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PubMed1983

The influence of amphetamine on preference for lateral hypothalamic versus prefrontal cortex or ventral tegmental area self-stimulation.

Rats were trained to bar-press for intermittent reinforcement on a concurrent schedule offering self-stimulation (SS) at the animal's choice of one of two different brain loci. On the concurrent schedule, the relative reward value of the two reinforcers is evaluated by the way the subject divides its session time responding for these reinforcers, thus yielding a rate-free measure of reward in addition to response rate data. In animals with electrodes in the lateral hypothalamus (LH) and prefrontal cortex (PFC), amphetamine dose-dependently increased response rates as well as the proportion of time allotted to LH stimulation, demonstrating that the reward value of LH stimulation was increased relative to PFC stimulation. This finding supports the hypothesis that DA systems modulate the rewarding value of LH but not PFC SS, and it suggests that differing neural mechanisms underlie these two behaviors. In animals with LH/ventral tegmental area (VTA) implants, amphetamine had no effect on preference, although it produced an overall increase in rate. This suggests that the drug elevates the rewarding value of LH and VTA stimulation to a similar degree, and that the two regions may have a common DA-related reward substrate. Finally, it was found that when the two reinforcers were equally preferred (50% session time allotted towards each reinforcer), response rates for the two rewards were not necessarily equal. This confirms that SS response rate is not a simple function of reward magnitude.

Animals↗

PubMed1984

Metabolic mapping of the brain during rewarding self-stimulation.

Local rates of cerebral glucose utilization were measured in rats by the quantitative 2-deoxy-D-[14C]glucose autoradiographic method during electrical stimulation of the ventral tegmental area. Rats trained in intracranial self-stimulation showed a pattern of changes in forebrain metabolic activity distinctly different from the pattern seen in rats stimulated by the experimenter. These findings provide information about the distribution of local cerebral activity specific to reinforced instrumental behavior.

Animals↗

PubMed1989

Effects of redesigning the physical environment on self-stimulation and on-task behavior in three autistic-type developmentally disabled individuals.

A study was conducted to assess the effects of redesigning the physical environment (i.e., the classroom) on the occurrence of self-stimulation, on-task behavior, inappropriate behavior, and inactivity. Three developmentally disabled males, diagnosed as autistic-type, participated. Data were collected using a withdrawal design. Results showed a decrease of self-stimulation and inactivity and an increase of on-task behavior. Inappropriate behavior remained unchanged across experimental conditions.

Adolescent↗

PubMed1989

Orosensory self-stimulation by sucrose involves brain dopaminergic mechanisms.

The most convincing body of evidence supporting a role for brain dopaminergic mechanisms in sweet taste reward has been obtained using the sham-feeding rat. In rats prepared with a chronic gastric fistula and tested with the cannula open, intake is a direct function of the palatability of the solution offered as well as of the state of food deprivation. Because essentially none of the ingested fluid passes on to the intestine, negative postingestive feedback is eliminated. Thus, the relative orosensory/hedonic potency of the food determines and sustains the rate of sham intake; long periods of food deprivation are not required. In this way, the sham feeding of sweet solutions may be considered a form of oral self-stimulation behavior and afford a preparation through which the neurochemical and neuranatomical substrates of sweet taste reward may be identified. The results obtained in the series of experiments summarized in this paper clearly indicate that central D-1 and D-2 receptor mechanisms are critical for the orosensory self-stimulation by sucrose in the rat. In conclusion, I suggest that such investigations of the roles of brain dopaminergic mechanisms in the sucrose sham-feeding rat preparation may further our understanding of normal and aberrant attractions to sweet fluids in humans (see Cabanac, Drewnowski, and Halmi, this volume), as an innate, positive affective response of human neonates to sucrose and the sustained positive hedonic ratings for glucose when tasted but not when consumed have demonstrated.

Animals↗

PubMedDate not supplied

[Self-stimulation reaction in normotensive and hypertensive rats].

