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PubMed1996

Dose-response functions of apomorphine, SKF 38393, LY 171555, haloperidol and clonidine on the self-stimulation evoked from lateral hypothalamus and ventral tegmentum.

The experimental animals were implanted with two bipolar electodes, one in the lateral hypothalamus including medial forebrain bundle (LH-MFB) and other in ipsilateral ventral tegmental area-substantia nigra (VTA-SN) and were trained to press a pedal for self-stimulation. This provided the scope to compare directly the effect of a given dose of a drug on the two reward regions in the same animal in the same testing situation. The current intensity was set to produce intracranial self-stimulation (ICSS) response rates of 50% less than the maximal shaping response rates for the respective animals (M60). Following systemic (intraperitoneal) administration of apomorphine (a dopamine receptor D1/D2 mixed agonist), SKF 38393 (D1 > D3 > D2 agonist), LY 17155 or quinpirole (D3 > D2 and D1) agonist), haloperidol (a DA-D2 antagonist), and clonidine (noradrenaline receptor alpha 2 agonist), the ICSS response rates evoked from LH-MFB and VTA-SN were compared with vehicle or saline-treated animals on the basis of dose-response functions. A dose-dependent inhibitory effect at M50 was observed with apomorphine (0.01-1.00 mg/kg) and haloperidol (0.05-0.30 mg/kg) for both the sites of stimulation. These doses of haloperidol did not produce any motor deficits like catalepsy and muscular rigidity. The dose-response and time-effect functions of SKF 38393 and LY 171555 at M50 showed the facilitation and suppression of ICSS of VTA-SN and LH-MFB respectively. Clonidine (0.05-0.25 mg/kg) also produced inhibitory effect on ICSS rates, but this suppression was of different magnitude with respect to the site of stimulation. These doses of clonidine were in the range that did not prevent active pedal pressing responses. ED50 (the dose required to reduce the ICSS response rate 50% of the rate after administration of vehicle) for LY 171555 was 0.8 and 4.4 mg/kg for the ICSS of VTA-SN and LH-MFB respectively and thus statistically different ED50 for apomorphine was 0.27 and 0.36 mg/kg; and for haloperidol was 0.75 and 0.90 mg/kg for LH-MFB and VTA-SN respectively and thus not different significantly. ED50 for clonidine was 0.25 and 0.08 mg/kg for VTA-SN and LH-MFB respectively and thus statistically different. The two-way analysis of variance (ANOVAR) of interaction of dose-response function of alpha 2 agonist with respect to LH-MFB and VTA-SN showed significant independence in their suppressive effects.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1981

A within-subject comparison of the effects of morphine on lateral hypothalamic and central gray self-stimulation.

The effects of chronic administration of morphine (20 mg/kg) on self-stimulation (SS) of the central gray and lateral hypothalamus were investigated in a within-subject design. The magnitude and time course of the drug-produced changes in SS at the two placements were similar within subjects but varied substantially across subjects. These results are interpreted in the light of evidence pertaining to the anatomical linkage of the substrates for the rewarding effects of central gray and lateral hypothalamic stimulation. The facilitation of SS may be due to a drug-produced sensitization of reward-related neurons. If so, morphine acts either beyond the point of convergence of the two substrates or at an earlier stage in each substrate. The across-subject variability is attributed to individual differences in sensitivity to the effects of the drug. The importance of controlling for this subject variable is stressed.

Animals↗
PubMed1986

Roles of catecholamine terminals and intrinsic neurons of the ventral tegmentum in self-stimulation investigated in neonatally dopamine-depleted rats.

Three series of experiments were undertaken to determine whether the residual catecholamine (CA) terminals or intrinsic neurons of ventral tegmentum (VT) in rats given 6-hydroxydopamine (6-OHDA) after desmethylimipramine (DMI) in the lateral ventricles at birth, mediated VT self-stimulation (SS). In Experiment I, male pups were injected bilaterally on days 3 and 5 with 6-OHDA (total dose 200 micrograms) or with the vehicle after pretreatment with DMI (50 mg/kg, IP) 30 min earlier. Each subject, 150 days old, was implanted bilaterally in the VT with electrode-cannula units. Both the dopamine (DA)-depleted and control groups yielded similar percentages of self-stimulators. The rate of responding was, however, slightly but significantly lower in the DA-depleted group than in the controls. In Experiment II, 8 DA-depleted and 7 control rats were pretreated with pargyline (50 mg/kg, IP) and then given unilateral injections of 6-OHDA in the VT, in the tissue below the SS electrode. These intracerebral injections of 6-OHDA had no effect on VT SS in both groups. Seventeen controls and 12 DA-depleted rats, in Experiment III, were given injections of kainic acid (KA; 5 nM) either ipsilaterally or contralaterally. The ipsilateral injection abolished SS (14 days of testing), whereas the contralateral injection had no effects on ipsilateral SS in both groups. Histochemical fluorescence study in Experiment I and II showed that the neonatal treatment with DMI + 6-OHDA had reduced the number of DA-containing perikarya in the VT and that reinjection of 6-OHDA into the VT caused the disappearance of the residual CA terminals in tissue surrounding the electrode tip.

