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PubMed1985

Behavioral and neurochemical effects of deprenyl and beta-phenylethylamine in Wistar rats.

The effects of 1-deprenyl (1-16 mg kg-1, 3.5 hr) on brain levels of endogenous beta-phenylethylamine were assessed in animals under three conditions: (1) experience of lateral hypothalamic self-stimulation; (2) electrode implantation but no self-stimulation experience; (3) no surgical intervention. The increase in striatal levels of beta-phenylethylamine with 1-deprenyl treatment was attenuated in the self-stimulation condition relative to conditions (2) and (3). This differential effect of 1-deprenyl was not observed at the level of the hypothalamus. Administration of 1-deprenyl did not affect self-stimulation behavior. Equivalent analysis of beta-phenylethylamine levels was carried out using animals injected with beta-phenylethylamine (0.5-4 mg kg-1, 0.5 hr 1P and 1-deprenyl (4 mg kg-1, 3.5 hr sc). Injected beta-phenylethylamine with deprenyl pretreatment increased self-stimulation rates; concomitant striatal levels of approximately 190 ng g-1 of beta-phenylethylamine were observed and were associated with increased brainstem 5-HIAA but no change in striatal HVA, indicating possible involvement of 5-HT in this response to beta-phenylethylamine. It is proposed that experience of electrical hypothalamic stimulation may alter endogenous striatal beta-phenylethylamine metabolism, possibly via an alteration of mechanisms governing synthesis and/or catabolism.

Animals↗
PubMed2005

Roles of pedunculopontine tegmental cholinergic receptors in brain stimulation reward in the rat.

RATIONALE: The brainstem pedunculopontine tegmental nucleus (PPTg) is proposed to mediate hypothalamic self-stimulation reward via cholinergic activation of the ventral tegmental area (VTA). However, to date there is little direct evidence to support this hypothesis. OBJECTIVES: To further study the role of PPTg in hypothalamic self-stimulation reward. METHODS: By using in vivo microdialysis, the levels of extracellular acetylcholine (ACh) in the PPTg and VTA were detected during lateral hypothalamic (LH) self-stimulation in rats. Rate-frequency curve shift procedure was used to evaluate the effects of nonselective muscarinic antagonist scopolamine (1 approximately 100 microg/microl) and nicotinic antagonist mecamylamine (5 approximately 100 microg/microl) microinjected into the PPTg on the rewarding efficacy of LH self-stimulation. Subsequently, the drugs were injected into the PPTg, and the extracellular ACh in the VTA was measured. RESULTS: LH self-stimulation produced a concurrent ACh release in the PPTg and VTA. Intra-PPTg injection of scopolamine (100 microg/microl) significantly reduced the frequency threshold for LH self-stimulation reward, but nicotinic antagonist mecamylamine did not shift the threshold. However, mecamylamine (10, 25 microg/microl) injected into the PPTg robustly diminished the nicotine-potentiated LH self-stimulation reward. The extracellular ACh in the VTA was dramatically increased by intra-PPTg scopolamine (10, 100 microg/microl), but not by mecamylamine. CONCLUSIONS: Results confirm that PPTg plays an important role in brain stimulation reward by modulating the cholinergic activity of the VTA. The PPTg muscarinic receptors contribute to an inhibitory modulation of reward effects by self-stimulation, whereas nicotinic receptors seem to be more involved in nicotine potentiation of brain stimulation reward.

Acetylcholine↗
PubMed1985

Elevation of pain threshold by vaginal stimulation in women.

In 2 studies with 10 women each, vaginal self-stimulation significantly increased the threshold to detect and tolerate painful finger compression, but did not significantly affect the threshold to detect innocuous tactile stimulation. The vaginal self-stimulation was applied with a specially designed pressure transducer assembly to produce a report of pressure or pleasure. In the first study, 6 of the women perceived the vaginal stimulation as producing pleasure. During that condition, the pain tolerance threshold increased significantly by 36.8% and the pain detection threshold increased significantly by 53%. A second study utilized other types of stimuli. Vaginal self-stimulation perceived as pressure significantly increased the pain tolerance threshold by 40.3% and the pain detection threshold by 47.4%. In the second study, when the vaginal stimulation was self-applied in a manner that produced orgasm, the pain tolerance threshold and pain detection threshold increased significantly by 74.6% and 106.7% respectively, while the tactile threshold remained unaffected. A variety of control conditions, including various types of distraction, did not significantly elevate pain or tactile thresholds. We conclude that in women, vaginal self-stimulation decreases pain sensitivity, but does not affect tactile sensitivity. This effect is apparently not due to painful or non-painful distraction.

