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At least 1,279 records · Page 71Linked to original sources
PubMed1994

Ventilatory conditioning by self-stimulation in rats: a pilot study.

This article describes an experimental attempt to condition breathing pattern in rats. In this experiment, a freely moving rat was first rewarded by an electrical stimulation of the medial forebrain bundle whenever inspiratory duration (TI) exceeded 300 ms. A bidirectional control was then used: TIs longer than 400 ms were rewarded, and then TIs shorter than 300 ms were rewarded. The frequency of TIs longer than 300 ms increased when this event was rewarded, further increased when TIs above 400 ms were rewarded, and decreased during reversal conditioning (TI < 300 ms). At the beginning of the experiment, stimulation caused increased arousal and motor activity, but after prolonged conditioning, the brain stimulation was associated with quiet wakefulness. Although the general procedure appears to be well-suited to the experimental study of voluntary breathing, some possible improvements are suggested for further, more extensive investigations.

Animals↗
PubMed1983

Dissociating the determinants of self-stimulation.

Four experiments were conducted to elucidate the determinants of the initiation of and escape from electrical stimulation of the lateral hypothalamus under several different reinforcement schedules. The first experiment of this series used correlational and factor analytic techniques to show that, under continuous reinforcement, the vigour of initiation is determined more by forcement than by positive reinforcement. Forcement is defined as all of the performance changes directly elicited and potentiated by the stimulation. Escape is determined by adaptation of positive reinforcement, not by negative reinforcement or aversion. Continuous reinforcement schedules are, therefore, not appropriate for studying either the positive or negative reinforcement produced by brain stimulation. The second experiment used fixed-interval reinforcement schedules to eliminate the effects of forcement on initiation and adaptation of positive reinforcement on escape. Parametric manipulations indicate that activity in the positive reinforcement and escape systems is a simple function of stimulation charge. The combination of parameters which make up a given charge is of relatively little importance. However, the positive reinforcement system becomes maximally activated at far lower charges than does the escape system. The third experiment used a T-maze technique to show that, after 5 sec, anterior hypothalamic stimulation becomes negatively reinforcing, but posterior hypothalamic stimulation does not. Since the escape from posterior hypothalamic stimulation on a fixed-interval schedule can be dissociated from both negative reinforcement and adaptation of positive reinforcement, it is suggested that such escape is reinforced by a positive process triggered by the offset of stimulation (OFF positive reinforcement). The fourth experiment showed that stimulation trains longer than 10 sec are significantly less positively reinforcing than much shorter trains. This reduction in positive reinforcement confirms the development of negative reinforcement in long trains of hypothalamic stimulation, even at posterior electrodes. Negative reinforcement appears to be as general a property of hypothalamic stimulation as is positive reinforcement. Thus, depending on the reinforcement schedule and electrode site, the initiation of lateral hypothalamic stimulation may be determined by ON positive reinforcement, OFF positive reinforcement and forcement. Escape may be determined by OFF positive reinforcement, adaptation of positive reinforcement and negative reinforcement.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

Prevention of stressor-induced disturbances of self-stimulation by desmethylimipramine.

Following exposure to uncontrollable footshock mice displayed a pronounced reduction of responding for electrical brain stimulation from the nucleus accumbens. In mice that received repeated treatment with the tricyclic antidepressant, desmethylimipramine, the shock induced reduction of responding was attenuated. It was suggested that, among other things, uncontrollable stressors result in disturbances of motivational/reward processes, which are antagonized by repeated treatment with desmethylimipramine.

Animals↗
PubMed1982

Increases in dopamine metabolism are not a general feature of intracranial self-stimulation.

Rats with electrodes implanted in the ventral tegmentum and posterior hypothalamus were trained to press a lever to obtain electrical stimulation through the electrodes. Stimulation in animals with ventral tegmental electrodes led to an increased concentration of homovanillic acid and dihydroxyphenylacetic acid in the forebrain of the animals. Stimulation in the posterior hypothalamus did not result in such raised concentrations in spite of the fact that the behaviour from the two sites was indistinguishable. Responding in the posterior hypothalamus was reduced by doses of neuroleptic drug similar to those reported to reduce responding in the ventral tegmental area.

Animals↗
PubMed1988

Analgesia produced by vaginal self-stimulation in women is independent of heart rate acceleration.

In the present study, the analgesia produced by vaginal stimulation (VS) in women was found to be dissociated from heart rate. The VS-produced analgesia was not accompanied by an acceleration of heart rate. Heart rate acceleration produced by exercise did not result in analgesia. The independence of VS-produced analgesia from this index of autonomic activity is consistent with recent findings in rats.