The part of noradrenergic mechanisms in self-stimulation (SS) operant behaviour was studied in rats. In all experiments systolic blood pressure (BP) in the tail artery was measured by means of photocells. It was found, that small doses of noradrenaline facilitate the SS, while high doses depress or stop it. The depressive effect is accompanied by a marked increase of BP. Effective blockade of beta-adrenoceptive structures by inderal suppresses SS, and the inhibitory effect is accompanied by a small decrease of BP. Suppressing effect of alpha-adrenoblocking agent, phentolamine, is even more pronounced, but is accompanied by a marked decrease of BP. Beta-agonist isadrin causes a marked facilitation of SS without changes of BP. It is suggested that positive reward in the lateral hypothalamus is due to a direct stimulation of beta-adrenoceptive noradrenergic neuronal elements. Chronic neurogenic hypertension is developed by an overloading of the higher nervous activity. In chronic hypertensive rats there is a pronounced suppression of SS. A transient fail of BP caused by injection of catapresan (hemiton) results in a temporary recovery of normal SS behaviour. It may be concluded that reduction of lever-pressing rate during acute and chronic neurogenic hypertensions is related to baroreceptor mechanisms. The role of the autonomic nervous system in SS behaviour is discussed.

Animals↗

PubMed1982

Elimination of medial prefrontal cortex self-stimulation following transection of efferents to the sulcal cortex in the rat.

Intracranial self-stimulation (ICSS) of the medial prefrontal cortex (MFC) was not affected by lesions of the medial forebrain bundle, the nucleus accumbens or medialis dorsalis. However, bilateral, parasagittal knife cuts that transected fibers interconnecting the medial and sulcal cortices eliminated ICSS from the MFC with no apparent recovery over a 21 day test period. Similar knife cuts produced only transient effects on lateral hypothalamic ICSS. These data suggest that the neural substrates of frontal cortex ICSS are very different than those that subserve ICSS along the medial forebrain bundle.

Animals↗

PubMed1981

Pentobarbital induces a naloxone-reversible decrease in mesolimbic self-stimulation threshold.

The effects of sodium pentobarbital and naloxone were tested on intracranial self-stimulation (ICSS) in rats implanted with electrodes in the ventral tegmental area. Threshold for ICSS was determined using a rate-independent current titration paradigm. A low dose of pentobarbital (5 mg/kg) did not have a significant effect on ICSS thresholds, while a high dose (20 mg/kg) rendered the subjects too ataxic to respond reliably in the operant task. An intermediate dose (10 mg/kg) induced a highly significant lowering of threshold (17% below saline baseline levels) without apparent deterioration in response capability. The concurrent administration of naloxone (2 mg/kg) significantly reversed the pentobarbital-induced threshold decrease, while naloxone treatment alone had no effect on the ICSS threshold.

Animals↗

PubMed1995

Poststimulation excitability of ventral pallidum self-stimulation neurons.

The degree of neural recovery from refractoriness was inferred in rats self-stimulating with pairs of pulses in the ventral pallidum. The prerecovery intrapair interval varied from 0.5 to 1.0 ms, depending on brain site. At some sites, recovery reached its maximum within less than 1.6 ms whereas, at the majority of sites, a substantial amount of recovery occurred at delays longer than 1.2 ms. The shortest recovery estimates were not fundamentally different from those obtained from sites lying along the medial forebrain bundle. The longest recovery estimates were similar to those obtained from cortical and basal forebrain sites. The differences in recovery noted between sites and the presence of step-like patterns in the recovery curves suggest the presence of neural heterogeneity within the ventral pallidal substrates of reward.

Animals↗

PubMedDate not supplied

[Effect of cholin- and serotoninergic substances on self stimulation in rats].

The influence of choline- and serotoninergic agents on the pedal self-stimulation (SS) was studied in male rats of Wistar line. Physostigmine decreased the frequency of pressing on the pedal whereas fluoxetine didn't influence SS. Scopolamine activated SS and lowered the threshold of the SS-reaction. P-chloroamphetamine effect depended on the action phase of the drug and was manifested both in depression and activation of SS. Preliminary administration of fluoxetine decreased the activating effect of scopolamine and enhanced the depressing effect of physostigmine. A combination of p-chloroamphetamine and cholinergic agents was accompanied by a tendency toward weakening of depressing effect of physostigmine and toward enhancing of activating effect of scopolamine. It is suggested that serotoninergic mechanisms in case of changes in activity of cholinergic processes, depress the system of positive reinforcement. A functional interaction of choline- and serotoninergic neurotransmitter systems seems probable.

Acetylcholine↗

PubMed1992

Neuromedin N decreases self-stimulation of the medial prefrontal cortex.