Adult↗
PubMedDate not supplied

Interrelationships of the emotionally positive and negative regions of the brain of the edible snail.

The changes in the behavior of the garden snail during self-stimulation through electrodes chronically implanted in specific regions of the brain are described in this study. The stimulation of the mesocerebral region led to an increase in the frequency of reinforced behavior, whereas stimulation of the rostral portion of the parietal ganglia led to a decrease in the frequency of reinforced behavior. An inference is reached regarding the emotional coloration of the effects of the stimulation of these regions. The interrelationships of the neurons located in the mesocerebrum and the parietal ganglia were studied in neurophysiologic experiments. It was found that the activation of the cells of the mesocerebrum inhibits the spontaneous activity of the serotoninergic cells of the pedal ganglia which sensitize the defensive reactions of the snail, and simultaneosly attenuate the sensory input of the command neurons of defensive behavior, which leads to the effective inhibition of the defensive reactions that is necessary during the activation of sexual behavior.

Animals↗
PubMed1989

Chronic imipramine does not block cocaine-induced increases in brain stimulation reward.

Self-stimulating rats implanted with ventral tegmental area electrodes were tested with 15 mg/kg cocaine HCl before and after chronic imipramine treatment. Chronic imipramine had no influence on cocaine's ability to lower brain stimulation reward thresholds, suggesting that tricyclic antidepressant treatment does not block cocaine-induced euphoria.

Animals↗
PubMed1999

Influence of bombesin on threshold for feeding and reward in the rat.

Bombesin's purported role in satiety mechanisms prompted this investigation of its effects on thresholds for stimulation-induced feeding and self-stimulation in the rat. Single electrodes were implanted in the lateral hypothalamus and the ability of each electrode to support self-stimulation and stimulation-induced feeding was evaluated at four current levels between 80 and 320 microA. The frequency thresholds associated with each current value were assessed following four intraperitoneal doses of bombesin, 2, 4, 8, and 16 micrograms/kg, as well as a saline dose. Bombesin increased the thresholds for stimulation-induced feeding at doses known to reduce food intake without influencing self-stimulation thresholds. From these findings we conclude that (1) the effects of peripheral bombesin on stimulation-induced feeding are analogous to its effects on normal feeding and (2) the data provide additional evidence for a pharmacological dissociation between stimulation-induced feeding and reward.

Animals↗
PubMed1986

Sex difference in reward asymmetry and effects of cocaine.

Male and female rats with bilaterally implanted electrodes in the lateral hypothalamus were tested daily for self-stimulation of each side of the brain, and rotation (circling behavior) was recorded concomitantly. All rats rotated in a preferred direction, regardless of the side of the brain stimulated, and all rats had asymmetries in the sensitivity for self-stimulation (thresholds and rate-intensity functions) related to the direction of rotation. However, the direction of the asymmetry of self-stimulation was sex-dependent: the side of the brain contralateral to the preferred direction of rotation was the more sensitive side in female rats, as reported previously, whereas the ipsilateral side was the more sensitive side in male rats. In both sexes, cocaine acted predominantly on the contralateral side: that is, cocaine lowered the thresholds and shifted the rate-intensity functions to the left on both sides of the brain, but the effects were much greater on the side of the brain contralateral to the preferred direction of rotation. When compared to baseline parameters, cocaine enhanced the asymmetry of self-stimulation in female rats, but reduced or reversed the asymmetry of self-stimulation in male rats; similar effects were produced by d-amphetamine. It is suggested that at least two separate systems (both lateralized) mediate self-stimulation of the lateral hypothalamus, that the relative importance of these systems differs between the sexes and that cocaine selectively affects one of these systems.

Animals↗
PubMed1980

Effects of d-amphetamine and naloxone on brain stimulation reward.

Self-stimulation thresholds were determined in rats by means of a modification of the psychophysical method of limits. Reinforcement values were determined after the administration of d-amphetamine alone, naloxone alone, and naloxone administered concurrently with d-amphetamine. d-Amphetamine yielded dose-related decreases in the threshold (0.25--2.00 mg/kg IP), while naloxone alone (2.0--16 mg/kg IP) caused no consistent changes. For each animal, a dose of d-amphetamine that substantially lowered the threshold was then selected to be administered with varying doses of naloxone. The threshold-lowering effect of d-amphetamine was blocked by naloxone at doses as low as 2.0 or 4.0 mg/kg. This finding suggests the possible involvement of an opiate receptor in the mediation of the enhancement by d-amphetamine of brain stimulation reward.

