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Results for “SELF STIMULATION”

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PubMed1980

[Interrelationship between the lateral hypothalamic self-stimulation reaction and the periodic motor activity of the stomach].

In 26 dogs, self-stimulation of the dorsal portion of the lateral hypothalamus at the level of anterior parts of ventromedial nuclei inhibits completely the stomach motor activity. Self-stimulation of the lateral portion of the middle hypothalamus at the level of posterior parts of ventro--medial nuclei does not affect at all the periodic contractions of the stomach. The intensity of self-stimulation depends on phase of the stomach periodic activity: during the contractions the number of lever-pressings is by 20% higher on the average than at resting. Bilateral supra-diaphragmal vagotomy increases the self-stimulation threshold in some animals and increases the number of lever--pressings in other animals at unaltered threshold.

Animals↗

PubMed1988

Electrical self-stimulation in the medial and lateral septum as compared to the lateral hypothalamus: differential intervention of reward and learning processes?

The characteristics of the electrical self-stimulation behavior elicited from the lateral hypothalamus (LH) and from both medial (MS) and lateral (LS) parts of the septal nucleus have been compared in male mice of the BALB/c strain. Using two different experimental situations (the lever-press box and a spatial discrimination test in a Y-maze) the self-stimulation rate-current intensity relations and the performances during both acquisition and reversal of a spatial discrimination were tested successively. In the lever-press box, it was observed that highest self-stimulation rates were obtained from LH placements while both MS and LS rates were lower. However, MS animals showed higher self-stimulation rates and lower self-stimulation thresholds than LS animals. Acquisition of the spatial discrimination in the Y-maze was achieved by all 3 groups with similar time courses. However, when tested for the reversal of the discrimination, the LS implanted mice were much more perturbed than the two other groups and exhibited marked perseveration. The incidence of convulsive episodes was more frequent in LS mice than in either MS or LH implanted animals during both phases of the discrimination task. These differences in the self-stimulation behavior elicited from medial and lateral parts of the septal complex are discussed in relation to the operation of positive reinforcement mechanisms and to internal inhibition processes operating during acquisition and reversal of the spatial discrimination.

Animals↗

PubMedDate not supplied

An electrophysiological and behavioural study of self-stimulation in the orbitofrontal cortex of the rhesus monkey.

It was found that neurons in the posterior orbitofrontal cortex, area 13, of the rhesus monkey were activated from self-stimulation electrodes (in 142 of 168 possible instances), and that neurons in the anterior orbitofrontal areas were much less likely to be activated from the self-stimulation electrodes (in only 28 of 177 possible instances). This activation of neurons in the posterior orbitofrontal cortex was found mainly from self-stimulation sites in the nucleus accumbens septi, lateral hypothalamus, and the orbitofrontal cortex itself. In a second investigation the orbitofrontal cortex was mapped for self-stimulation, and it was found that self-stimulation occurred in the posterior orbitofrontal area. These results implicate the posterior or caudal orbitofrontal cortex, mainly area 13, but not the more anterior orbitofrontal areas, in self-stimulation.

Amygdala↗

PubMed1985

Differential effect of naloxone on food and self-stimulation rewarded acquisition of a behavioral response pattern.

The involvement of endogenous opioids in self-stimulation reward was investigated by repeated administration of the opioid antagonist naloxone to rats during acquisition of a behavioral response pattern that was rewarded with electrical (self-)stimulation of the ventral tegmental area. A control experiment was performed using food deprived rats in which a comparable response pattern was rewarded with food pellets. The response patterns consisted of gradually decreasing amounts of reward per response, which could be reset to maximal reward by another response. It was found that naloxone disrupted the acquisition of the stimulation rewarded response pattern, while it did not influence the food rewarded behavior. It is suggested that endorphin systems are actively involved in the acquisition of self-stimulation reward procedures, and that this involvement may be specific for self-stimulation reward.