Intracerebral microinjections of neurotensin (NT) decrease intracranial self-stimulation (ICSS) of the medial prefrontal cortex (MPC) in the rat. This effect could be due to the ability of NT to bind dopamine. To test this hypothesis we studied the effects of intracerebral microinjections of neuromedin N, a natural NT analogue that does not bind dopamine, on ICSS of the rat MPC. Unilateral microinjections of neuromedin N into the MPC at doses of 2.5, 5, 10, 20 and 40 nmol produced a dose-related decrease in ICSS of the ipsilateral MPC. ICSS of the contralateral MPC, used as a control, was not affected by the microinjections. These results suggest that the inhibitory effect of NT on ICSS is independent of NT-dopamine binding. Because neuromedin N is also present in the MPC, these results also suggest a possible neuromodulatory role of this neuropeptide on ICSS of the prefrontal cortex.

Animals↗

PubMed1989

Assessment of the neural substrate for intracranial self-stimulation by the postreinforcement pause technique.

The poststimulation excitability of neurons mediating intracranial self-stimulation (ICSS) was evaluated by the paired-pulse method. Stimulus effectiveness was assessed by the postreinforcement pause (PRP) and by frequency threshold (FT) determinations in 7 rats performing ICSS in the medial forebrain bundle (MFB) and in the ventral tegmental area (VTA). Stimulus effectiveness values were minimal at conditioning-test (C-T) pulse intervals of 0.6 and 0.8 ms for MFB and VTA animals, respectively, because of neuronal refractoriness. Local potential summation could account for the increase in effectiveness at very short C-T intervals, and an additional peak of enhanced effectiveness at a C-T interval of 2.0 ms, perhaps reflecting synaptic events, was observed only in VTA animals with the PRP method. Important advantages of the PRP method were that the C-T interval was the only stimulus parameter that was varied, and the behavioral output of the animal remained relatively constant.

Animals↗

PubMed1988

Effects of current intensity on behavioral and autonomic heat-loss responses in intracranial self-stimulating rats.

We investigated the effects of current intensity on behavioral and autonomic heat-loss responses in intracranial self-stimulating (ICSS) rats. At an ambient temperature (Ta) of 22 degrees C, the tail vasodilation during ICSS behavior began at higher hypothalamic temperature (Thy) at higher current intensity. At a Ta of 36 degrees C, body extension, a typical heat-loss response in rats, appeared during ICSS behavior and frequently interrupted lever pressing. When the body extension first began, Thy was elevated if current intensity was high. In experiments in which current intensity was varied between two levels at a Ta of 22 degrees C, if current intensity was lowered after tail vasodilation began and Thy reached a steady level, the rat interrupted pressing the lever to lose heat through grooming or body extension. Rectal temperature (Tre) dropped in the process. If, on the other hand, current intensity was raised, the rate of lever pressing increased and Tre rose with tail vasoconstriction. The data suggest that the magnitude of the reward, as reflected in current intensity, affects both behavioral and autonomic heat-loss responses.

Animals↗

PubMed1983

Region-specific reductions of intracranial self-stimulation after uncontrollable stress: possible effects on reward processes.

Rates of responding for intracranial self-stimulation from the medial forebrain bundle, nucleus accumbens and substantia nigra were evaluated in mice that had been exposed to either escapable shock, yoked inescapable shock or no shock treatment. Whereas performance was unaffected by escapable shock, marked reductions of responding from the medial forebrain bundle and nucleus accumbens were evident following the uncontrollable shock treatment. Responding from the substantia nigra was unaffected by the stress treatment. Uncontrollable shock is thought to reduce the rewarding value of responding for electrical brain stimulation from those brain regions in which stressors are known to influence dopamine activity.

Animals↗

PubMed1983

Increasing the work requirements lowers the threshold of naloxone for reducing self-stimulation in the midbrain of rats.

Rats were trained to lever-press for intracranial self-stimulation (ICSS) with electrodes in the midbrain central gray area. The effects of naloxone (0.1-30.0 mg/kg, SC) on a continuous reinforcement (CRF) schedule were determined. Rats were then re-trained on higher fixed-ratio (FR) schedules, and naloxone was re-tested at FR: 5, 10, 15 and 20. Only moderate reductions in lever-pressing rates were obtained at the highest dose of naloxone under CRF and FR: 5 schedules. In contrast, pronounced, dose-dependent reductions in ICSS rates occurred at FR: 10, 15 and 20. The time-course for this reduction at FR: 20 was consistent with an opiate-antagonistic action of naloxone. The modest decrease in locomotor activity produced by naloxone in a matched group of control rats was not sufficient to account for the effects on ICSS. The threshold of naloxone for reducing the rate of ICSS lever-pressing was lowered by increasing the effort and/or time requirement for each reinforcement.

Animals↗

PubMed1979

Suppression of self-stimulation: three alternative strategies.

