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PubMed2003

Alpha2-adrenoceptor antagonism is neither sufficient nor necessary for the distinctive action of atypical neuroleptics on intracranial self-stimulation in the rat.

Response rates in variable-interval intracranial self-stimulation (ICSS) in rats can provide a continuous record of drug-induced changes in brain function. Use of this procedure has been found to distinguish between typical and atypical neuroleptics, with the latter producing a similarly intense but much briefer depression of responding. This difference has been ascribed to the alpha2-adrenoceptor antagonist properties of atypical neuroleptics, but the evidence is ambiguous. The role of alpha2-adrenoceptors was examined in the present study using ventral tegmental ICSS to track the depressant effects of the typical and atypical neuroleptics, haloperidol (0.075 mg/kg) and olanzapine (0.9 mg/kg), injected alone or in combination with an alpha2-adrenoceptor agonist or antagonist. Neither haloperidol nor olanzapine (despite its atypical features) shows appreciable affinity for the alpha2-adrenoceptor. In the present study, olanzapine was found to depress self-stimulation responding dose-dependently, but with considerable recovery after 4 h. Simultaneous administration of alpha2-adrenoceptor receptor agonists or antagonists (respectively clonidine 0.015 mg/kg or idazoxan 3.0 mg/kg) failed significantly to increase or decrease the action of either haloperidol or olanzapine. These results indicate that alpha2-adrenoceptor antagonism does not necessarily promote recovery from neuroleptic-induced depression, and that 'atypical' features do not necessarily depend on alpha2-adrenoceptor antagonism. Various other explanations remain possible, but the accelerated time course of the atypical agents appears to support more recent explanations, based on their rapid dissociation from the D2 receptor.

Adrenergic alpha-2 Receptor Agonists↗

PubMed1987

Evaluation of stressor effects on intracranial self-stimulation from the nucleus accumbens and the substantia nigra in a current intensity paradigm.

The effect of uncontrollable footshock was evaluated in animals responding for intracranial self-stimulation from the nucleus accumbens and the substantia nigra (pars compacta) in a descending current intensity paradigm. Responding for brain stimulation from the nucleus accumbens was found to be affected by the stressor at the upper end of the rate-intensity curve. In contrast, responding for brain stimulation from the substantia nigra was unaffected by the stressor at any of the current intensities employed. The variations of responding for self-stimulation from the nucleus accumbens were unrelated to alterations of locomotor activity or rearing. It is suggested that stressor-provoked reductions of responding for intracranial self-stimulation are not a result of the brain stimulation taking on aversive properties, but rather reflect a reduction in the reinforcing or motivational value associated with the stimulation.

Animals↗

PubMed1979

Self-stimulation of the sulcal prefrontal cortex in the rat: direct evidence for ascending dopaminergic mediation.

Intracranial self-stimulation (ICSS) of the prefrontal cortex dorsal to the rhinal sulcus in rats has been abolished by means of injections of 6-hydroxydopamine (6-OHDA) (4 micrograms/2 microliters) into the ascending trajectory of the A10 mesocortical dopaminergic fibers ipsilateral to the stimulation electrodes. Similar injections made contralateral to the stimulation electrodes produced a transient attenuation of this self-stimulation. All cases of such lesions were confirmed with the use of Vibratome histochemical fluorescence examination of each of the dopamine projection areas in the forebrain.

Animals↗

PubMed1983

Neurobehavioral evidence for mesolimbic specificity of action by clozapine: studies using electrical intracranial self-stimulation.

The ability of chronic treatment with the atypical neuroleptic clozapine to induce functional dopaminergic hypersensitivity in laboratory rats was assessed. The intracranial electrical self-stimulation paradigm, known to be sensitive to changes in functional dopaminergic sensitivity, was used. Animals with electrodes in the ventral tegmental nucleus (mesolimbic dopamine cell body area) showed a marked increase in self-stimulation rate following 3 weeks of chronic clozapine. This increase was similar in magnitude and duration to that shown by animals given 3 weeks of chronic haloperidol. In contrast, animals with electrodes in the substantia nigra (nigrostriatal dopamine cell body area) showed no change in self-stimulation rate following 3 weeks of chronic clozapine. These data are interpreted in the light of previous suggestions that clozapine and other atypical neuroleptics may possess functional selectivity for the mesolimbic dopamine system.

Animals↗

PubMed1990

Application of in vivo electrochemistry to the measurement of changes in dopamine release during intracranial self-stimulation.

