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At least 163 records · Page 9Linked to original sources

PubMed1975

Effects of intraventricular 6-hydroxydopamine and replacement therapy with norepinephrine, dopamine, and serotonin on self-stimulation in diencephalic and mesencephalic regions in the rat.

Although 6-hydroxydopamine (6-OHDA) reduced the rate of hypothalamic self-stimulation, it is not known whether the same effect is produced at other reinforcing sites remote from the hypothalamus. This was investigated in rats implanted with rewarding probes in the hypothalamus, in the substantia nigra, in the midbrain, and in the pontine region. Two patterns of self-stimulation emerged in each subject. One, characterized by short, medium and long-stimulus-train durations, was seen in the hypothalamus, in the substantia nigra, and in selected sites in the pons. The other, which comprised only short stimulus-trains, was found in the medial midbrain and in the pontine region. 6-OHDA (250 mug intraventricular route) reduced the rate of responding in the regions where responding was for short, medium, and long stimulus trains. It has a minor effect on responding in regions where the brain rewards were exclusively of short duration. Thus, self-stimulation in the hypothalamus, in the substantia nigra and in the pons was suppressed after 6-OHDA, while self-stimulation in the medial midbrain and at sites in the pons, where selection was for short trains, was only slightly below control levels after 6-OHDA. L-Norepinephrine (L-NE) (10, 20 and 30 mug) injected into the lateral ventricle of the 6-OHDA-treated rats temporarily reinstated self-stimulation in the lateral hypothalamus but not in the substantia nigra and not in the pontine region where the pattern of selection had been for long brain rewards. Dopamine (DA) was not effective as an antagonist of the suppressant action of 6-OHDA. Serotonin (5-HT) reinstated self-stimulation behavior in the lateral hypothalamus but not in the other positive regions. Its action was less than that of NE and did not take place in all animals tested.

Animals↗

PubMed1976

Non-selective enhancement of locus coeruleus and substantia nigra self-stimulation after termination of chronic dopaminergic receptor blockade with pimozide in rats.

Self-stimulation of substantia nigra and locus coeruleus were assessed before and after an 8-day regimen in which pimozide was given twice daily at a dose of 0.5 mg/kg (first 4 days) or 1.0 mg/kg (last 4 days). At 48 hours after termination of pimozide treatment self-stimulation was increased to 25% above pre-pimozide baseline levels: this was true for both self-stimulation sites. Rates remained high the following day but returned to normal by the third day of post-pimozide-testing. These data are interpreted as reflecting pimozide-induced supersensitivity in a dopamenergic substrate. This substrate appears to be critical for intracranial self-stimulation even when its fibers are not themselves activated at the tip of the stimulating electrode.

Animals↗

PubMed1983

Reversal of haloperidol induced deficits in self-stimulation by anti-Parkinsonian drugs.

The effects of 0.1 mg/kg dose of haloperidol on self-stimulation were assessed in rats having 3 stable self-stimulation response rates of approximately 10, 50 and 100 responses per min generated by 3 levels of current intensity. Haloperidol reduced overall response rates at all current intensities and generated extinction-like response patterns. Concurrent anti-Parkinsonian (benztropine 4.0 mg/kg or diphenhydramine 4.0 mg/kg) eliminated the within session extinction performance pattern and at the highest current intensity benztropine restored self-stimulation to a non-drug performance level. These results suggested that haloperidol induced impairments in self-stimulation are secondary to a motoric rather than reinforcement dysfunction.

Animals↗

PubMed1976

The effects of ethanol upon threshold and response rate for self-stimulation.

The hypothesis that ethanol would reduce the threshold for self-stimulation of the medial forebrain bundle was not supported. Ten rats, implanted with electrodes in the lateral hypothalamus, were shaped to bar press for electrical brain stimulation. The effects of 0.6, 0.9, and 1.2 g/kg ethanol injections upon threshold and response rate for self-stimulation were measured. The lowest dose had no effect upon self-stimulation threshold while 0.9 and 1.2 g/kg ethanol raised thresholds. Rate of bar pressing was increased by 0.6 g/kg ethanol but was not affected by higher doses. Results were discussed in terms of a postulated dual effect of ethanol upon a brain arousal system and upon a reward system.