Animals↗

PubMed1982

Comparative studies with linear and cyclic somatostatin on the self-stimulation of rats.

In the present study the dose-related effects of linear and cyclic somatostatin were compared on the self-stimulation rate of rats. Twenty micrograms of linear somatostatin administered intracerebroventricularly (icv.) markedly decreased the self-stimulation rate, while 5 micrograms and 10 micrograms was ineffective. Cyclic somatostatin in a dose of 1 microgram caused a transitory but not significant increase in the self-stimulation rate, which later returned to the control level. Five micrograms and 10 micrograms of the peptide decreased the self-stimulation rate. These results indicate that the cyclic somatostatin is more effective in inhibiting the self-stimulation rate than the linear one.

Animals↗

PubMed1999

Amelioration of fornix lesion induced learning deficits by self-stimulation rewarding experience.

Intracranial self-stimulation (ICSS) rewarding experience is known to modulate learning and memory and induce morphological and neurochemical changes in hippocampus. Therefore, we studied the effect of ICSS on the hippocampus-dependent operant and the spatial learning tasks in rats with bilateral electrolytic lesioning of fornix. Bilateral lesioning of fornix induced deficits in acquisition and performance of both the tasks, whereas exposure to 10 days of ICSS experience from ventral tegmental area reversed these behavioural deficits. Hence, we propose that the ICSS experience ameliorates the fornix lesion induced behavioural deficits, by inducing neuronal plasticity in the hippocampus which may act as a compensatory mechanism for the deficits produced by the lesioning of fornix.

Animals↗

PubMed1994

Changes in self-stimulation response during chronic morphine treatment and after withdrawal of morphine in rats.

Morphine (5-20 mg/kg, s.c.) dose-dependently inhibited the hypothalamic self-stimulation response 1-2 hr after administration of the drug. Thereafter, slight increase in the self-stimulation response was seen 4-8 hr after drug administration. The depressant effect induced by 10 mg/kg, s.c. of morphine on the self-stimulation response was antagonized by 1 mg/kg, s.c. of levallorphan. Repeated administration of morphine (10 mg/kg, s.c.) resulted in an increase of the self-stimulation response. The self-stimulation response rate was increased significantly 24 and 48 hr after withdrawal of morphine in chronic-morphine-treated rats; In these rats, the initial dose of morphine (10 mg/kg, injected s.c. twice daily 7 days a week) was increased gradually until at the end of 5 weeks, each dose was 50 mg/kg, s.c.

Animals↗

PubMedDate not supplied

[Effect of stimulation of structures causing an escape reaction on the self stimulation reaction in rats].

The effect of emotionally negative actions with various intensities, on the activity of the positively reinforcing brain system was studied in chronic experiments on rats. In each rat "purely" negative and positive sites were determined by well-known methods of pedal self-stimulation, of reactions of active and passive avoidance. It was shown that elimination of both central and peripheral negative actions enhances the activity of the positive reinforcement system; complex neurophysiological relations exist between systems of positive and negative reinforcement which cannot be defined solely as a reciprocal interaction.

Animals↗

PubMed1993

Exercise training alters cardiovascular and hormonal responses to intracranial self-stimulation.

Both reinforcing intracranial self-stimulation (ICSS) and physical exercise result in heightened cardiovascular and endocrine responses. This study compared the cardiovascular and endocrine responses to ICSS in rats after either chronic ICSS or treadmill running. Male rats (n = 35) were implanted with bipolar electrodes aimed at the ventral tegmental area of the brain, and those that performed vigorous lever pressing for ICSS (> 50 presses/min; n = 30) were counter balanced into three groups: chronic ICSS (PRESS), chronic run training (RUN), or sedentary controls (CONT). PRESS, RUN, and CONT rats performed ICSS, ran on a motorized treadmill, or sat quietly in cages for 30 min/day, 5 day/wk, for 12 wk, respectively. All animals then performed 30 min of lever pressing for ICSS and were immediately killed. Oxygen consumption, heart rate, blood pressure, rectal temperature, and plasma norepinephrine, epinephrine, and corticosterone increased (P < 0.05) for all groups during lever pressing. PRESS rats did not differ from CONT rats for any variable studied. However, heart rate was lower and oxygen consumption, norepinephrine, and corticosterone were higher in RUN than in CONT rats. Heart and ventricle weights were higher in PRESS and RUN than in CONT rats; body weights were not different. These data suggest that chronic treadmill running results in adaptations that influence cardiovascular and hormonal responses to ICSS.

