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At least 37 records · Page 2Linked to original sources
PubMed1992

Modelling drug kinetics with brain stimulation: dopamine antagonists increase self-stimulation.

The rewarding effects of brain stimulation and drugs are believed to depend on a common neural system. However, the pattern of responding produced by drug reinforcers is different from the pattern produced by conventional brain stimulation. Furthermore, pharmacological antagonists of reinforcement increase the rate of drug self-administration but depress self-stimulation. To test the hypothesis that the differences in the characteristics of brain stimulation and drugs as reinforcers are due to differences in the kinetics of drugs and brain stimulation, we modelled drug kinetics with frequency-modulated trains of brain stimulation. We report that animals will self-administer such brain stimulation in a manner that resembles drug self-administration and that, under these conditions, dopamine antagonists can increase the rate of self-stimulation.

Animals↗
PubMed1980

Effects of GABA receptor blockade on stimulation-induced feeding and self-stimulation.

Frequency thresholds for eating elicited by electrical stimulation of the lateral hypothalamus of rats decreased in a dose-dependent manner after intraperitoneal (IP) administration of picrotoxin, a gamma-aminobutyric acid (GABA) antagonist that blocks GABA-mediated synaptic inhibition. Strychnine IP, a glycine antagonist that blocks glycine-mediated synaptic inhibition, had no effect. By contrast, frequency thresholds for self-stimulation at the same electrode site significantly increased after picrotoxin. Again, strychnine had no effect. These findings indicate that GABAergic mechanisms are involved in both electrically-elicited feeding and self-stimulation. They also suggest a dissociation of the neural substrates which subserve these behaviors.

Animals↗
PubMed1982

Differential effects of d-amphetamine, pipradrol and bupropion on shuttlebox self-stimulation.

The shuttlebox self-stimulation test is claimed by Atrens to differentiate drug effects on brain stimulation reward from those on performance variables. Thus, for example, drug-induced enhancement of the reward value of stimulation should be reflected in a selective reduction of the latency to initiate stimulation (the ON latency), as compared with the latency to terminate stimulation (the OFF latency). The effects of the psychostimulant drugs, d-amphetamine and pipradrol, and the antidepressant, bupropion, were evaluated in this procedure as well as in a bar-pressing test of self-stimulation. Pipradrol (3 and 10 mg/kg) and bupropion (54 mg/kg) reduced ON latencies by 40% or more but failed to shorten OFF latencies, indicating that performance variables were not involved in the ON latency decrements. Although d-amphetamine (0.3 and 1.0 mg/kg) shortened ON latencies, the 1.0 mg/kg dose also reduced OFF latencies. Drug doses that reduced ON latencies also increased bar-pressing self-stimulation. The shuttlebox self-stimulation test appears to be capable of discriminating drug-induced enhancement in brain stimulation reward from performance variables.

Animals↗
PubMed1976

Separation of inhibiting and stimulating effects of morphine on self-stimulation behaviour by intracerebral microinjections.

The effects on self-stimulation behaviour of 5 mug morphine HCl applied into the ventricular system and into different areas throughout the brain were studied. Injections into the ventricular system and in areas intermediate between the posterior hypothalamus and the periaqueductal grey matter had biphasic effects: an inhibition followed by an excitation. Injections into the posterior hypothalamus resulted in increased self-stimulation whereas injections into the periaqueductal grey matter and into the locus coeruleus were only inhibiting.

Animals↗
PubMed1973

Some characteristics of self-stimulation behavior of dogs.