Four boys with autistic-like behavior were treated for self-stimulatory behavior with three different treatment procedures--time out, differential reinforcement of other behavior (DRO), and overcorrection. All four boys showed a rapid response to the overcorrection procedure. Three boys demonstrated some evidence of decrement in responding with time-out. During the DRO procedure, one showed a modest decrease, two showed no change, but one exhibited a consistent increase in responding under this condition. A multiple baseline applied to one of the subjects failed to reveal any generalization of suppression from one setting to another. A strong but not perfect relationship was found between a frequency and a duration measure of self-stimulation. There was some evidence of negative side effects for one boy during overcorrection and for another during time-out. None of these negative side effects was enduring. There was also some indirect evidence that overcorrection facilitated appropriate play.

Autistic Disorder↗

PubMedDate not supplied

[Mechanisms causing repeated pedal pressing during self stimulation of the brain].

Mono- and polymodal histograms of pauses duration were obtained in rats during self-stimulation (SS) through electrodes implanted in the lateral hypothalamus. Changes in motivational state (deprivation--satiation) did not markedly affect the histogram pattern. It is concluded that the SS drive mechanism is not connected with natural motivations. In all experiments, a high negative correlation between "optimal criterion" parameters and model pause duration is obtained. It is suggested that one and the same mechanism underlies both the SS-reinforcement and drive. Reinforcement is probably connected with current excitation of reinforcing structures during stimulation, whereas the drive is caused by trace activation of the same cerebral structures after the stimulation.

Animals↗

PubMed1986

Antagonism of footshock stress-induced inhibition of intracranial self-stimulation by naloxone or methamphetamine.

Rats were trained to lever-press for intracranial self-stimulation (ICSS) with electrodes implanted in the ventral tegmental area (VTA). The effect of inescapable footshock on response rates to ICSS was examined in the present study. Markedly decreased response rates to ICSS were observed 15 min to 24 h following inescapable footshock. Naloxone (10.0 mg/kg) itself was without effect on response rates to ICSS, but completely antagonized the decreased response rates by the stressor treatment. A relatively low dose of methamphetamine (0.5 mg/kg), which showed no effect on ICSS rates in naive rats, also antagonized the decreased response rates to ICSS. The present results suggest that inescapable footshock may release endorphin in the mesolimbic or mesocortical area; the released endorphin may act on dopaminergic nerve endings and interrupt dopaminergic transmission. The decreased activity of dopaminergic neurons may cause the decreased response rates to ICSS.

Animals↗

PubMed1986

Evidence implicating descending fibers in self-stimulation of the medial forebrain bundle.

The role of ascending and descending fibers in self-stimulation of the lateral hypothalamus and ventral tegmental area in the rat was assessed by noting whether anodal hyperpolarization of one of these sites could reduce the rewarding effect of stimulating the other site. Strength-duration curves were obtained by psychophysical means, with one of the depth electrodes serving as the cathode and the other as the anode. It was anticipated that at long pulse durations, conduction in some of the fibers stimulated at the cathode would be blocked at the anode. At shorter durations, the anodal hyperpolarization should have dissipated before the arrival of the action potentials triggered by the cathode. Thus, the predicted effect of the block was to bend the strength-duration curves obtained with two depth electrodes upward at long pulse durations, provided that the anode lay between the cathode and the efferent stages of the pathway responsible for the rewarding effect. To control for possible differences in the density of the reward substrate in the lateral hypothalamic and ventral tegmental areas, the strength-duration curves obtained with a given cathode and a depth anode were compared to curves obtained with the same cathode but with an anode consisting of a set of skull screws. It was expected that the concentrated current entering from the depth anode would much more effectively block conduction in the medial forebrain bundle than the diffuse current entering from the large, distant skull screws. The predicted change in the shape of the strength-duration curves was observed only when the ventral tegmental electrode served as the anode and the lateral hypothalamic electrode as the cathode. This is consistent with the notion that in at least some of the neurons responsible for the rewarding effect, action potentials elicited by the lateral hypothalamic electrode had to pass through the ventral tegmental area in order to reach the efferent stages of the reward pathway. In the simplest anatomical arrangement consonant with this view, the somata of these cells lie in the forebrain and give rise to descending axons. As a test of the hypothesis that anodal block was responsible for changing the shape of the strength-duration curve obtained with the ventral tegmental anode, a psychophysical version of the collision test was used to determine whether the tips of the lateral hypothalamic and ventral tegmental electrodes were indeed linked by a common set of reward-related fibers.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