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PubMedDate not supplied

[Effect of peptides introduced into the central nucleus of amygdala on the hypothalamic self-stimulation in chronically alcoholized rats].

The reinforcing properties of neuropeptides (substance P, corticoliberin, leu-enkephalin, alaptide) and 70 kDa heat shock protein (HSP) administered into the extended amygdala were studied on the hypothalamic self-stimulation model in rats reared in community or social isolation since the 17th day after birth. Since that time (17th day) half of rats were given 5 - 15 % ethanol solution instead of water (semiforced alcoholization). In the age of 90 - 100 days, all rats were implanted electrodes into lateral hypothalamus and cannulas into the central nucleus of amygdala. In the group of alcohol-dependent rats, the alcohol administration was continued. In rats reared in community, corticoliberin, leu-enkephalin and substance P increased the reinforcing properties of self-stimulation in dose-dependent manner, but alaptide and HSP decreased self-stimulation moderately. In rats reared in social isolation, the vector of neuropeptide effects was retained, although the magnitude of the effects was lower. Therefore, the neuropeptides differently participate in the reinforcing mechanisms of hypothalamus. It is suggested that the extended amygdala modulates the reinforcing properties of lateral hypothalamus, probably by means of extrahypothalamic corticoliberin-containing neurons.

Alcoholism↗
PubMed1993

Differential effects of ondansetron, haloperidol and clozapine on electrical self-stimulation of the ventral tegmental area.

The effects of 5-HT(3), receptor blockade with ondansetron (0.025-0.2mg/kg) on intracranial self-stimulation of the ventral tegmental area were compared with effects of the typical antipsychotic drug haloperidol (0.01-0.3mg/kg) and the atypical antipsychotic drug clozapine (1.25-10mg/kg). Rats were trained to self-stimulate using unipolar ventral tegmental electrodes (200µm diameter) to deliver 1s trains of 0.2ms cathodal pulses of constant current stimulation as a reinforcer. The animals were tested daily in frequency threshold tests. The frequency that maintained half maximal response rates (M50) and the maximal number of responses at a single frequency (RMAX) and the number of responses per session (TRESP) were used to measure drug effects. Ondansetron had no effects on the behavioural measures in this study. Haloperidol induced a significant increase in M50 at 0.3mg/kg without altering RMAX; TRESP was reduced by 0.1 and 0.3mg/kg of this drug. Clozapine increased M50 at 5.0mg/kg; following 10.0mg/kg of clozapine responding was completely abolished and no M50 measure could be calculated. Clozapine reduced RMAX at 1.25, 5.0 and 10.0mg/kg; TRESP was decreased by 5.0 and 10.0mg/kg of clozapine. The present results indicate that ondansetron had no measurable effects under conditions in which haloperidol and clozapine increase reinforcement thresholds and decrease response rates maintained by ventral tegmental self-stimulation.

Journal Article↗
PubMed1989

Diazepam modulates lateral hypothalamic self-stimulation but not stimulation-escape in rats.

Rats electrically stimulated via chronically implanted lateral hypothalamic (LH) electrodes were assessed with and without diazepam (DZ), for thresholds of stimulation-bound feeding (SBF) and for barpressing rates to administer and to escape from the same current, Six pure-reward rats, who self-stimulated but did not escape LH stimulation, exhibited SBF. Their electrode tips lay in medical forebrain bundle (MFB) and zona inserta along the entire rostral-caudal extent of the ventromedial nucleus of the hypothalamus (VMH). Six reward-escape rats, who self-stimulated and escaped from LH stimulation, did not (with one histologically deviant exception) show SBF. Reward-escape electrode tips were anterior to all the pure-reward placements. They lay in MFB rostral to the VMH up to the level of the bed nucleus of the stria terminalis (with the deviant electrode tip located on the zona inserta/ventral thalamic border). After i.p. injections of DZ, self-stimulation (SS) rates increased for both groups of animals and SBF thresholds decreased. Stimulation-escape (SE) rates, however, remained unchanged by the drug. The results are consistent with the existence of dual substrates: a DZ-sensitive reward system, present in both groups of animals, and a simultaneously stimulated, drug-resistant aversion system which is powerfully engaged in reward-escape animals only.

Animals↗
PubMed1982

Effects of kainic acid lesions of the striatum on self-stimulation in the substantia nigra and ventral tegmental area.