Animals↗

PubMed1976

Attenuation of self-stimulation from substantia nigra but not dorsal tegmental noradrenergic bundle by lesions of sulcal prefrontal cortex.

Rats that self-stimulated from electrodes implanted in either the substantia nigra pars compacta (SNC) or the dorsal tegmental noradrenergic bundle (DTB) received bilateral electrolytic lesions of the prefrontal cortex dorsal to the rhinal sulcus. Immediately after the lesions, animals with SNC electrodes (n = 9) showed significant and permanent reductions in self-stimulation rates. The average reduction in the SNC group was 67% of prelesion bar-pressing scores. In contrast, rats with DTB electrodes (n = 11) were not significantly affected by similar sulcal lesions. Subsequent examination of the brains for prograde degeneration using procedure I of Fink and Heimer 11 revealed a descending system of sulcal efferents that was very dense in the region of the SNC but only scattered in the area of the DTB. The close relation between the effects of sulcal lesions on self-stimulation and the resultant density of degeneration as a function of stimulation site is discussed in terms of the contribution of prefrontal cortex to self-stimulation in general, and of the implications for the catecholamine hypothesis of self-stimulation in particular.

Animals↗

PubMed1982

Dopaminergic and noradrenergic inhibition of hypothalamic self-stimulation: differentiation of reward and performance effects.

Dopaminergic and noradrenergic inhibition of lateral hypothalamic self-stimulation was investigated in a new signalled, discrete-trials shuttle-box paradigm. The differential inhibitory effects of drugs and stimulation frequency reductions within small blocks of trials differentiate reward inhibition from a variety of performance deficits. They further differentiate among the deficits produced by fatigue, sedation, dyskinesias, akinesia and sensory disruption. Pimozide's selective inhibition of the first response within each block of trials shows that its inhibition of self-stimulation is not due to either an inhibition of reward or to a general performance deficit. Instead, it suggests that pimozide specifically inhibits the initiation of motor responding. Pimozide-induced akinesia appears to be partly reversible by hypothalamic stimulation. Thus the pimozide data do not support a role for dopamine in mediating brain-stimulation reward. Since the inhibitory effects of clonidine were very similar to those of pimozide, it is suggested that clonidine also produces a stimulation-reversible akinesia. Thus the clonidine data do not support a role for noradrenaline in mediating brain-stimulation reward. LU 5-003, which selectively inhibits the presynaptic reuptake of noradrenaline, inhibited self-stimulation in almost exactly the same way as did reducing reward by reducing stimulation frequency. These data do support a primary role for noradrenaline in mediating brain-stimulation reward. However, it is suggested that LU 5-003 inhibits self-stimulation, not by inhibiting reward, but by enhancing reward and making the electrical stimulation superfluous.

Animals↗

PubMed1982

Effect of methylglucamine orotate on intracranial self-stimulation.

The effect of the memory improving substance methylglucamine orotate (MGO) on intracranial self-stimulation was investigated in rats. Self-stimulation (0.2 mn square pulses; 100 Hz frequency; 400 mn chain; 100-300 micro A current) was performed using electrodes in the lateral hypothalamus. MGO was administered intraperitoneally in doses of 112.5 mg/kg and 225 mg/kg or intraventricularly in a dose of 225 micrograms per rat. In chronic experiments, daily intraperitoneal injections of 225 mg/kg MGO were given during 10 days. The results show that intracranial self-stimulation is scarcely influenced by a single injection of retention improving MGO doses, but increased significantly by repeated MGO application.