Stearate-modified graphite paste recording electrodes were acutely or chronically implanted into the nucleus accumbens along with bipolar stimulating electrodes in the ipsilateral ventral tegmental area (VTA). Chronoamperometry was used to monitor changes in electrochemical signals that may correspond to the oxidation of dopamine (DA) during experimenter-administered stimulation (EAS) and intracranial self-stimulation (ICS). Application of EAS to stimulating electrodes in the VTA produced increases in the electrochemical signal in both the anesthetized and conscious preparation. The magnitude of both effects increased as a function of current intensity. Initiation of ICS was also accompanied by an immediate increase in the electrochemical signal. Rate-intensity experiments revealed a corresponding increase in both the ICS rates and the electrochemical signal with successive increases or decreases in current intensity. In subsequent experiments, intraperitoneal injections of DA uptake blockers nomifensine and GBR-12909 produced significant increases in the amplitude of the chronoamperometric signal which corresponded to drug-induced increases in bar press rates. The noradrenergic uptake blocker desipramine had no significant effect on either ICS rates or oxidation current. These data indicate that ICS of the VTA may produce concurrent increases in DA neurotransmission in the nucleus accumbens. The pharmacological studies are consistent with a dopaminergic substrate of brain stimulation reward at electrode sites in the VTA.

Anesthesia↗

PubMed2003

Facilitation of electrical brain self-stimulation behavior by abused solvents.

Animal models are needed to study the abuse-related behavioral and pharmacological effects of inhaled solvents. Previous studies have suggested that intracranial self-stimulation techniques may be successfully adapted for testing the effects of solvent exposure. The present study aimed to assess the effects of toluene, cyclohexane, acetone, and petroleum benzine (a widely used mixture of hexanes and heptanes) in rats trained to lever press or nose-poke for electrical stimulation delivered through electrodes implanted into the medial forebrain bundle. It was found that toluene, cyclohexane, and benzine but not acetone, increased rates of responding, particularly at the lower stimulation intensities. In another set of experiments utilizing an auto-titration procedure, all tested solvents significantly reduced self-stimulation thresholds. However, only for toluene and benzine were these effects observed at the exposure levels that did not impair rates of operant performance. There may not be such a clear separation of effects for acetone and cyclohexane. Thus, toluene and benzine appear to selectively affect brain reward systems in a manner similar to that for most other abused drugs. Data from intracranial self-stimulation studies of solvents may be useful in abuse potential assessment of individual compounds and for examining neural and behavioral processes involved in inhalant abuse.

Animals↗

PubMed1985

Spatio-temporal integration in the substrate for self-stimulation of the prefrontal cortex.

The number of stimulation pulses required to maintain a half maximal rate of self-stimulation of the prefrontal cortex (PFC) was determined for various currents. Over a restricted range, the effects of decreasing the stimulation frequency could be compensated for by increasing the current. This finding cannot easily be reconciled with the hypothesis that the rewarding impact of PFC stimulation is unaffected by increments in current. The minimum current that would support self-stimulation of the PFC at high frequencies was larger than has been reported at medial forebrain bundle sites.

Animals↗

PubMed1983

Effect of cholecystokinin on self-stimulation behavior in rats.

Experiments were performed to examine the effects of intracerebroventricularly administered cholecystokinin octapeptide sulfate ester (CCK-8-SE) and unsulfated cholecystokinin octapeptide (CCK-8-NS) on electrical self-stimulation behavior elicited from the medial forebrain bundle. CCK-8-SE and CCK-8-NS in 80 pmol doses reduced the response rate of self-stimulation behavior 22-30 min following injection, while 400 pmol doses of these peptides attenuated self-stimulation behavior between 13 and 36 min. It is suggested that CCK-8-SE and CCK-8-NS interact with central rather than peripheral nervous mechanisms.

Animals↗

PubMed1981

Electrical stimulation of the septal area in the rat: prolonged suppression of water intake and correlation with self-stimulation.

The role of the septal region in the control of drinking and self-stimulation behavior in the rat was investigated under conditions of forced and self-delivered brain stimulation. Sixty minutes of intermittent septal stimulation significantly reduced post-stimulation water consumption in water deprived rats without affecting the consumption of solid food or a liquid diet following food deprivation. In addition, those animals demonstrating the greatest suppression of water intake after forced stimulation also emitted the highest response rates to obtain rewarding brain stimulation from the same electrodes. These results support the hypothesis that the septal region plays an inhibitory role in the control of drinking behavior and suggests a relationship between the reward obtained by electrical brain stimulation and the central neural systems controlling thirst in the rat.

Animals↗

PubMed1985

Comparison of deficits in electrical self-stimulation after ibotenic acid lesion of the lateral hypothalamus and the medial prefrontal cortex.