Animals↗
PubMed1994

Experimental estimation of addictive potential of a mixture of organic solvents.

In the present study we investigated in rats the reinforcing properties of glue vapours which are a mixture of four organic solvents (toluene 25%, benzine fraction 37%, ethyl acetate 31% and methylene chloride 7%). This mixture is used as a glue thinner and is a very popular among glue-sniffing children. Immediately after inhalation at a concentration of 7200 ppm, the glue vapours increased locomotor activity in the open field and response rate of self-stimulation in the lateral hypothalamus. Contrary to classical drug abuse, glue vapours enhanced the threshold current of self-stimulation. While the response rate of self-stimulation decreased to the control level 30 min after inhalation, the threshold current was still enhanced. Increasing the concentration of the vapours produced a decrease in response rate of self-stimulation and locomotor activity. When glue vapours were inhaled at a concentration of 14,400 ppm and higher, the response rate of self-stimulation was completely suppressed. The discriminative stimulus effects of the glue vapours appeared to be similar to those of general anaesthetics such as ether and pentobarbital. At vapour concentrations of 7200 and 14,400 ppm, conditioned place preference was established. The ability of solvents to reinforce conditioning in the place preference paradigm and to activate the brain reward system in intracranial self-stimulation experiments may be useful for predicting the addictive potential of inhalants.

Administration, Inhalation↗
PubMed1995

The bidirectional interaction between ventral tegmental rewarding and hindbrain aversive stimulation effects in the rat.

We used the curve-shift procedure in self-stimulating rats to examine the interaction of aversive and rewarding electrical stimuli in terms of duration and direction. The subjects were implanted with two moveable electrodes, one in a region supporting self-stimulation (the ventral tegmental area, VTA) and another in a region supporting escape (the nucleus reticularis gigantocellularis, Gi). The function relating self-stimulation rate to pulse frequency (RF function) was first obtained and then replicated in a condition where each VTA pulse was followed 0.2 or 2.0 ms later by a Gi pulse. The intensity of Gi pulses was set at a value previously found to elicit escape within less than 5 sec. The following observations were made: (1) rats self-stimulated consistently, despite the presence of Gi pulses, (2) the presence of Gi pulses shifted the RF function rightward (decreased the rewarding efficacy of VTA stimulation), with little effect on the maximum rate, (3) after 2 to 5 VTA-Gi self-stimulation sessions, the Gi pulses progressively lost their ability to shift the RF function, and (4) at the end of testing, escape was no longer detectable using Gi pulses alone. It was concluded that (1) the interaction between rewarding VTA and aversive Gi stimulation effects is bidirectional, thus suggesting the presence of algebraic summation; (2) the effect of Gi on VTA reward is transient whereas that of VTA on Gi aversion cumulates and eventually results in total abolition of Gi aversion. The present study represents the first account of cumulative and long-lasting suppression of aversion following brain stimulation in the rat.

Animals↗
PubMed2002

Study of cannabinoid dependence in animals.

Different animal models have been used to clarify the consequences of chronic exposure to cannabinoid agonists and their abuse liability. Following the chronic administration of cannabinoids, tolerance develops to most of their pharmacological effects. The development of cannabinoid tolerance is particularly rapid, and seems to be due to pharmacodynamic events. A cross-tolerance among different exogenous cannabinoid agonists has been reported. Somatic signs of spontaneous withdrawal have not been reported after chronic Delta(9)-tetrahydrocannabinol (THC) treatment, but were observed after chronic treatment with the cannabinoid agonist WIN-55,212-2. The administration of the CB(1) cannabinoid antagonist SR141716A in animals chronically treated with THC and other cannabinoid agonists precipitated somatic manifestations of withdrawal. The potential ability of anandamide to induce physical dependence has not been clarified. Subjective drug effects of cannabinoids have been reported by drug discrimination studies, which show cross discrimination among different natural and synthetic agonists. The rewarding effects of cannabinoids have been revealed by using several paradigms: place conditioning, intracranial self-stimulation, and self-administration. Cannabinoids have been reported to lower intracranial self-stimulation thresholds in rats. However, particular experimental conditions are required to induce conditioned place preference with cannabinoids. Numerous studies have shown that THC is unable to induce a self-administration behaviour in animals. However, WIN-55,212-2 was intravenously self-administered in mice, and monkeys that had a previous history of cocaine self-administration also self-administered THC. The mesolimbic dopaminergic system seems to be the substrate for the rewarding properties of cannabinoids.

