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PubMedDate not supplied

Compulsive somatosensory self-stimulation inducing epileptic seizures.

Three children who had been diagnosed as having infantile spasms with major psychomotor retardation were referred for the persistence of series of spasm-like seizures, which were resistant to antiepileptic drug treatment, beyond infancy. Serial seizures were elicited by a compulsive self-stimulating behavior that was documented by long-term video-polygraphy. These behaviors implicated proprioceptive inputs: tapping on the chin in one case, flexion and external rotation of the leg with dislocation of the femur in one case, a particular posturing of the body followed by rhythmic shaking of the head in the last case. This clinical picture seems to constitute a particular type of outcome for infantile spasms and is particularly resistant to therapy.

Cerebral Cortex↗

PubMed1981

Brain site variations in effects of morphine on electrical self-stimulation.

Pairs of bipolar electrodes were stereotaxically aimed at two of three sites: the locus coeruleus (LC), the substantia nigra, pars compacta (SNC), and the median forebrain bundle (MFB). Rats were shaped to bar-press for trains of intracranial electrical stimulation presented as pairs of monophasic pulses. The first pulse of a pair (the C, conditioning pulse) was followed by a second pulse (the T, test pulse) after a parametrically varied interval. The effects of chronic morphine administration were tested in a paradigm of 7 days saline, 7 days morphine, 1 day morphine+naloxone, and 6 days post-drug saline. High doses of morphine (5 mg/kg) depressed response rates for intracranial self-stimulation (ICSS). LC placements and those just lateral or ventral to the LC showed large increases in ICSS rates under morphine (2.5 mg/kg). This area was delimited on either side by tips that showed response rate depressions under morphine. MFB placements yielded response rate facilitations under morphine. Sites medial to the MFB and ventral within the MFB showed rate depressions under morphine. Dorsal substantia nigra placements showed facilitated rates, whereas placements ventral within the SNC and substantia nigra, pars reticulata (SNR) produced more variable results, with rates tending to be depressed by morphine. The ICSS procedure may be a useful animal model for detecting the abuse potential of drugs.

Animals↗

PubMed1976

Effects of various inhibitors of tyrosine hydroxylase and dopamine beta-hydroxylase on rat self-stimulation after reserpine treatment.

The behavioral effects of low doses of the catecholamine (CA) synthesis inhibitor, alpha-methyl-p-tyrosine (alpha-MPT, 50 mg/kg i.p.), or the norepinephrine (NE) synthesis inhibitors (FLA-63, 15 mg/kg i.p., U-14624, 50 mg/kg i.p., or disulfiram 150 mg/kg i.p.) were studied in rats pretreated with reserpine (1 mg/kg i.p.) 24 h before. Rats were implanted either in the area ventralis tegmenti (AVT) or in the lateral hypothalamus (LH). The modifications of CA synthesis and endogenous CA levels were estimated in a parallel experiment. Reserpine treatment produced a slow decrease in self-stimulation (SS) rates during the first 12 h; SS rates were 85% of control values 24 h after reserpine treatment. Injection of alpha-MPT in reserpine-pretreated rats inhibited SS (85% decrease 3 h after administration either in AVT or LH rats), whereas dopamine beta-hydroxylase inhibition had no great effect on SS. The administration of very low doses of alpha-MPT (20 mg/kg i.p.) to rats treated with reserpine (24 h before) plus FLA-63 (1 h before) induced an important decrease in SS rates in AVT-implanted rats only. The major conclusion is that dopaminergic neurons seem to be involved in AVT and LH SS. The last experiment suggests the involvement of a balance between dopaminergic and noradrenergic neurons in AVT SS.

Animals↗

PubMed1992

Rat exploratory behavior controlled by intracranial self-stimulation improves the study of place cell activity.