Unilateral kainic acid lesions of the dorsal striatum provided evidence for a dissociation of neural substrates of brain-stimulation reward at sites in the ventral tegmental area and substantia nigra. The lesions caused a significant increase in current intensity thresholds at substantia nigra placements, whereas similar lesions had no effect on self-stimulation thresholds at sites in the ventral tegmentum. In addition, the rate-increasing effects of D-amphetamine (0.1-1.0 mg/kg) on self-stimulation were determined before and after lesions to the dorsal striatum. No significant changes in dose-response curves were observed at either loci. Amphetamine-induced rotation was used to confirm damage to the dorsal striatum and lesioned animals were observed to rotate towards the side of the lesion. In contrast, sham-lesioned animals showed turning away from the side stimulated electrically in previous tests. The results of the self-stimulation and rotation experiments are discussed in the context of neural substrates of reward and motor activity.

Animals↗
PubMed1986

Opioid-receptor blockade reduces nose-poke self-stimulation derived from medial entorhinal cortex.

Rats were trained to nose-poke for intracranial self-stimulation (SS) with electrodes unilaterally implanted in the medial entorhinal cortex. The acute effects of naloxone (NX; 0.1-10 mg/kg, IP) on a continuous reinforcement schedule were determined. Reductions in the self-stimulation rates occurred only at moderate doses (median of individual changes = -36% at 1 and 5 mg/kg), whereas the high dose (10 mg/kg) was ineffective. None of the doses influenced operant behavior. These results are consistent with the hypothesis that endogenous opioid-opiate receptor mechanisms play a modulatory role in SS reward. Considering that NX was administered systemically the action of the drug on reinforcement levels may be mediated by a site distinct from the locus of stimulation.

Animals↗
PubMed1977

Brain self-stimulation: direct evidence for the involvement of dopamine in the prefrontal cortex.

Rats were trained to self-stimulate the medial prefrontal cortex, a region rich in dopaminergic terminals. After the region adjacent to the electrode site was labeled with [14C]dopamine, it was perfused repeatedly by means of push-pull cannulas. Electrical stimulation of this cortical area in six animals enhanced the release of dopamine and its associated metabolites in nine of 16 experiments. Thus in vivo evidence is provided that dopamine is involved in the brain self-stimulation mechanism within the frontal cortex.

Animals↗
PubMed1971

Effect of 6-hydroxydopamine on electrical self stimulation of the brain.

In rats, after a single intracisternal injection of 6-hydroxydopamine (6-OHDA) electrical self stimulation was reduced by approximately 50%. The concentrations of noradrenaline and dopamine in the brain were reduced by 83%. A second injection of 6-OHDA reduced the concentration of these amines to 7% of control values and virtually eliminated self stimulation.

Animals↗
PubMed1997

Cholinergic and GABAergic modulation of self-stimulation of lateral hypothalamus and ventral tegmentum: effects of carbachol, atropine, bicuculline, and picrotoxin.

This study aimed at investigating the effects of modulators of acetylcholine-muscarinic (ACh-M) and GABAA.B-receptors in the lateral hypothalamus and ventral tegmentum on the electrical self-stimulation evoked from these regions. In each Wistar rat, a bipolar electrode and an ipsilateral insulated cannula-cum-electrode were implanted chronically in the right hemisphere. There were two placement combinations: 1. Bipolar electrode in lateral hypothalamus-medial forebrain bundle (LH-MFB) and cannulacum-electrode in ventral tegmental area-substantia nigra (VTA-SN) or 2, bipolar electrode in VTA-SN and cannula-cum-electrode in LH-MFB. The stimulation parameters were kept at a level to obtain 50% of the maximum possible asymptotic intracranial self-stimulation (ICSS) rates (M50) from each site. Carbachol injected into VTA-SN increased the ICSS responding rate of VTA-SN as well as, indirectly, that of LH-MFB, and atropine injections had an opposite effect. Similar injections of these ligands into LH-MFB again had facilitatory and inhibitory effects on its ICSS: however, there was no indirect effect on the ICSS of VTA-SN. Bicuculline injection into VTA-SN had no effect on either its ICSS or that of LH-MFB. On the other hand, bicuculline injected into LH-MFB decreased its ICSS and, indirectly, the ICSS of VTA-SN in a dose-dependent manner. In contrast, intra VTA-SN injections of picrotoxin decreased its ICSS and, indirectly, ICSS of LH-MFB. Similar injections into LH-MFB had no effect on the ICSS of VTA-SN. The results suggest that ICSS of VTA-SN is Ach-M receptor mediated and, also, this mediation influences the ICSS of LH-MFB. On the contrary, changes in ICSS of LH-MFB following Ach-M receptor ligands do not influence the ICSS of VTA-SN. The direct effects of GABA-receptor antagonists have shown disassociation because ICSS of LH-MFB was more sensitive to bicuculline, whereas the ICSS of VTA-SN was more sensitive to picrotoxin. Thus, the cholinergic and GABAergic mechanisms of the self-stimulation of lateral hypothalamus and ventral tegmentum are different.