Analgesia↗
PubMed1976

Bromperidol, a new potent neuroleptic of the butyrophenone series. A comparison of the effects of bromperidol and haloperidol in intracranial self-stimulation.

Bromperidol, a new potent and long-acting neuroleptic of the butyrophenone series, and haloperidol were injected s.c. at the doses 0.01, 0.02, 0.04 and 0.08 mg/kg, in rats implanted with electrodes in the lateral hypothalamic region of the medial forebrain bundle. A dose-related response inhibition was found with both compounds and the graphically estimated ED50 value was 0.041 mg/kg for bromperidol and 0.047 mg/kg for haloperidol. These data are in complete agreement with our previous findings that bromperidol is a new potent and specific neuroleptic.

Animals↗
PubMed1989

Effects of D2 dopamine receptor blockade with raclopride on intracranial self-stimulation and food-reinforced operant behaviour.

To examine the involvement of D2 dopamine receptors in the neural mechanism of reinforcement, raclopride tartrate, a D2 specific dopamine antagonist with a relatively fast central action, was injected into 32 rats. The D2 antagonist reduced bar-pressing responses reinforced with electrical stimulation of the ventral tegmental area (ED50 = 0.079 mumol/kg) and those reinforced with food (ED50 = 0.58 mumol/kg) in 18-30 min after IP injection. The reduction in response rates could not be attributed to an interference with motor functions. An increase in the frequency of brain-stimulation pulses and a change in the schedule of food reinforcement, which respectively increased the baseline rate of responding, did not alter the effectiveness of raclopride. SCH 23,390, a D1-specific dopamine antagonist, was sensitive to similar manipulation of reinforcement. These results seem to suggest that D1 and D2 antagonists may be acting at different locations in the neural mechanism underlying the reinforcement of operant behaviour.

Animals↗
PubMed1975

Differential antagonism by the antichlolinergic dexetimide of inhibitory effects of haloperidol and fentanyl on brain self-stimulation.

Haloperidol (0.08 mg/kg) or fentanyl (0.16 mg/kg) injected subcutaneously suppressed bar-pressing for brain-stimulation in rats, implanted with electrodes in the lateral hypothalamic area of the medial forebrain bundle. Increasing doses: 0.04, 0.16, 0.63 and 2.50 mg/kg of the central anticholinergic dexetimide gradually antagonized the haloperidol effects. The highest dose of dexetimide did not reduce the fentanyl-induced inhibition. The results, together with a literature survey on the anticholinergic effects on neuroleptic-induced catalepsy and inhibition of avoidance behavior, are related to biochemical findings and clinical effects.

Animals↗
PubMed2000

Hypoinsulinemia may mediate the lowering of self-stimulation thresholds by food restriction and streptozotocin-induced diabetes.

7 days beyond cessation of insulin treatment) elevation of threshold in ad libitum fed rats and, more transiently, reversed the threshold-lowering effect of food restriction. Acute insulin treatment (3 mU, 15 min prior) also elevated threshold in food-restricted rats. These results are consistent with the hypothesis that insulin modulates sensitivity of a brain reward system and that hypoinsulinemia may be the common factor in food restriction and diabetes that accounts for the enhancement of perifornical LHSS.

Animals↗
PubMedDate not supplied

Effects of intracranial self-stimulation on brain opioid peptides.

The neurochemical system(s) underlying brain stimulation reward (ICSS) has been investigated for many years. The catecholamine hypothesis is currently most accepted with predominant emphasis on the role of dopamine. The present report examines the role of three opioid peptides--Methionine and Leucine Enkephalin (ME and LE) and beta-Endorphin (beta-E) in this behavior. Peptide levels from pituitary, hypothalamus and whole brain were determined by independent RIAs and analyzed according to treatment: low, moderate and high ICSS responders, sham controls, animals receiving nonspecific stimulation, and naloxone--with and without ICSS. Not only did naloxone reduce ICSS from high responders by 74%, it also was able to reduce peptide levels--most notably for ME and beta E in most regions. Additionally, the effects of ICSS on endorphin levels was found to be related to the rate category of responding. Since endorphins are known to interact with dopamine systems, it is therefore considered likely that the endogenous opioid peptides play an important role in ICSS either directly or indirectly via their influence on catecholamine systems.

Animals↗
PubMed1999

A dopamine D1 agonist elevates self-stimulation thresholds: comparison to other dopamine-selective drugs.