Self-stimulation was studied in dogs chronically implanted with electrodes in different points within the basal forebrain. The animals exhibiting pure self-rewarding behavior were defined as "optimal" and "good self-stimulators", whereas those with concomitant aversive phenomena were incorporated into the third category called "self-stimulation-withdrawal". In "optimal self-stimulators" a remarkable resistance of the response to extinction was noted. A strong negative attitude toward food was found in four dogs upon stimulation of the self-rewarding loci. Penile erection accompanied self-stimulation in two animals. Sniffing at first always followed incentive brain stimulation, but later it appeared at the beginning of each experiment and/or preceded the bouts of pressing. A rise of hypothalamic temperature was noted in mast of the animals. In some cases this was equal to or exceeded 1 degree Celsius. The temperature increase was accompanied by intense panting between the bouts. Seizures appeared locally as contractions of masticatory muscles and sometimes developed into a generalized fit. Anatomically the "reward area" in the dog extends from the septum and the preoptic area to the mammillary bodies and reaches laterally to the internal capsule.

Animals↗
PubMedDate not supplied

Designing of a brain stimulator suitable for intracranial self-stimulation experiments for studying the brain-stimulation reward system.

A circuit design has been developed and described for fabricating and using in the intracranial self-stimulation experiments on rat to study the brain-stimulation reward behaviour, and to explore into the underlying mechanisms of drives and motivated behaviours. The stimulator can be fabricated with parts available in India. It has been continuously used and tested during the last four years in different research studies.

Animals↗
PubMed1994

Post-stimulation excitability of diencephalic self-stimulation neurons.

We used the double-pulse technique with moveable electrodes to estimate the refractory periods of self-stimulation neurons within the rat's dorsal diencephalon and surrounding areas. Refractory period estimates varied substantially depending on the site of stimulation. For some sites, recovery from refractoriness was noted at post-stimulation intervals as short as 0.5 ms, an estimate similar to that reported for the MFB axis and the dorsal raphe and periaqueductal grey. The longest recovery intervals were similar to those reported for the prefrontal cortex, caudate, and substantia nigra. Step-like recovery (believed to indicate the presence of neural populations with non overlapping refractory periods) was also noted in several sites. The large range of recovery intervals found in the present study may suggest that the diencephalon plays an integrative role for rewarding signals arriving from various brain areas.

Animals↗
PubMed1995

Withdrawal from chronic amphetamine elevates baseline intracranial self-stimulation thresholds.

Intracranial self-stimulation was assessed before, within, and after a chronic amphetamine treatment regimen. Amphetamine was given twice daily 5 days per week for 6 weeks at dosages escalating from 1 to 10 mg/kg per injection. Lateral hypothalamic self-stimulation rate-frequency functions were taken 36 h after the last injection in each weekly series and weekly for 3 weeks following the last injection. Frequency thresholds increased and maximal response rates decreased progressively as a function of amphetamine withdrawal during treatment; each returned to near normal levels within 2 weeks of the last injection. When subsequently tested under amphetamine, animals previously receiving the 6-week amphetamine treatment regimen had self-stimulation thresholds and maximal response rates that did not differ significantly from those of saline-treated control animals. These data confirm that chronic amphetamine treatment results in a dependence syndrome characterized in part by a phasic depression in the brain mechanism mediating the reinforcing effects of lateral hypothalamic electrical stimulation.

Amphetamine↗
PubMed1984

Self-stimulation in the ventral tegmental area suppresses self-mutilation in rats with forelimb deafferentiation.

In rats which received section of 5 dorsal roots corresponding to the brachial plexus, self-mutilation of the forelimb develops during the first 2 months after deafferentation. The extent of self-mutilation was measured for 90 days in a control group of animals and in a group with an electrode implanted in the ventral tegmental area and which were allowed to self-stimulate at freedom. The animals which self-stimulated for 35 days did not develop the self-mutilation even after the self-stimulation was stopped.

Afferent Pathways↗
PubMed1991

Cocaine enhances the reward value of medial prefrontal cortex self-stimulation.

Intracranial self-stimulation (ICSS) of at least some brain sites is thought to be mediated by mesolimbic dopamine (DA) neurons. However other ICSS sites, especially those in the medial prefrontal cortex (MFC), have been shown to be relatively insensitive to drugs (e.g. amphetamine, neuroleptics) that alter DA synaptic transmission. In the present study, rats with ICSS electrodes implanted in both the medial forebrain bundle (MFB) and the MFC were treated once per day for 10 days with cocaine (15.0 mg kg-1). Cocaine decreased the thresholds for both MFB (-51.4%) and MFC (-23.0%) ICSS. Cocaine also increased rates of responding for MFC but not MFB ICSS. These data provide additional support for the view that the MFC contributes to the rewarding effects of cocaine.