The aim of the present study was to compare the self-stimulation deficit produced by a unilateral injection of the neurotoxin, ibotenic acid, in the lateral hypothalamus (LH) to the deficit produced by the same unilateral injection in the medial prefrontal cortex (MPC). Four groups of adult male Sprague-Dawley rats were used: in two control groups, electrodes were bilaterally implanted in the LH (5 rats) or in the MPC (6 rats) and self-stimulation (ICSS) was obtained separately with the right and left electrodes. In the two experimental groups the intrinsic neurons of the LH (8 rats) or of the MPC (10 rats) were destroyed unilaterally by local injection of ibotenic acid (4 micrograms in 0.5 microliter); the other side served as the sham-lesioned control. Ten days later ICSS electrodes were implanted bilaterally, one in the lesioned area, the other in the contralateral region. As in the case of the control rats, ICSS was determined separately for each electrode, first by a rate dependent test (nose-poke) then by a 'rate-free' test (shuttle-box). In the LH and MPC control rats, ICSS responses were the same with stimulation on either side. In the LH-lesioned rats, the ICSS rates measured with the nose-poke test were significantly decreased with stimulation on the lesioned side, whereas rates with stimulation of the non-lesioned LH were normal. Likewise, while shuttle responses with stimulation of the non-lesioned LH were normal, the OFF-time was increased and the ON-time was decreased with stimulation of the lesioned LH. In the MPC-lesioned rats, ICSS (nose-poke) was totally suppressed and the shuttle responses were disorganized since neither the ON- nor the OFF-times changed in response to increasing current intensities. Nose-poke responses with stimulation of the non-lesioned MPC were just about normal. These results show that in the two brain regions studied local neurons are involved in ICSS. The difference in the magnitude of the deficit observed suggests, that the neuronal circuits involved in MPC self-stimulation are poorly represented whereas in the LH many neuronal circuits involved in these mechanisms overlap.

Animals↗

PubMed1998

Activation of reward-relevant neurons in the caudate-putamen influences the development of medial prefrontal cortex self-stimulation: a moveable electrode mapping study.

Two hundred fifty five medial prefrontal cortical (MPFC) and 187 caudate-putamen (CPu) sites were evaluated for intracranial self-stimulation in 67 animals using moveable electrodes and collecting trade-off functions between current and frequency. Eleven percent of the examined areas, located predominantly in the ventromedial aspects of MPFC and CPu, showed reliable self-stimulation and the average charge of 1.12 and 1.11 microC respectively, values that are in line with those reported for the Medial forebrain bundle. The distribution of charge, however, was greater than reported for the latter region, and ranged between 0.68 to 1.63 microC across sites. Some subjects were implanted with two electrodes, one aimed at the MPFC, and the other at the CPu, ventral tegmental area, or lateral hypothalamus. Only animals with CPu placements showed transference of self-stimulation to the MPFC, suggesting that these two regions might form part of the same reward substrate, a view that has anatomical, electrophysiological and recently behavioral support.

Animals↗

PubMed1976

[The effect of neurotropic substances on the self-stimulation reaction at the thalamic level].

The effect of d-amphetamine, cocaine, caffeine, morphine, imipramine, phenobarbital, LSD-25, benactyzine, meprobamate, diazepam, chloridiazepoxide on the lateral hypothalamic self-stimulation of rats was investigated. D-amphetamine, cocaine, caffeine, morphine, imipramine decreased the threshold of selfstimulation. Meprobamate, diazepam, chlordiazepoxide failed to influence this index, but increase the intensity of self-stimulation during the threshold, the optimum and more than the optimum cirrent intensity. Benactyzine, LSD-25, phenobarbital decreased the threshold and increased the frequency of self-stimulation during all the current intensities. A comparative study of the above results showed the agents of the first group to exert a direct stimulating action on the positive reinforcement system. Tranquillizers activated this system due to their depressive action on the negative reinforcement system. Benactyzine, LSD-25, phenobarbital activated the system and depressed the system of negative reinforcement.

Animals↗

PubMed1984

The effects of feeding and fasting on self-stimulation.

The effects of ad libitum feeding and 72 hr fasting on intracranial electrical self-stimulation behaviour (ICSS) were tested in cats. In contrast to previous studies it was found that the opposite manipulations in food intake, i.e. ad libitum feeding fasting, often induced identical changes in lever-pressing rate even in cases of lateral hypothalamic self-stimulation. Both increase and decrease in lever-pressing rate for ICSS could be observed depending rather on the electrically elicited behaviours than the precise anatomical location of the stimulating electrodes. It is concluded that changes in ICSS induced by food intake and food deprivation are probably secondary to the changes in activity level.

Animals↗

PubMed1985

Reinforcement delay of one second severely impairs acquisition of brain self-stimulation.