Animals↗
PubMed1987

Strain-specific effects of inescapable shock on intracranial self-stimulation from the nucleus accumbens.

Responding for electrical stimulation from the nucleus accumbens was assessed in 3 inbred strains of mice (DBA/2J, C57BL/6J and BALB/cByJ) following exposure to uncontrollable footshock. While the operant response was most readily acquired in the DBA/2J strain, exposure to inescapable shock in this strain induced a marked deterioration of self-stimulation responding, which tended to dissipate over a 168-h period. In contrast to these mice, the stressor did not affect self-stimulation responding in the C57BL/6J strain, and produced a transient enhancement of responding in BALB/cByJ mice. It appears that although uncontrollable aversive events may engender an anhedonic effect, such an outcome is strain-dependent. These data suggest the importance of considering individual and genetic differences in the development of animal models of depression.

Animals↗
PubMed1986

Rat strain differences in the acquisition of hippocampal self-stimulation.

The rate of acquisition of lever-pressing for electrical stimulation of the hippocampus (HPC) was compared in two strains of rat: barrier-sustained Wistar and Sprague-Dawley. Sprague-Dawley rats initially bar-pressed at very low rates and took a median of 11 days to self-stimulate, according to the criterion used. Wistar rats all reached the same criterion in the first test session. Differential sensitivity to the activating effects of stimulation as an explanation for this difference was ruled out by the observation that both strains decreased response rates at the same rate and to the same level if stimulation was made non-contingent on lever-pressing. Differential threshold for reward was ruled out by the observation that rate-intensity curves yielded the same threshold currents and peak rates in both strains. Finally, it was shown that the rate of development of kindled seizures in the two strains of rats is different: Wistars kindle to full seizures faster than do Sprague-Dawleys. The relationship between the quicker onset of self-stimulation and of kindled seizures in Wistars is discussed.

Animals↗
PubMedDate not supplied

Investigation of influence of diazepam, valproate, cyproheptadine and cortisol on the rewarding ventral tegmental self-stimulation behaviour.

Experiments were carried on in the Wistar rats having self-stimulation (SS) electrodes implanted chronically in substantia nigra-ventral tegmental area (SN-VTA) to examine whether modulations of GABAergic, serotonergic, histaminergic, dopaminergic, and glucocorticoid neuronal receptor functions will affect or not the brain reward system and the SS behaviour. The modulators are the wellknown drugs: diazepam which is a facilitator of some of the GABA receptors, and used clinically for its tranquilizing, anxiolytic, sedative-hypnotic and anti-convulsant properties; sodium valproate which is known to enhance the GABA synapse function, and used clinically for its anti-convulsant property; haloperidol which is a dopaminergic receptor (D2) blocker, and clinically used for its anti-psychotic property; cyproheptadine which is both anti-histaminic and anti-serotonergic (blocks 5-HT2 receptor), used clinically for its antihistaminic and other beneficial properties; and hydrocortisone which is the stress-resisting glucocorticoid having direct effects on both brain and body cells, used clinically for the wide-ranging glucocorticoid therapeutic effects. The results revealed that systemic administration of these drugs, except haloperidol, caused no significant influence on the SS behaviour, thereby indicating that these nondopaminergic drugs have no effect on brain-reward system and also these categories of synaptic actions are not likely to be involved in the primary organization of the mechanisms of the brain-reward system.

Animals↗
PubMed1993

The tuberomammillary nucleus region as a reinforcement inhibiting substrate: facilitation of ipsihypothalamic self-stimulation by unilateral ibotenic acid lesions.