Animals↗

PubMed1985

Site of rewarding action of morphine in the mesolimbic system determined by intracranial electrical self-stimulation.

Systemic treatment with morphine has been shown to facilitate intracranial electrical self-stimulation reward elicited from the ventral tegmental area (VTA) as was determined using a response rate-insensitive threshold measurement. In the present experiment graded doses of morphine were microinjected into the mesolimbic system to determine the site of this morphine action. Morphine injected into the nucleus accumbens did not affect the threshold and response rate of self-stimulation by electrodes in the VTA, while relatively high doses of morphine injected into the VTA produced a long-lasting decrease of the threshold of self-stimulation by electrodes in the nucleus accumbens. It is concluded that morphine can facilitate self-stimulation when injected into the VTA, and that a concerted action of morphine on multiple brain sites may be involved in the interaction of the drug with brain reward.

Animals↗

PubMed1986

Changes in self-stimulation at stimulation-bound eating and drinking sites in the lateral hypothalamus during food or water deprivation, glucoprivation, and intracellular or extracellular dehydration.

These studies were designed to examine the effects of "hunger" induced by food deprivation, 2-deoxy-D-glucose (200 mg/kg), or insulin (2 U/kg) and "thirst" induced by water deprivation, sodium chloride (4 M), or polyethylene glycol (5 ml of 30% w/w) on lateral hypothalamic self-stimulation in 40 male Long-Evans rats. Changes in self-stimulation were evaluated at electrodes that produced stimulation-bound eating and/or drinking or neither behavior. Daily 30-min test sessions consisted of three 5-min periods of self-stimulation alternated with three 5-min periods when bar presses resulted in a 5-s time-out from experimenter-delivered stimulation (stimulation escape). Food deprivation significantly increased self-stimulation; insulin, 2-deoxy-D-glucose, and sodium chloride significantly suppressed self-stimulation; water deprivation mildly inhibited self-stimulation; and polyethylene glycol had no effect. This pattern of findings was noted at electrodes that did and those that did not elicit eating and/or drinking. These findings argue against the hypothesis that the magnitude of lateral hypothalamic self-stimulation is differentially and predictably controlled by specific drive mechanisms indexed by the consummatory behaviors also elicited by the stimulation.

Animals↗

PubMed1981

Inhibition of intracranial self-stimulation in brain stem-transected cats--a proposed mechanism of aversive effects produced by brain stimulation.

Effects of intracranial self-stimulation of central 'punishment areas' were studied on an operant conditioning of vertical eye movements in the midpontine pretrigeminal cats as well as in the encéphale isolé cats. In 36 pretrigeminal cats, the ventromedial hypothalamus (VMH), basal amygdaloid nuclei (AMY), dorsal central gray (CG) of the midbrain and the thalamic nuclei such as the ventralis posteromedialis (VPM) and ventralis posterolateralis (VPL) were tested. No suppression of eye movements indicating a passive avoidance conditioning from stimulation of these 'punishment areas' was obtained in 92 electrode tip sites. In 49 encéphale isolé cats, stimulation of the VPM associated with contraction of the facial muscles, demonstrated a marked passive avoidance effect on the eye movements. After blocking both the trigeminal (5N) and facial nerves (7N), VPM stimulation no longer produced an increase of facial EMG activity and the suppressive effect on eye movements was abolished. Extracranial blockade of 7N alone, which induced facial muscle paralysis also showed similar effects. Bilateral blockade of cranial nerves from acoustic (8N) to hypoglossal (12N) nerves had no significant effect on the avoidance conditioning. The mass neural activity recorded from the 5N showed a marked increase of discharge by VPM stimulation which was reduced significantly after 7N blockade. These results may suggest a possibility that punishing effects of brain stimulation depend on feedback from the periphery (muscles, blood vessels and visceral organs), whereas reward effects essentially depend on neural circuitry confined within the forebrain above the rostral pons.