The effect of delayed reinforcement on the acquisition of lateral hypothalamic self-stimulation was investigated. Brain stimulation reinforcement minimizes cues associated with reinforcement delivery (secondary reinforcement) and, by eliminating consummatory responses, permits precise temporal control of the interval between the operant response and reinforcement. Different groups were trained in daily 1-h sessions for brain stimulation reinforcement at one of 4 delay intervals (1, 2, 3 or 6 s). Responses made during the delay interval were not reinforced and reset the delay timer. Control groups (IMMEDIATE) were reinforced immediately, but were required to space responses--according to a delayed reinforcement of low rates (DRL) schedule--for an interval corresponding to one of the delay of reinforcement intervals. The DRL schedule equalized opportunities for reinforcement and non-reinforcement. At all intervals, rats trained with delayed reinforcement had significantly lower bar-press rates than controls trained with immediate reinforcement under DRL. When reinforcement schedules were switched (DELAY groups now get IMMEDIATE and vice versa), response rates rapidly shifted to levels appropriate to the new schedule. The pre-switch results indicate that delays even as short as 1 s markedly impede the acquisition of self-stimulation behavior. The post-switch results suggest that delay of reinforcement, like stimulation intensity, may determine the strength of hypothalamic reinforcement and hence final levels of performance.

Animals↗

PubMedDate not supplied

[Changes in the level of cortisol in the blood of rabbits during self stimulation].

The time-course of changes in the blood plasma cortisol level during activation of the positive reinforcement system was studied in experiments on adult chinchilla male rabbits. The self-stimulation status of the brain lateral hypothalamus was utilized as a model for positive reinforcement. The basal cortisol level in intact rabbits, determined by means of radioimmunoassay, was equal to 5.31 +/- 0.87 micrograms% over a period of 10 to 2 hours p.m. The blood collection procedure, using the method of the ear marginal vein dissection, increases the cortisol concentration 30 minutes after blood collection by 19.4%, i.e. augments its level up to 6.37 +/- 0.90 micrograms%. A significant rise (P less than 0.01) of hormone release into the blood (two-fold) is seen 5 to 15 minutes following the self-stimulation test. Cortisol level remains heightened 1 hour after the self-stimulation experiment. The intensity of the corticotropic activity was not dependent on the hypothalamus, stimulated by force or by animals themselves. On the basis of the data obtained it is concluded that the hormonal response is directly dependent both on hypothalamic electric stimulation and on the motivative mechanism activation. The very positive reinforcement, timing to the post-stimulating period and being of full value only during the adaptive behavioral act, is not stress-inducing.

Animals↗

PubMed1988

Effects of cholecystokinin-related peptides on self-stimulation behaviour in rats.

The effects of cholecystokinin octapeptide sulfate ester (CCK-8-SE), its N-terminal tripeptide (CCK-2-4-SE) and its C-terminal tetrapeptide (CCK-5-8) were investigated on hypothalamic self-stimulation in rats. CCK-8-SE and CCK-5-8 in 400 pmole doses inhibited self-stimulation behaviour, while CCK-2-4-SE was ineffective. In 80 pmole doses the peptides showed no effect. It is suggested that CCK-5-8 itself influences self-stimulation behaviour.

Animals↗

PubMed1989

Increased locomotor activity of rats by self-stimulation in a running wheel.

A method was developed in which the intracranial self-stimulation of rats was dependent on their locomotor activity. During each rotation of a running wheel (= 0.75 m), six stimulus trains were administered via electrodes in the medial forebrain bundle. Under these conditions, animals increased their locomotor activity 112-fold, compared to a control condition without self-stimulation. This method may be a valuable procedure in various research fields where extreme increases in motor activity of laboratory animals are advantageous.

Animals↗

PubMed1977

Cardiovascular responses and lateral hypothalamic self-stimulation: anatomical differentiation and functional significance.

Heart rate was telemetrically recorded from rats self-stimulating in a two-day shuttle-box. Blood pressure changes to intracranial stimulation (ICS) were determined in acute studies with the same subjects. Stimulus-bound heart rate decreases were found only at sites in the anterodorsal aspect of the lateral hypothalamus, whereas no changes in heart rate were observed at ventral or posterior sites. In the acute experiments, stimulation of the anterodorsal sites produced either decreases or no change in blood pressure. Stimulus-bound blood pressure increases were observed only in the ventrolateral hypothalamus. The differential topographical distribution of the electrode sites producing the heart rate and blood pressure changes suggests that these two aspects of cardiovascular function are subserved by separate neural systems in the hypothalamus and that the bradycardia during self-stimulation is a primary response to ICS and is not a reflex elicited by blood pressure increases. Blockade of the bradycardia with the peripheral cholinergic blocker methyl-hyoscine HBr had no effect on the initiation of or escape from ICS indicating that peripheral parasympathetic activity is not causally related to either the rewarding or aversive components of hypothalamic ICS.

Animals↗