Animals↗
PubMed1979

Serotonergic mediation of reward within the medial raphe nucleus: some persistent problems in interpretation.

Adult male Sprague Dawley rats were implanted with unipolar stimulating electrodes aimed at the medial forebrain bundle (MFB) or the medial raphe nucleus (MR). All MFB implanted subjects self-stimulated at high stable rates for at least three weeks. Only a minority (1/3) of MR rats self-stimulated at all. Rates for the MR group were considerably more variable, and could not be maintained for more than two weeks. Treatment with methysergide increased MFB self-stimulation but decreased MR self-stimulation. While this result suggests serotonergic mediation of self-stimulation this conclusion must be interpreted cautiously since parachlorophenylalanine (PCPA) reinstated self-stimulation in raphe animals which had spontaneously ceased responding.

Animals↗
PubMed1978

Sensory extinction: a procedure form eliminating self-stimulatory behavior in developmentally disabled children.

This study was designed to investigate the role of sensory reinforcement in the motivation of self-stimulation. If self-stimulatory behavior is maintained by its sensory consequences, such as the proprioceptive, auditory, or visual stimulation it produces, then such behavior should extinguish when those sensory consequences are not permitted. The present study introduces a new procedure, Sensory Extinction, in which certain sensory consequences are masked or removed, to examine whether self-stimulation is operant behavior maintained by sensory reinforcement. The effectiveness of Sensory Extinction was assessed by a reversal design for each of three autistic children, and the results showed the following. First, self-stimulation reliably extinguished when a certain sensory consequence was removed, then increased when that consequence was permitted. This was replicable within and across children. Second, different Sensory Extinction procedures were required for different self-stimulatory behaviors, since the sensory reinforcers supporting them were idiosyncratic across children. Finally, regarding clinical gains, the data suggest that Sensory Extinction may be a relatively convenient and rapid alternative for the treatment of self-stimulation. The present findings extend the efficacy of extinction as a behavior-modification technique to instances in which the reinforcer is purely sensory. The implications of these results for the treatment of other forms of deviant behavior are discussed.

Autistic Disorder↗
PubMed1981

Amphetamine enhancement of reward asymmetry.

Rats with bilaterally implanted lateral hypothalamic electrodes were tested daily for self-stimulation to each side of the brain; rotation (circling behavior) was recorded concomitantly. All rats rotated in a perferred direction regardless of the side of the brain stimulated and all rats had asymmetries in self-stimulation sensitivity (threshold and rate-intensity functions) related to the direction of rotation. Amphetamine both enhanced rotation and potentiated the asymmetry in self-stimulation sensitivity. Subsequently rats were tested in a choice procedure providing concurrent access to rewarding stimulation of either side of the brain; currents were titrated such that, under baseline conditions, rats continually alternated between self-stimulating one side of the brain or the other. Amphetamine induced a robust preference for stimulation to the more sensitive side of the brain (the side having a lower threshold). The results are discussed in relation to mechanisms of drug reinforcement and to biological etiologies of schizophrenia. It is proposed that schizophrenia results from a lateralized overactivity of dopaminergic neuronal systems mediating reward and that amphetamine mimics schizophrenic symptomatology by enhancing lateralization of the same systems.

Amphetamine↗
PubMed1980

Neurophysiological analysis of brain-stimulation reward in the monkey.

Neuronal activity related to brain-stimulation reward and to feeding was analyzed in rhesus monkeys and squirrel monkeys as follows. First, self-stimulation of the lateral hypothalamus, orbitofrontal cortex, amygdala and nucleus accumbens was found. Second, a population of single neurones in the lateral hypothalamus was found to be trans-synaptically activated from one or several self-stimulation sites. It was also found to populations of neurones in the orbitofrontal cortex and amygdala were activated from at least some of the self-stimulation sites. Thus, in the monkey, there is evidence for an interconnected set of self-stimulation sites, stimulation in any one of which may activate neurones in the other regions. These sites include the lateral hypothalamus, amygdala, and orbitofrontal cortex. Third, in one sample of 764 neurones in the lateral hypothalamus and substantia innominata which were activated from brain-stimulation reward sites, 13.6% were also activated during feeding, by the sight and/or taste of food. The responses of the neurones with activity associated with taste occurred only while some substances (e.g. sweet substances such as glucose) were in the mouth, depended on the concentration of the substances being tasted, and were independent of mouth movements made by the monkeys. Fourth, the responses of these neurones occurred to food when the monkeys were hungry, but not when they were satiated. Fifth, self-stimulation occurred in the region of these neurones in the lateral hypothalamus and substantia innominata, and was attenuated by satiety. These results suggest that self-stimulation of some brain sites occurs because of activation of neurones in the lateral hypothalamus and substantia innominata activated by the sight and/or taste of food in the hungry animal, and that these neurones are involved in responses to food reward.