Amygdala↗

PubMed1981

Presynaptic alpha-adrenergic mediation of self-stimulation in locus coeruleus in rats treated neonatally with 6-hydroxydopamine.

Rats self-stimulating in the region of the locus coeruleus and treated neonatally with 6-hydroxydopamine (6-OHDA) injected bilaterally in the same region were tested for effects of adrenergic receptor blockers on a lever-pressing behavior to obtain the brain reward. The neonatally treated animals (16 microgram total dose, 8 microgram X 2) self-stimulated at abnormally high rates compared with controls. Yohimbine (5 mg/kg i.p.) and phentolamine (5 mg/kg) suppressed self-stimulation in controls and treated subjects. Phenoxybenzamine (10 mg/kg) reduced the response rate for the brain reward but did not abolish the behavior in the 6-OHDA-treated animals and had minor effects in controls. Propranolol (10 mg/kg) had no effects. The 6-OHDA subjects tested for the effects of D-amphetamine and L-amphetamine (0.5 mg/kg) showed facilitation of responding after the former but not after the latter. Self-stimulation in the 6-OHDA subjects was suppressed by treatment with alpha-methyl-p-tyrosine and pimozide. The significance of these findings is discussed in terms of the use of alpha-adrenoreceptor antagonists to separate the pre- from the post-synaptic action of released norepinephrine and in terms of the norepinephrine hypothesis of rewarding effects of brain stimulation in the dorsal pons.

Animals↗

PubMed1979

Effects of satiety on self-stimulation of the orbitofrontal cortex in the rhesus monkey.

Self-stimulation of the orbitofrontal cortex of the rhesus monkey was found to be attenuated after the monkeys were fed to satiety. Self-stimulation at some other sites (e.g. the nucleus accumbens septi, the region of the substantia nigra, and the caudate nucleus) was relatively unaffected in the same test sessions by the satiety. In recordings from single neurons in the monkey orbitofrontal cortex, neurons of the type found in the lateral hypothalamus with sustained responses associated with the sight of preferred foods were not found. However, some orbitofrontal neurons did respond to the removal of food or other desired objects. These experiments show that self-stimulation of the monkey orbitofrontal cortex in modulated by hunger, and show that some orbitofrontal neurons have complex responses which could be related to the control of feeding.

Animals↗

PubMed1997

Effects of microinjections of cholecystokinin and neurotensin into lateral hypothalamus and ventral mesencephalon on intracranial self-stimulation.

Changes in intracranial self-stimulation (ICSS) evoked from ventral tegmental area-substantia nigra (VTA-SN) and lateral hypothalamus-medial forebrain bundle (LH-MFB) before and after microinjections of sulfated cholecystokinin octapeptide (CCK-8S) and unsulfated cholecystokinin (CCK-8US), neurotensin tridecapeptide ([D-Tyr11]NT(1-13) or [DTrp11]NT(1-13)) into either VTA-SN or LH-MFB were assessed. The current intensity was fixed at a level to obtain 60-70% of the maximal asymptotic rate. CCK-8S (0.10 microg/0.5 microl and 0.25 microg/0.5 microl) into VTA-SN resulted in dose-dependent decreases in VTA-SN ICSS of 38-42% and 78-92%, respectively, without affecting the ICSS of LH-MFB. Similar doses of CCK-8S injected into LH-MFB changed neither LH-MFB ICSS nor VTA-SN ICSS. CCK-8Us injected into VTA-SN or LH-MFB had no effect on ICSS in either site. Intra-VTA-SN injections of the neurotensin-1 (NT1) receptor agonist [DTyr11]NT(1-13) and the NT1 receptor antagonist [D-Trp11]NT(1-13) at doses of 5 microg/0.5 microl and 10 microg/0.5 microl decreased VTA-SN ICSS. NT1 receptor agonist and antagonist injections did not alter LH-MFB ICSS in any significant manner. Similar injections of these peptides into LH-MFB did not change the responding rates for LH-MFB ICSS or VTA-SN ICSS. Increasing the current intensity reversed the inhibitory effect of CCK-8S and [D-Trp11]NT(1-13) on VTA-SN ICSS and restored basal preinjection rates of responding. These results suggest that CCK(A) and NT1 receptor mechanisms in the ventral tegmentum in association with dopamine neurotransmission may be important in mediating the rewarding effects of VTA-SN ICSS but not LH-MFB ICSS.