Animals↗
PubMed1984

Contraction stress testing with mammary self-stimulation.

One hundred fifty-six women with high-risk pregnancies performed mammary self-stimulation 256 times in an attempt to induce uterine contractions that would meet contraction-stress-test criteria. One hundred forty-nine, or 57%, of the attempts resulted in contractions of adequate duration and frequency to satisfy those criteria. Patient acceptance of the procedure was very high; only one patient refused to participate. Performing a contraction stress test through mammary self-stimulation was found to shorten the time that successful patients stayed in the testing area and eliminated the need for an intravenous oxytocin challenge test.

Adolescent↗
PubMedDate not supplied

[Effect of self-stimulation of the septum pellucidum on disrupted delayed reactions in cats].

The effect of self-stimulation of the septum on impaired delayed reactions was studied on cats in a state of neurotization. Reduction of intervals between tests from 3-5 min to 30-40 s produced a complex of motor and vegetative reactions testifying to augmentation of emotional stress. This was followed by disturbance of short-term memory of complex perception of the location of food. Self-stimulation of the septum by animals in a state of experimental neurosis caused considerable improvement and then recovery of the maximum of delayed reactions This testifies to the important role of the septum in regulation of the level of emotional stress, and hence, a normal course of higher brain functions.

Animals↗
PubMed1985

Long-term desipramine treatment attenuates clonidine-induced suppression of ventral tegmental self-stimulation.

Long-term administration of the tricyclic antidepressant desipramine did not change the rate of self-stimulation responding in the A10 (ventral tegmental) area but significantly attenuated the suppressive effect of the selective alpha 2-adrenergic agonist clonidine on this behavior. These findings demonstrate an involvement of noradrenergic mechanisms in the regulation of ventral tegmental self-stimulation and further suggest that adaptive changes in inhibitory presynaptic noradrenergic receptors may be involved in desipramine's antidepressant effects.

Animals↗
PubMed1976

Effect of lithium and other alkali metals on brain chemistry and behavior. II. Intracranial self-stimulation behavior.

Rats implanted with bipolar electrodes aimed at the medial forebrain bundle (MFB) were trained to self-stimulate. Six daily injections of 2 mEq/kg of the chloride salts of Li+, Rb+ or Cs+ were administered and the rate of intracranial self-stimulation (ICSS) was recorded. Lithium caused a reversible decrease in ICSS rate, beginning on the second day and returning to pretreatment rate on the fourth day of injections. The decrease was more pronounced in animals with high baseline rate (over 500 responses/10 min) than in low responders. Rubidium enhanced ICSS rate whereas cesium had no effect. These results agree with other accumulating data showing the opposite effects of Li+ and Rb+, but their relevance to effective disorders is not clear.

Affective Symptoms↗
PubMed1986

The role of intrinsic neurons in lateral hypothalamic self-stimulation.

