and self-stimulation in infantile autism and in generalized development disorders. We summarize 20 years of study and investigation in the treatment of these serious behaviour disorders, in a pioneer institution in Spain: the centre for rehabilitation 'El Cau' in Castellon. DEVELOPMENT: We describe the most frequent behaviour disorders, with particular reference to self-injury and self-stimulatory behaviour. Models explaining the aetiology and treatment are described in a brief general review of the subject, and we consider explicative models which integrate different treatments (in family and institutional contexts) by means of family therapy, psychoeducational models and social support networks.

Autistic Disorder↗

PubMed1997

Intracranial self-stimulation in rats: sensitization to an opioid antagonist following acute or chronic treatment with mu opioid agonists.

Acute mu opioid agonist pretreatment (4 hr) dose-dependently sensitizes rats responding for food reinforcement to the rate-decreasing effects of naltrexone (NTX). In the present study, adult rats were trained to respond in an intracranial self-stimulation autotitration procedure in which responding resulted in electrical stimulation of the medial forebrain bundle that decreased in frequency until reset to the initial value. In an acute sensitization experiment, pretreatment (4 hr) doses of 3.0 and 10 mg/kg morphine reduced the ED25 value for the intracranial self-stimulation rate-decreasing effect of NTX from 28.2 mg/kg to 0.29 and 0.02 mg/kg, respectively. All mu-selective opioid agonists tested, fentanyl > levorphanol > methadone > morphine > meperidine (listed in order of decreasing potency), produced similar large increases in sensitivity to NTX. Acute sensitization was not induced by the kappa-selective opioid agonist spiradoline, the dextrorotary enantiomer of levorphanol, dextrorphan, or the nonopioid drugs d-amphetamine and pentobarbital. Pretreatment with morphine for 10 days by continuous subcutaneous infusion (15 mg/kg/day) reduced the ED25 value of NTX from 28.2 to 0.002 +/- 1.48 mg/kg. The correlation of decreases in ED25 values for the rate-decreasing effect of NTX after both acute and chronic morphine administration is consistent with the theory that acute agonist-induced sensitization reflects receptor-mediated changes occurring early in the development of physical dependence.

Animals↗

PubMed1992

Apomorphine and electrical self-stimulation of rat brain.

The participation of dopamine neurons in reward produced by electrical stimulation of the brain was examined by measuring self-stimulation thresholds after injections of apomorphine, a direct agonist of dopamine receptors. Rats were trained to press a lever to obtain 0.3-s trains of electrical stimulation applied to lateral hypothalamic electrodes in a paradigm where the pulse frequency was decreased every eight stimulations by approximately 20%. The pulse frequency interpolated at 50% of maximum rate was taken as threshold. In a completely within-subject design, five doses of apomorphine from 0.01 to 1.00 mg/kg and the ascorbic acid vehicle were injected in a random order and thresholds were tracked at intervals of 5 min for 2 h postinjection. Low doses from 0.01 to 0.10 mg/kg caused thresholds to increase while the two higher doses, 0.30 and 1.00 mg/kg, caused thresholds to drop; the switch in the direction of the behavioural effect is thought to parallel the shift in apomorphine's action from presynaptic to predominantly postsynaptic activation of dopamine receptors as the concentration of apomorphine increases.

Animals↗