This report is limited to the description of a procedure that should help to resolve the question whether firing fields of hippocampal place cells are relatively stable or modifiable by learning. Rats implanted with lateral hypothalamic electrodes for rewarding intracranial self-stimulation (ICSS) were trained to explore a circular open field (100 cm in diameter) while their locomotion was tracked by a computerized video system which also delivers ICSS whenever the animal's exploration has met certain experimenter defined criteria. The 3 following conditions were examined. (1) Homogeneous exploration of the entire field: ICSS was delivered after the animal repeatedly visited 5 equal segments of the field (central annulus and remainders of the 4 quadrants), entered randomly located circular areas of the field, and/or traveled a criterion distance. (2) Place field contingent reward or non-reward: ICSS was delivered when the animal entered a circular area (23 cm in diameter) corresponding to the place field after a previous visit to a similar area outside the place field. These conditions were reversed in the following task. (3) Delayed reward: ICSS was delivered when the animal entered the circular area and remained in it for 2 s. Each condition was tested for 600 s or until 50 ICSS were delivered. The behavioral procedures described make it possible to propose an experimental protocol that allows examination of the same place cell under conditions of homogeneous exploration with a segment condition or randomly distributed reward and under conditions with the place field signaling reward or non-reward. The delayed reward condition increases the accuracy of the target location and allows assessment of the phasic versus tonic nature of the place cell firing.

Animals↗

PubMed2005

Slower extinction of responses maintained by intra-cranial self-stimulation (ICSS) in an animal model of attention-deficit/hyperactivity disorder (ADHD).

Children with attention-deficit/hyperactivity disorder (ADHD) show performance deficits and excessive motor activity during extinction and in situations where no reinforcer can be identified, suggesting an extinction deficit in ADHD possibly linked to dopamine dysfunction. The present study examined extinction of responding previously maintained by intra-cranial self-stimulation (ICSS) in spontaneously hypertensive rats (SHR), an animal model of ADHD using three different extinction procedures. Delivery of electrical pulses were terminated altogether or presented independently of responding using two different current intensities. The results showed that more responses were retained in the SHR, especially during the initial transition from ICSS-maintained responding to response-independent delivery of electrical pulses with current reduced relative to that given during reinforcement. Slower extinction of previously reinforced behavior is suggested as an alternative explanation for the frequently observed increased behavioral output that has previously been interpreted as "disinhibition" of behavior in ADHD.

Analysis of Variance↗

PubMed1976

[Changes in the substantia nigal self-stimulation behavior caused by intraventricular injection of norepinephrine, dopamine and GABA].

A bipolar electrode was stereotaxically implanted in the substantia nigra of male albino Wistar-Imamichi rats. Effects of l-norepinephrine (NE), dopamine (DA) and gamma-aminobutyric acid (GABA), injected into the lateral ventricle, on the substantia nigral self-stimulation (SS) behavior, and the effect of alpha- and beta-adrenergic receptor antagonists on the facilitation induced by NE were investigated. NE but not DA facilitated the SS behavior and GABA showed no constant effects on the behavior. Facilitation by NE of SS behavior was inhibited by phentolamine, but not by propranolol. These results suggest that the noradrenergic system in the brain may play a more significant role in the positive reinforcement of the substantia nigral SS behavior than does the dopaminergic or GABA-ergic system, and that the action of NE may be facilitated through alpha-receptors rather than through beta-receptors.

Aminobutyrates↗

PubMed1988

Brain self-stimulation, locomotor activity and tissue concentrations of ethanol in male rats.

These studies were aimed at correlating the effects of ethanol on operant behavior and on locomotor activity with its distribution in selected tissues in the body. One group of male rats was trained on a continuous reinforcement schedule for intracranial self-stimulation (ICSS) with electrodes in the lateral hypothalamus. Another group was studied in a locomotor activity apparatus, and both groups were given ethanol intraperitoneally over the dose-range 0.3-1.7 g/kg. Urine was collected 15 min and 60 min after ethanol administration and samples of blood, brain, heart, lung, liver, muscle and testis were obtained at both time points. Depressions of ICSS and of locomotor activity occurred, and these changes in behavior were correlated with increasing concentrations of ethanol in blood, urine and tissue. Thus, the disrupting effects of ethanol on behavior which occurred shortly after its acute administration were closely linked to its concentrations throughout the body.

Animals↗

PubMed1979

Intracranial self-stimulation thresholds: a model for the hedonic effects of drugs of abuse.