Animals↗
PubMed1975

A role for dopamine in the psychopharmacology of electrical self-stimulation.

The psychopharmacology of electrical self-stimulation of the lateral hypothalamus was studied using 6-hydroxydopamine, alpha-methyltyrosine, U-14, 624, and d-amphetamine. Reduction of brain dopamine, but not norepinephrine, with 6-hydroxydopamine produced an acute depression of responding which eventually recovered to pretreatment levels. A low dose of alpha-methyltyrosine, which did not affect responding in control rats, significantly depressed responding in the rats with brain dopamine reduced. This treatment did not alter responding of rats with norepinephrine reduced by 6-hydroxydopamine. A dopamine-beta-hydroxylase inhibitor, U-14, 624, depleted norepinephrine an additional 70% yet failed to alter self-stimulation in any of the groups. In other experiments, the 6-hydroxydopamine treatment which reduced brain dopamine was found to block the facilitation of self-stimulation produced by d-amphetamine. This facilitation of lateral hypothalmic self-stimulation was not influenced by treatments which reduced brain norepinephrine. An experiment suggesting that dopamine is of importance to locus coeruleus self-stimulation is also described. Implications of these data indicating a role for dopamine in self-stimulation responding are discussed in relation to the "catecholamine hypothesis of self-stimulation".

Animals↗
PubMed1985

An investigation of the factors affecting development of frontal cortex self-stimulation.

Intracranial self-stimulation (ICSS) of the medial prefrontal cortex (MFC) is acquired gradually, taking 4 or more days to establish. One explanation for this finding is that the stimulation becomes more rewarding with repetition. Four experiments were conducted to test this hypotheses. In Experiment 1, the MFC ICSS frequency thresholds remained constant over the first 3 weeks of testing while the rate of lever pressing response increased. In Experiment 2, it was found that acquisition of MFC ICSS was much more rapid when a motorically simpler response (nose-poking) was employed. Similarly, Experiments 3 and 4 further demonstrated that response factors such as task complexity may ultimately determine the rate of development of frontal cortex ICSS. Overall, these data suggest that independent of the rewarding effects of MFC stimulation there are other effects that initially interfere with learning of complex operant responses.

Animals↗
PubMed1990

Ketamine blocks the plasticity associated with prefrontal cortex self-stimulation.

Intracranial self-stimulation (ICSS) at sites within the medial prefrontal cortex (MFC) is acquired slowly but can be hastened by prior exposure to a regimen of noncontingent stimulation delivered to the MFC ICSS electrode. The facilitatory effects of noncontingent MFC stimulation on subsequent ICSS acquisition were blocked by pretreatment with ketamine, a noncompetitive antagonist of the N-methyl-D-aspartate (NMDA) receptor. These findings provide further support for the view that the NMDA receptor is importantly involved in mechanisms of neural plasticity.

Animals↗
PubMed1998

Alterations in the density of excrescences in CA3 neurons of hippocampus in rats subjected to self-stimulation experience.

Self-stimulation (SS) rewarding experience induced alterations in the density of excrescences in the apical dendrites of CA3 neurons were studied in adult male Wistar rats. SS experience was provided daily for an hour over a period of 10 days, through bipolar stainless steel electrodes implanted bilaterally in lateral hypothalamus and substantia nigra-ventral tegmental area. The results revealed a significant (P<0.001) increase in the number of excrescences in both main shaft and sub branches of the apical dendrites in SS experienced group compared to control groups of rats. The increased number of excrescences in CA3 neurons might be due to an enhancement in the synaptic transmission in the mossy fiber pathway following SS experience.

Animals↗