Animals↗

PubMedDate not supplied

Peptides and self-stimulation of the medial prefrontal cortex in the rat: effects of intracerebral microinjections of substance P and cholecystokinin.

The effects of intracerebral microinjections of substance P and cholecystokinin on self-stimulation of the medial prefrontal cortex of the rat were studied. Intracerebroventricular administration of substance P at doses of 2.5, 5, 10 and 20 micrograms produced a dose-related decrease in self-stimulation of the medial prefrontal cortex; spontaneous motor activity, measured as a control, was not affected. Unilateral microinjections into the medial prefrontal cortex of substance P at doses of 10 and 20 micrograms produced a decrease of self-stimulation of the ipsilateral side, but self-stimulation of the contralateral cortex, used as a control, was not affected. On the contrary, cholecystokinin in both intracerebroventricular administration at doses of 100, 200 and 400 ng, or intracortical microinjections into the medial prefrontal cortex at doses of 200, 400 and 800 ng, had no effect on self-stimulation of this cortical area. These results suggest that substance P, but not cholecystokinin, could be part of the neurochemical substrate underlying self-stimulation of the medial prefrontal cortex in the rat.

Animals↗

PubMed1997

Ventral pallidum self-stimulation induces stimulus dependent increase in c-fos expression in reward-related brain regions.

Neuronal expression of Fos, the protein product of the immediate early gene c-fos has been used as a high resolution metabolic marker for mapping polysynaptic pathways in the brain. We used Fos immunohistochemistry to reveal neuronal activation following self-stimulation of the ventral pallidum. Four groups of rats were allowed to self-stimulate for 30 min with 0.4 s trains of cathodal rectangular pulses of constant intensity (0.4 mA) and duration (0.1 ms). Each group was assigned a different pulse frequency, (3, 17, 24 and 50 pulses/stimulation train). Which was preselected from within each animal's rate-frequency function. The subjects that were assigned three pulses failed to self-stimulate and were considered as controls. The subjects that were assigned 17 pulses self-stimulated at half-maximal rate, whereas those that were assigned 24 and 50 pulses self-stimulated at maximal rates. The animals were sacrificed 90 min after the self-stimulation session and their brains were processed for Fos-like immunoreactivity. Fos-like immunoreactivity was found to increase as a function of pulse frequency in several brain regions known to be involved in drug and/or brain stimulation reward (medial prefrontal cortex, lateral septum, nucleus accumbens; lateral hypothalamus and ventral tegmental area), whereas it was not affected in structures devoid of such involvement (substantia nigra reticulata and dorsolateral striatum). The level of Fos expression induced by trains of 50 pulses was considerably higher than that produced by 24 pulses although both frequencies supported the same (maximal) self-stimulation rate. This finding indicates that Fos expression correlated with reward magnitude (known to increase between these frequencies), not with bar-pressing rate, thus suggesting the presence of a reward-specific effect. The finding of a frequency-dependent Fos expression in a behavioural paradigm can be considered analogous to a pharmacological dose-response curve and, as such, our results may open new avenues for the use of Fos immunohistochemistry in quantitative neurobehavioural studies.

Animals↗

PubMed1994

[The dopaminergic and serotoninergic components of the self-stimulation reaction of the lateral hypothalamus in rats with disruption of the medial prefrontal cortex].

Amphetamine (1 mg/kg) promoted a pedal self-stimulation of lateral hypothalamus of Wistar rats in the Skinner box. An unipolar lesion of medical prefrontal cortex with kainic acid 10-14 days prior to an experiment did not prevent the facilitating effect of amphetamine on self-stimulation, though the levels of hypothalamic noradrenaline and dopamine are 43% and 4.5-fold decreased respectively, the hypothalamic serotonin concentration not changing. Lysergic acid diethylamid (10 mkg/kg) did not influence on self-stimulation response in rats with damaged medial prefrontal cortex, but after preliminary administration prevented the stimulating effect of amphetamine on self-stimulation of lateral hypothalamus. The data are discussed from the point of view of a hypothesis that the phenomenon obtained is associated with the presence of a hypothalamic autoregulatory dopaminergic system providing the realization of self-stimulation. However, it does not exclude that the modulating influence of medial prefrontal cortex on lateral hypothalamus is connected with not only dopaminergic but with serotoninergic axons too.