Animals↗

PubMed1981

Rewarding effects of hypothalamic self-stimulation altered by unilateral lesions of superior colliculus in rats.

The effects of unilateral lesions of the superior colliculus were determined on self-stimulation of the medial forebrain bundle. It was found that the lesions had different effects depending upon the precise location of the stimulating electrode: self-stimulation on far-laterally located electrodes was abolished while on more medially placed electrodes this behaviour was enhanced. These data are inconsistent with explanations of intracranial self-stimulation which treat it as a unitary phenomenon.

Animals↗

PubMedDate not supplied

[The effect of different activating influences on the self stimulation reaction].

A study was made of the influence on self-stimulation of non-painful sensory stimuli of different modalities, and of intra-brain stimulations of emotionally positive and neutral points with the wiew to elucidate the specificity of certain functional relations appearing during interaction between emotionally negative and positive conditions. The data obtained attest that the influence of various excitation sites on self-stimulation reactions depends not so much on the strength of the stimuli, as on the specific neurophysiological organization of emotionally negative zones in the brain. A reciprocal enhancement of excitation of self-stimulation zones points to a certain non-specificity of positively reinforced structures.

Acoustic Stimulation↗

PubMed1975

Intracranial self-stimulation effects along the route of the nigro-striatal bundle.

Recent evidence suggesting a possible dopaminergic nigro-striatal substrate of self-stimulation led us to map this route for both self-stimulation and stimulus-bound motor effects. The results of 128 electrode placements show that the route of the nigro-striatal projection supports strong self-stimulation effects from the substantia nigra to the ento-peduncular nucleus. Beyond this level, such effects disappear. Our results indicate that the striatum itself is neutral with regard to reinforcement, and suggest that such apparent neutrality cannot be ascribed to motor or other artifacts. These findings require a reappraisal of the hypothesis of a dopaminergic self-stimulation system, although they are not in conflict with the idea that dopaminergic manipulations may affect self-stimulation through some more general regulatory influence on operant responding.

Animals↗

PubMedDate not supplied

[The effect of the NMDA-receptor antagonist (+/-)-CPP on the conditioned-reflex activation of an operant reaction in the brain electrical self-stimulation test in rats].

Self-stimulation behaviour was studied in rats with implanted bipolar electrodes in ventral tegmental area (VTA) and guide cannulae in nuclei accumbens septi (NAC). Conditioned activation of the operant response was induced by the stimuli associated with rewarding electrical stimulation of VTA, i.e., light or subthreshold stimulation. Bilateral administration of NMDA receptor antagonist ( +/- )-CPP (2.5 mcg in each cannula) significantly attenuated the facilitating effect of the conditioned stimuli. These data provide evidence for the role of glutamatergic transmission in NAC in realization of responses with conditioned reinforcement.

Animals↗

PubMed1979

Self-stimulation of the nucleus accumbens and ventral tegmental area of Tsai attenuated by microinjections of spiroperidol into the nucleus accumbens.