The effects of the high-efficacy D1 receptor agonist SKF 81297 and the D2/3 receptor agonist 7-OH-DPAT on brain stimulation reward thresholds and on response latencies in responding for the stimulation, were compared to the effects of subtype-selective receptor antagonists and a dopamine uptake blocker. SKF 81297 produced dose-dependent elevations in reward thresholds but did not alter response latencies. In contrast, 7-OH-DPAT produced inconsistent reward threshold elevations, yet dose dependently increased response latencies. Both the dopamine D1 receptor antagonist SCH 23390 and the D2 antagonist raclopride elevated reward thresholds, but only raclopride significantly increased response latencies. The dopamine uptake inhibitor GBR 12909 lowered reward thresholds and did not influence response latencies. The present results provide a clear demonstration that a selective, high-efficacy D1 receptor agonist elevates brain stimulation reward thresholds without producing performance deficits. Furthermore, it was observed that the effects upon reward measures of D1-selective compounds, but not D2/D3-selective compounds, are dissociable from their effects upon response latency in this task. These results are discussed with regard to a distinction between the effects of indirect and direct dopamine agonists on reward thresholds, a distinction that does not depend upon the subtype-selectivity of the direct agonists tested.

Animals↗
PubMed1990

Chronic low-dose haloperidol effects on self-stimulation rate-intensity functions.

Animals responding for biphasic square wave stimulation to the VTA were treated for 26 days with a low dose (0.07 mg/kg) of the neuroleptic haloperidol and tested at 1 h post-injection. Initially the drug induced a pronounced lateral displacement of the baseline rate-intensity function, concomitant with a depression in slope. Over the course of chronic treatment, partial tolerance was observed to the drug-induced increases in threshold concomitant with the onset of a significant suppression in peak response rate. Biochemical tolerance to stimulated dopamine metabolism (as per cent non-drug control) was significant only for mesolimbic (versus neostriatal) regions, in animals receiving haloperidol according to pre- and post-test administration schedules. The observation of sensitization to peak rate reductions parallels previous reports for spontaneous locomotor activity measures and is compatible with depolarization inactivation mechanisms proposed to account for delayed-onset clinical effects. Further, selective biochemical tolerance in mesolimbic regions supports suggestions that mesolimbic dopamine is important as a substrate for subtle low dose neuroleptic effects which may be relevant for studying pharmacotherapeutic treatment issues.

Animals↗
PubMed1989

Regional neuroleptic microinjections indicate a role for nucleus accumbens in lateral hypothalamic self-stimulation reward.

Bilateral microinjections of the neuroleptic, cis-flupenthixol, were made into 56 forebrain targets distributed across various dopamine (DA) terminal fields in the forebrain. Drug effects on medial forebrain bundle (MFB) stimulation-produced reward were assessed with a rate-frequency procedure implemented in a runway paradigm in a discrete-trial fashion. This method generated independent measures of drug-induced changes in the MFB stimulation reward and operant motor/performance capacity. Control experiments were run with the inactive isomer, trans-flupenthixol. Results indicate a major role for accumbens DA in MFB reward, but not for the DA in caudate and medial frontal cortex. Few drug-induced motor/performance deficits were found at any site. In 14 selected subjects, 6-OHDA-induced chronic DA lesions were made at the same site as neuroleptic microinjection. These results confirmed the reward effects of acute DA receptor blockade, but produced a greater associated motor/performance impairment. Both behavioral effects of the lesion recovered within 2 weeks in many, but not all subjects.

Animals↗
PubMed1991

The effects of dopaminergic agonists and antagonists on the frequency-response function for hypothalamic self-stimulation in the rat.

The function of dopaminergic synapses in generating the reinforcing effect of brain stimulation was examined in 8 rats. The animals were implanted with bipolar electrodes and trained to press a bar for lateral hypothalamic stimulation. The frequency of stimulation pulses was systematically changed, and a frequency-response curve was plotted for each rat after intraperitoneal injection of a test agent. Dopamine agonists and antagonists selective to either D1 or D2 subtypes of receptors were used. The curve was shifted to a high-frequency range by either SCH 23390 (D1 antagonist) or raclopride (D2 antagonist). SKF 38393 (D1 agonist) failed to shift the curve, and quinpirole and CV 205-502 (D2 agonists) shifted the lower part of the curve to a low-frequency range. The results suggest that an activation of D2 receptors generates a reinforcing effect, and that the effect is expressed only if D1 receptors are activated to an optimal level.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1976

Comparison of the effects of morphine on hypothalamic and medial frontal cortex self-stimulation in the rat.