Amphetamine↗

PubMed1988

Effects of somatostatin on self-stimulation behaviour in rats pretreated with a receptor blocker.

The effects of somatostatin on lateral hypothalamic self-stimulation were investigated in rats pretreated with haloperidol, bicuculline, phenoxybenzamine or propranolol. Somatostatin decreased the rate of self-stimulation. Halperidol, bicuculline and phenoxybenzamine potentiated the somatostatin-induced depression of self-stimulation behaviour. Propranolol had no effect. It is suggested that dopaminergic, GABAergic and noradrenergic systems are involved in the somatostatin-induced depression of self-stimulation.

Animals↗

PubMed1989

Effects of opiate antagonists and their quaternary analogues on nucleus accumbens self-stimulation.

Naloxone and naltrexone were compared with their quaternary analogues naloxone methobromide and naltrexone methobromide for efficacy in suppressing intracranial self-stimulation behavior. These quaternary analogues effectively block opiate receptors in the periphery, but since they do not readily cross the blood-brain barrier they have little effect on central receptors. Rats with electrodes in the nucleus accumbens were trained to self-stimulate in daily 60-min sessions. Naloxone (0.2, 2.0 and 20 mg/kg) and naltrexone (20 mg/kg) potently suppressed self-stimulation behavior. In contrast, neither naloxone methobromide (0.2 and 20 mg/kg) nor naltrexone methobromide (20mg/kg) had any significant effects on this behavior. These results suggest that blockade of peripheral opiate receptors alone is insufficient to suppress self-stimulation, and therefore support the idea that opiate antagonists suppress self-stimulation by blockade of central receptors that mediate reinforcement.

Animals↗

PubMed1999

Self-stimulation rewarding experience induced alterations in dendritic spine density in CA3 hippocampal and layer V motor cortical pyramidal neurons.

Self-stimulation rewarding experience induced alterations in the numerical density of spines in CA3 hippocampal and layer V motor cortical pyramidal neurons in adult male Wistar rats was evaluated. Self-stimulation experience was provided 1 h daily over a period of 10 days through stereotaxically implanted bipolar stainless steel electrodes bilaterally in lateral hypothalamus and substantia nigra-ventral tegmental area. After 10 days, rats were killed and the hippocampus and motor cortex were processed for rapid Golgi staining procedure. The dendritic spine densities were studied in CA3 hippocampal and layer V motor cortical pyramidal neurons. The spine densities were quantified in five successive segments of 15.2 microm up to a distance of 76 microm. Apical dendrites were classified as mainshaft, sub branch, oblique shaft-I, oblique shaft-II, primary branch; and basal dendrites as main shaft, primary branch and secondary branch. A grand total of 864 CA3 hippocampal and 1008 layer V motor cortical dendrites were analysed for spine counting in different groups of rats. The results revealed a significant (P<0.001; ANOVA, F-test) increase in the number of spines in all the categories of dendrites in apical and basal regions in both hippocampal and motor cortical neurons in self-stimulation group of rats. Such changes were not observed either in sham control, experimenter-administered or normal control groups of rats. The self-stimulation induced increase in the spine density suggests an increase in the postsynaptic receptive field in CA3 hippocampal and layer V motor cortical neurons. This might enhance the efficacy of synaptic transmission in these neurons. Our study clearly demonstrated the self-stimulation rewarding experience induced postsynaptic plasticity in hippocampal and motor cortical pyramidal neurons.

Animals↗