The tuberomammillary nucleus (TM), located in the posterior hypothalamic region, consists of five subgroups and is the only known source of brain histamine. Knowledge about the function of this nucleus is still scarce. In a previous study we found an increase in the rate of ipsihemispheric hypothalamic self-stimulation following a dc lesion in the rostroventral part of this nucleus, suggesting that this region has an inhibitory action on a neuronal reward system or on the brain's reinforcement mechanism. In the present study we examined whether this facilitating effect on reinforcement was due to the destruction of fibers passing through the lesion area or of intrinsic cells, by lesioning subgroups of the TM with ibotenic acid, an excitatory amino acid, that selectively destroys neural cell bodies, leaving fibers largely intact. Following such lesions in the rostroventral part of the TM the operant response rates increased over the six days of testing when the animals stimulated themselves in the lateral hypothalamus in the hemisphere located ipsilateral but not contralateral to the lesion. No significant changes in response rate occurred following the lesion in the caudal part of the ventral TM. The results indicate that the region influenced by the lesion exerts inhibitory control over lateral hypothalamic self-stimulation, and that it is possible that histamine-containing neurons are involved in this effect.

Animals↗
PubMed1981

The ecology of anxiety: situational stress and rate of self-stimulation in Turkey.

Twelve community behavior settings in Ankara, Turkey, were ranked with high agreement by 30 judges (average r = .80, p less than .001) according to the amount of situational stress, defined as evaluative apprehension and uncertainty, generated by each setting. The rate of hand-to- face or body (self-stimulation) behavior was observed systemically in stressful compared to relaxed settings. Analysis by a stepwise multiple regression procedure showed higher rates in stressful settings, F(1, 587) = 9.33, p less than .01. This finding was successfully replicated one year after the original study with new samples of settings, observers, and observed individuals, F(1, 351) = 7.38, p less than .01. Sex of the observed individuals had no relationship to rate of self-stimulation, and smoking appeared to act as a suppressor variable. These results suggest that other sources of variance from persons and Person X Situation interactions can be safely ignored if one's purpose in an investigation is to make ecological comparisons in anxiety rates.

Anxiety↗
PubMedDate not supplied

[Inhibitory effect of hydrocortisone and corticotropin on the self stimulation reaction].

The effect of hydrocortisone and ACTG on the frequency of self-stimulation reaction (SS) was studied. It was shown that hydrocortisone markedly suppresses the central mechanism of the positive reinforcement. SS frequency is lowered 10-15 minutes after the drug administration and recovered in one hour. The changes in the frequency of SS in response to ACTG are simular to the hydrocortisone effect, but are less intensive and in some cases depend on the location of the stimulating electrodes.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

[The effect of self-stimulation of the lateral hypothalamus on the sleep-waking cycle in rats during alcoholization].

Directed activation of a system of positive emotional reinforcement induces regulatory effect on limbic-neocortical mechanisms of the sleep-waking cycle organization in rats after chronic alcoholization carried out in periods of decreased and increased circadian rhythms of emotional activity. In animals with high level of positive emotional drive after the alcoholization self-stimulation of the lateral hypothalamus suppresses hypersynchronous paroxysmal activity in waking EEG, decreases the content of waking in the sleep-waking cycle, restores the paradoxical phase of sleep. In animals with inhibition of positive emotional drive in consequence of alcoholization self-stimulation of the lateral hypothalamus has no essential effect on the mechanisms of regulation of the sleep-waking cycle.

Alcohol Drinking↗
PubMedDate not supplied

Effects of an alcohol diet on locomotor activity and the acquisition of brain self-stimulation in rats.

Male rats (n = 45), implanted with stimulating electrodes in the lateral hypothalamus for intracranial self-stimulation (ICSS), were allocated to three groups equalized for body weights. One group was given an alcohol liquid diet (Lieber-DeCarli) diet as the sole source of food; a second group was given a control liquid diet in which carbohydrates were substituted for alcohol; and a third group was maintained on standard laboratory chow and water. After four weeks on these diets, all animals were tested during the fifth week of the diets for locomotor activity in five daily 15-min sessions, and their reactivity to handling was also measured. During the sixth and seventh weeks of the diets, animals were allowed to self-train for ICSS during daily 15-min sessions. In the eighth week blood alcohol levels were measured. There were no differences between groups in locomotor activity or reactivity to handling. However, when tested for the acquisition of ICSS, animals on the diet containing alcohol made fewer responses than did those receiving the two control diets (p less than 0.001). The mean blood level of alcohol in the alcohol-consuming group at the time of day of behavioral testing was 50.6 +/- 5.0 mg/dl. These results suggested that the chronic ingestion of an alcohol-containing diet which resulted in only moderate blood levels of alcohol may not affect simple behavior such as locomotor activity, but may produce decrements in the performance of a more complex task such as lever pressing for ICSS.

Analysis of Variance↗
PubMed1980

Effects of chronic amphetamine or reserpine on self-stimulation responding: animal model of depression?