The effect of morphine (3.75, 7.5, and 15.0 mg/kg, s.c.) on medial frontal cortex (MF) and hypothalamic self-stimllation (SS) was determined 1, 3, 5, and 7 h after injection for 5 consecutive days. Morphine suppressed or enhanced SS responding as a function of dose, time after injection, and the site stimulated. The MF SS groups were less sensitive to the toxic effects of morphine, and evidenced elevated rates of responding earlier after injection than the hypothalimic animals. The dose-response relationship of the MF rats, thus, clearly differed from that of the hypothalamic rats. With repeated administration, tolerance was rapidly (3-4 days) developed to the suppressive effect while the excitatory effect appeared earlier and tended to be enhanced, peaking 1 and 3 h after injection in the MF and hypothalamic groups, respectively. These data provide additional evidence against the hypothesis that the effect of morphine on SS behavior is non-specific. If it were, the time course and degree of effects should be similar, regardless of the electrode site tested. Furthermore, an inhibitory effect was not observed in the groups receiving 3.75 mg/kg although both showed a significant increase in responding 1 and/or 3 h after injection. This observation indicates that the excitatory effect is not dependent on the depressant effect and, therefore, probably is not a rebound phenomenon. It also suggests that the toxic effects of morphine can either mask or delay the appearance of its facilitatory action on SS responding.

Animals↗
PubMed1985

Effects of opioid antagonists and their quaternary derivatives on locomotor activity and fixed ratio responding for brain self-stimulation in rats.

Rats were implanted with stimulating electrodes aimed at the midbrain-central gray area (MID-CG) and trained to lever press for brain stimulation (ICSS) on a fixed ratio:30 (FR:30) schedule of reinforcement. When response rates were stable, animals were administered either naloxone hydrochloride, naltrexone hydrochloride, naloxone methobromide or naltrexone methobromide in a dose range of 0.1-30 mg/kg. Fifteen minutes after the subcutaneous administration of either drug or vehicle, animals were tested for 45 min in the ICSS procedure and changes in response rates following drug administration were compared with those following vehicle administration. Both naloxone and naltrexone hydrochloride produced graded decreases in responding over the entire dose range, while naloxone and naltrexone methobromide did not alter response rates at any dose level. In a separate testing procedure, 30 mg/kg naloxone and naltrexone hydrochloride produced modest reductions in motor activity, while the methobromide derivatives did not. These results demonstrated that the fixed ratio procedure was sensitive to changes in responding for ICSS produced by opioid antagonists, and this effect depends upon the entry of these opioid antagonists into the brain.

Animals↗
PubMed1989

Interactions of diazepam and pentobarbital with RO 15-4513 on intracranial self-stimulation discrimination behavior in rats.

Rats implanted with electrodes in the lateral hypothalamus were trained in a discrete trial procedure to make a differential response (right or left lever press) in the presence or absence of brain stimulation. When a high level of accuracy (95% correct) was attained in the discrimination, testing with vehicle, RO 15-4513, diazepam (1.0-10 mg/kg), diazepam plus RO 15-4513 (1.0 mg/kg), pentobarbital (1.0-17.5 mg/kg) and pentobarbital plus RO 15-4513 began. Diazepam, at 10 mg/kg, disrupted the discrimination behavior, and it also decreased the total number of lever-presses and increased the time to complete the session. These effects were blocked by the coadministration of 1.0 mg/kg RO 15-4513. Pentobarbital produced effects similar to those of diazepam, but these effects were only reversed to a limited extent by RO 15-4513. By itself, however, RO 15-4513 also decreased the total number of lever presses and increased the time to complete the session. Results were consistent with our previous findings with alcohol and RO 15-4513, and supported the notion that diazepam and alcohol have some similar effects at the GABA-benzodiazepine receptor complex.

Animals↗
PubMed1975

Effects of d- versus l-amphetamine, food deprivation, and current intensity on self-stimulation of the lateral hypothalamus, substantia nigra, and medial frontal cortex of the rat.

Intracranial sefl-stimulation (ICSS) was studied in rats with chronically implanted lateral hypothalamic, substantia nigra, or medial frontal cortex bipolar electrodes. A comparison of the effects of d- and l-amphetamine on ICSS response rate indicated that the d isomer had a greater facilitatory effect than the l isomer at lateral hypothalamic and substantia nigra electrode sites but that neither isomer significantly affected medial frontal cortex ICSS. d-Amphetamine resulted in a dose-related increase in motor activity, but the same doses of the l isomer resulted in decreased motor activity. Only lateral hypothalamic ICSS response rates increased significantly in response to food deprivation. Increases in current intensity above the level used for amphetamine and food-deprivation testing facilitated lateral hypothalamic and substantia nigra ICSS response rates but did not significantly affect medial frontal cortex response rates. The responsiveness of ICSS at each electrode site appeared to be correlated with the fiber- and cell-body densities of catecholaminergic systems in the brain.

Amphetamine↗