Amygdala↗
PubMed1987

Summation and saturation properties in the rewarding effect of brain stimulation.

We used a two-lever self-stimulation chamber and rats with central grey and hypothalamic electrodes to obtain a choice-frequency (C/F) function, which plots the relative choice of an electrical stimulus of fixed pulse frequency (the standard stimulus) as a function of the frequency of a second competing stimulus (the alternative stimulus). A family of C/F functions was obtained using increasing frequencies for the standard. A choice index, varying from -1.0 (exclusive choice of the fixed stimulus) to 1.0 (exclusive choice of the alternative stimulus) was computed by using the barpressing rates on the two levers. Reward saturation was assumed to occur when the C/F function obtained with the largest standard reached an asymptote below the value of 1.0. For the hypothalamic subjects, the pulse frequency at the point of reward saturation was twice as high as the frequency required for the maximum rate of self-stimulation in the usual single-lever chamber. Decreasing the pulse intensity always increased the saturation frequency, indicating that the saturation was not due to a frequency blocking effect in the directly activated neurons. Reward saturation occurred with a considerably higher frequency in the central grey than in the hypothalamus. Thus, the asymptotic rate of self-stimulation in the usual single-lever chamber is not conditioned by the processes that summate the central grey and hypothalamic rewarding effects. From the central grey data we obtained the relation between the slope and the position of the C/F function on the frequency axis. We used the slope/frequency profile to delimit the most probable profile of summation rate in the rewarding process. We found that the slope/frequency function has an early plateau followed by a rapidly decelerating phase. We proposed that these two distinct phases reflect an early accelerating rate of summation, followed by a decelerating rate of summation. In other words, reward summation would be predicted by a sigmoid growth model.

Animals↗
PubMedDate not supplied

Neurochemical correlates of brain-stimulation reward measured by ex vivo and in vivo analyses.

Evidence from ex vivo analyses of dopaminergic function following self-stimulation behavior is reviewed and compared to in vivo analyses of extracellular dopamine measured by chronoamperometry during self-stimulation. Both data bases provide strong support for a dopaminergic substrate for brain-stimulation reward obtained by electrical stimulation of the ventral tegmental area (VTA). Data obtained from in vivo measures of dopamine release are particularly compelling as a positive correlation was observed between the rate/intensity function for self-stimulation and increments in the oxidation current for dopamine. An examination of the effects of the dopamine uptake blockers, cocaine and GBR 12909 on self-stimulation and stimulated release of dopamine revealed a facilitation of both measures. In contrast, the noradrenaline uptake blocker desipramine had no effect on either self-stimulation or extracellular dopamine. These pharmacological experiments also are consistent with a dopaminergic substrate of brain-stimulation reward at electrode sites in the VTA.

Animals↗
PubMed1986

Amphetamine withdrawal: a behavioral evaluation.

The effects of withdrawal from long-term amphetamine treatment of intracranial self-stimulation, forced swim-induced immobility, shuttle escape performance, acoustic startle and locomotor activity were evaluated. Mice implanted with stimulating electrodes in the lateral hypothalamus demonstrated stable and reliable rates of self-stimulation responding. After exposure to a chronic schedule of amphetamine treatment response rates were severely depressed. In addition to modifying intracranial self-stimulation responding, amphetamine withdrawal increased the duration of immobility in a forced-swim situation. Although chronic amphetamine exposure induced pronounced behavioral changes in the intracranial self-stimulation and forced swim tasks, drug withdrawal had little effect on shuttle escape performance, acoustic startle and locomotor activity. Based on these findings it was suggested that the development of post-amphetamine depression in the self-stimulation and forced swim paradigms was not related to variations in motoric or arousal mechanisms resulting from amphetamine withdrawal, but rather involved drug-induced changes in motivational processes.

Acoustic Stimulation↗