The mood-altering properties of amphetamine (AMPH) in humans (euphoria and depression) have been postulated to be related to the increases and decreases respectively which this drug produces in the sensitivity of the reward system of the brain. The present study further evaluated this relationship by testing the effects of chronic reserpine (RES), another treatment that produces depression in humans, on self-stimulation responding. Separate groups of animals implanted with stimulating electrodes in the medial forebrain bundle were administered daily injections of saline, d-AMPH (5 mg/kg X 7 days followed by 10 mg/kg X 7 days), or RES (0.05 mg/kg X 18 days). At treatment termination, both drug groups showed a significant elevation of the reinforcement threshold, with no recovery occurring during 18 subsequent days. Thus, drug-induced depression of self-stimulation responding may serve as an animal model for studying the underlying physiological basis for clinical depression, or at the very least, for drug-induced depression.

Animals↗
PubMed1979

Arterial blood pressure and heart rate changes during self-stimulation by dogs in the basal forebrain region, lateral preoptic area, hypothalamus, ventral midbrain and amygdala.

In dogs pressing a lever for a brain-stimulation reward, arterial blood pressure (ABP) was elevated for 20 out of 24 sites tested, but this effect was usually conspicuous only at twice the threshold current sustaining stable performance. Hypertension was seen only in one ventral tegmental and two hypothalamic sites. In three anterior placements the ABP and heart rate (HR) increased more upon a fixed ratio than on continuous reinforcement. In most sites, self-stimulation was accompanied by cardiac acceleration; however, in some placements the HR was similar to or even less than control values. Continuous stimulation (5-10 sec) at one nucleus accumbens and four hypothalamic sites by the experimenter was aversive and produced a clearcut pressor response. The cardiovascular changes seem to depend on a spread of current to brain centres controlling circulatory functions and also, to some extent, on the animal's motor activity. The results contradict the claim that a causal relationship exists between the autonomic concomitants of self-stimulation and the intrinsic nature of the brain-stimulation reward.

Amygdala↗
PubMed1978

Hypothalamic-pituitary responses to intracranial self-stimulation in the rat.

The effects on pituitary and adrenal hormones of intracranial self-stimulation (ISS) and forced stimulation in rewarding (PS) and non-rewarding (NSS) sites were investigated in adult male rats. Growth hormone (GH) was suppressed during periods of ISS and PS and rose sharply to a peak within 15 min of cessation. The interval between GH secretory episodes was significantly shortened during all 3 types of stimulation when compared to the normal rhythmic discharge observed in freely behaving baseline (BL) sampled rats. ISS, PS and NSS resulted in a rapid rise in prolactin (Prl), which returned to normal by the end of each hourly period of stimulation. There was a significant reduction of Prl elevation in the second and third periods of stimulation, suggesting that the first exposure to ISS had a greater stimulatory effect than subsequent stimulations. There was a rapid and sustained release of corticosterone (CS) during ISS and PS. As with Prl, the initial period of either ISS or PS caused a greater effect that subsequent periods. These studies provide data to compare the relationship between ISS and neuroendocrine responses. The hormonal responses, with minor exceptions, were similar under all experimental conditions, and could not be clearly dissociated from previously described stress responses. Neural pathways and substrates involved in GH, Prl and CS secretion are discussed in relation to pathways activated by LH-MFB stimulation. Potential differential functions of monoamines and hypothalamic neuropeptides in behavioral and neuroendocrine regulation are hypothesized.

Animals↗
PubMed1983

Effects of apomorphine on self-stimulation responding: does the drug mimic the current?

The effects of apomorphine (APO) on self-stimulation responding were examined as a function of drug dose and stimulation current intensity. The lowest dose tested (0.02 mg/kg) significantly elevated the stimulation threshold, presumably reflecting the drug's preferential affinity for presynaptic dopamine (DA) receptors at this dose. At a dose which stimulates postsynaptic DA receptors (0.2 mg/kg), the rats responded with a pattern of behavior that resembled that obtained when non-drugged animals are given non-contingent current. However, during extinction, drugged animals were identical to non-drugged rats in their pattern of responding. These data indicate an interaction of APO with the stimulating current and suggest that APO may be mimicking only one component of the stimulation--perhaps the rewarding but not the motivating one.

Animals↗
PubMed1977

Hypothalamic self-stimulation under the chronic morphine treatment in the rat.

The influence of morphine on self-stimulation (SS) under chronic morphine administration (30 injections for 15 days) in increasing doses (from 20 to 20 mg/kg/injection) has been studied. Initial doses had a depressive effect varying in degree in different animals. Subsequent injections activated "reward" behavior. This activation is suggested as one of the neurophysiological mechanisms of morphine abuse and addiction.

Animals↗