The contribution of dopaminergic neurons to self-stimulation of the ventral tegmental area, nucleus accumbens and prefrontal cortex was investigated. The ventral tegmental area is the site of non-striatal dopaminergic neurons and their axons project to the nucleus accumbens and prefrontal cortex. Injections of spiroperidol, a dopamine antagonist, into the nucleus accumbens significantly reduced self-stimulation of the ipsilateral ventral tegmental area but did not influence self-stimulation of the contralateral ventral tegmental area. Injections of spiroperidol into the prefrontal cortex did not reduce self-stimulation of the ipsilateral or contralateral ventral tegmental area. Electrical stimulation of sites in the nucleus accumbens positive for self-stimulation antidromically activated neurons of the ventral tegmental area, and a reduction of discharge of these neurons following administration of apomorphine suggested that they were dopaminergic neurons. These observations provide additional evidence implicating dopaminergic neurons in brain-stimulation reward and suggest that dopaminergic neurons contribute to self-stimulation of the nucleus accumbens but not the prefrontal cortex.

Animals↗

PubMed1977

Effect of substance P on medial forebrain bundle self-stimulation in rats following intracerebral administration.

The effect of Substance P infused intracerebrally via chronically implanted electrode-cannulae on self-stimulation induced from the same site was studied in rats. Substance P caused a significant depression of self-stimulation at 60 and 120 microgram/rat. Morphine infused into this site also caused significant depression of self-stimulation, but the doses were considerably lower than those of Substance P (5 and 10 microgram/rat). Pretreatment with naloxone, a narcotic antagonist, significantly antagonized the effects of Substance P on self-stimulation. It is proposed that Substance P modulates self-stimulation by the release of an endogenous morphine-like substance, but the possibility of a direct effect of Substance P was not ruled out.

Animals↗

PubMed1989

Opiate antagonists and self-stimulation: extinction-like response patterns suggest selective reward deficit.

The present study investigated the response decrement patterns produced by opiate antagonists on intracranial self-stimulation behavior, in order to determine if these drugs affect the reinforcement value of the stimulation or interfere with the ability of the animal to respond. Male rats lever-pressed in 60-min sessions on a continuous reinforcement schedule for self-stimulation of the nucleus accumbens. Naloxone (2.0 and 20 mg/kg) and naltrexone (2.0 and 20 mg/kg) suppressed self-stimulation only after a significant delay, in an extinction-like response decrement pattern, mimicking the effects of reductions in current intensity (75% and 50% of baseline). The increasing behavioral effects characteristic of the extinction pattern were observed despite the fact that testing began after the time point at which maximal suppression of self-stimulation occurs with these drugs, and when brain concentrations of these drugs were declining. Since normal responding was observed for several minutes after the beginning of the session, the results may explain why long sessions are necessary to observe suppression of self-stimulation by opiate antagonists. The extinction-like pattern produced by these drugs suggests that opiate antagonists suppress self-stimulation by reducing the reinforcement value of the stimulation, rather than by interfering with the ability of the animal to respond. These findings are consistent with a role for endogenous opioid peptides in brain stimulation reward.

Animals↗

PubMed1980

[Effects of procaine and apomorphine injected into the ventral tegmental area on self-stimulation of the nucleus accubens (author's transl)].

In the present study, microinjection of procaine and apomorphine were made into the ventral tegmental area (VTA) during self-stimulation of the nucleus accumbens (NAS). By blocking the VTA input to NAS with procaine, it should be possible to influence self-stimulation of the NAS. In addition, since it has been suggested that dendrites of VTA dopaminergic neurons contain dopamine "autoreceptors", the effect of microjections of apomorphine a dopamine agonist, into the VTA on self-stimulation of the nucleus accumbens was also investigated. Reseult obtained were as follow: The injection of procaine to VTA reduced self-stimulation of the ipsilateral NAS and the administration of apomorphine to the VTA significantly attenuated self-stimulation of the ipsilateral NAS completely suppressing it for 3--4 min. Self-stimulation of NAS has been suggested to activate fiber projection of mesolimbic dopamineric neurons (A10) from VTA.

Animals↗