In this brief review, we summarize some of our recent work concerning the effect of a specific lesion of the intrinsic neurons located in the middle part of the lateral hypothalamus on electrical self-stimulation of this structure by electrodes implanted along the medial forebrain bundle. In a first experiment the neurons of the lateral hypothalamus were destroyed unilaterally by local injection of ibotenic acid (4 micrograms in 0.5 microliter). The contralateral side served as the sham-lesion control. Between 10 and 20 days later, electrodes were bilaterally implanted, one in the lesioned area, the other in the contralateral hypothalamus. Intracranial self-stimulation (ICSS) was obtained separately for each electrode, at various current intensities, using a nose-poke response. ICSS from electrodes implanted in the lesioned area was decreased in all cases, whereas ICSS of the sham-lesioned side was normal. In a second experiment, two groups of rats lesioned and implanted as above, received two additional electrodes either in the anterior hypothalamus or in the posterior hypothalamus. In rats with electrodes in the anterior hypothalamus, the lesion produced a large deficit in self-stimulation when stimulation was applied to the anterior electrode ipsilateral to the lesion. Only 3 of 6 rats showed a decrease in ICSS with stimulation of the posterior hypothalamic electrode ipsilateral to the lesion. These results suggest that ICSS in the anterior part of the medial forebrain bundle is sustained by long fibers originating in the middle part of the lateral hypothalamus, while ICSS in the posterior part of the lateral hypothalamus may not depend on the neurons located in the lesioned area.

Animals↗
PubMed1990

Effect of intracerebroventricular and systemic injections of caerulein, a CCK analogue, on electrical self-stimulation and its interaction with the CCKA receptor antagonist, L-364,718 (MK-329).

Systemic administration of caerulein (10-100 micrograms/kg SC), a potent analogue of cholecystokinin, caused a profound dose-related depression of variable-interval self-stimulation, followed by progressive recovery within 60 min. Intracerebroventricular injection of caerulein (3-1000 ng) was not more effective than systemic injection, while injections into the nucleus accumbens (3-100 ng bilaterally) were without detectable effect. Systemic injections of L-364,718 (70-700 micrograms/kg IP), a specific competitive antagonist of CCKA ("peripheral-type") receptors, had no effect on self-stimulation when given alone. When given in combination with caerulein, L-364,718 (200 micrograms/kg IP) significantly reduced the inhibitory effect of caerulein (30 micrograms/kg SC); however, this dose, and higher doses of L-364,718, failed to confer complete protection. It is concluded that self-stimulation performance may be subject to modulation by CCK receptors distributed predominantly in the peripheral nervous system and that some but not all of these receptors are CCKA receptors.

Animals↗
PubMed1983

Nigral transplants reinnervating the dopamine-depleted neostriatum can sustain intracranial self-stimulation.

Transplants of embryonic substantia nigra reinnervated the striatum and were able to sustain intracranial self-stimulation in rats with brain lesions induced by 6-hydroxydopamine. Dopaminergic drugs and alterations in current intensity produced typical changes in response rates. Animals with electrodes implanted into cortical grafts or into the denervated striatum failed to exhibit self-stimulation. These findings suggest that transplanted dopamine neurons convey specific, temporally organized information axonally to the striatum.

Animals↗
PubMed1992

Comparison of mu opioid receptors in brains of rats bred for high or low rate of self-stimulation.

Opiates and endogenous opioid peptides play an important role in reward-mediated behaviors, including self-stimulation. Two strains of rats, LC2-Hi and LC2-Lo, selectively bred for high vs. low rate of lateral hypothalamic self-stimulation, were employed in the present study. Quantitative autoradiography was performed on brains of adult male rats of each strain, using the mu opioid receptor agonist 3H-DAGO. Strain differences in receptor density were observed in the nucleus accumbens and in ventral areas of the hippocampus.

Animals↗
PubMed1987

Reward saturation in medial forebrain bundle self-stimulation.

A rate-frequency curve in self-stimulation experiments plots the response rate as a function of the frequency of stimulation pulses, yielding a steeply rising, roughly sigmoidal curve. Altering stimulation reward efficacy results in lateral shifts of this curve, while altering the operant performance capacity of the rat results in primarily vertical shifts. One hypothesis explaining the lateral stability of the curve in the face of performance-altering manipulations is that the stimulation reward effect saturates at the frequency where the curve asymptotes. In the first experiment we determined the frequency of rate-frequency curve asymptote in two paradigms, runway and lever-pressing, and compared it to the reward saturation frequency determined in a discrete choice procedure. Results indicate that reward often saturates at frequencies above the rate-frequency asymptote point, which does not support the above hypothesis; levelling-off of the rate-frequency function is most likely a result of performance ceiling factors. In a second experiment, increases in stimulation current reduced the saturation frequency, indicating that saturation is not determined by an upper limit on the signal carrying capacity of the directly excited axons.

Action Potentials↗