We present the thesis that many drugs of abuse are used for their hedonic effects and that a relevant animal model for the study of these effects is the action of these drugs on the pathways that support rewarding intracranial self-stimulation. A relationship between abuse potential of a drug and its ability to lower the threshold for rewarding brain stimulation in the rat was found. Of all the compounds we have studied, morphine and cocaine were the drugs that caused the maximum lowering of the rewarding threshold. Phencyclidine hydrochloride and the mixed agonist-antagonist pentazocine also lowered the threshold to a lesser degree, while the mixed agonist-antagonists cyclazocine and nalorphine hydrochloride had inconsistent effects. Naloxone hydrochloride, at the doses tested, had no effect on the threshold. Further, there is no evidence that tolerance develops to the threshold-lowering effect of morphine, suggesting that continued use of narcotics by the physically dependent individual is not simply due to an effort to avoid the pain of withdrawal.

Animals↗

PubMed1991

The effects of excitotoxin lesions of the lateral hypothalamus on self-stimulation reward.

Unilateral microinjection into rat lateral hypothalamus (LH) of the excitotoxins ibotenic acid (IBO) and N-methyl-D-aspartic acid (NMDA) produced a local zone of neuronal death but also produced a zone of demyelination. The size of this demyelination zone was related to excitotoxin dose and was smaller than the zone of neuron killing. In behavioral testing, MFB self-stimulation reward and performance were measured with a rate-frequency curve-shift method before and after IBO or NMDA lesions of the LH. Excitotoxin lesions were made anterior or posterior to the LH electrode so that the zone of neuronal death, but not demyelination, extended to the electrode tip. These lesions produced small, temporary LH stimulation reward deficits, leading to the conclusion that intrinsic LH neurons are not a major substrate of MFB stimulation reward.

Animals↗

PubMed1997

Fos-like immunoreactivity in the caudal diencephalon and brainstem following lateral hypothalamic self-stimulation.

Fos immunohistochemistry was used to stain neurons in the caudal diencephalon, midbrain and hindbrain driven by rewarding stimulation of the lateral hypothalamus (LH). Increases in Fos-like immunoreactivity were most pronounced ipsilateral to the site of stimulation and tended to be confined within discrete structures such as the posterior LH, arcuate nucleus, ventral tegmental area (VTA), central gray, dorsal raphé, pedunculopontine area (PPTg), parabrachial nucleus, and locus coeruleus. At least two of these structures, the VTA and PPTg, have been implicated in medial forebrain bundle self-stimulation.

Animals↗

PubMed1967

An inexpensive electro-fistular swivel for negative feedback control of self-stimulation.

A swivel was developed for concurrent intraorganismic fluid injection and intracranial electrical stimulation of the unrestrained rat. Effects of various intragastric injections on bar-pressing maintained by electrical stimulation of the hypothalamus were studied. In some subjects, intragastric injections of either water or milk decreased the rate of responding. This decrease resulted from pauses in responding rather than from decreases in the local rates of responding. The decrement in responding occurred at a lower gastric volume during milk injection than during water injection. In other subjects, however, neither water, milk, nor 32% sucrose injections affected the rate of self-stimulation.

Animals↗

PubMed1992

Effects of the preferential dopamine autoreceptor antagonist (+)-AJ76 in the intracranial self-stimulation paradigm.

As revealed by locomotor activity experiments in rodents, cis-(1S,2R)-5-methoxy-1-methyl-(2-n-propylamino)tetralin [(+)-AJ76] is a preferential dopamine autoreceptor antagonist that produces stimulatory or weak inhibitory behavioral effects in animals that display low or high baseline activity, respectively. In the present study, the possible positive reinforcing properties of (+)-AJ76 were studied by means of the intracranial (median forebrain bundle) self-stimulation (ICSS) technique in rats. The current intensity of the electrical stimuli was used as the independent variable. The resulting rate/intensity curves were analyzed by computer, and the half-maximal response (called EC50) was calculated for each animal. When starting on a suprathreshold current intensity, (+)-AJ76 dose dependently (3.1-52.0 microM/kg, SC) increased the EC50 without producing any apparent motor deficits like muscular rigidity or catalepsy. A clear-cut and more potent inhibitory action was also noted for haloperidol (0.033-0.133 microM/kg, SC) and the di-N-methyl analog of (+)-AJ76 called (+)-AJ118 (0.8-3.5 microM/kg, SC), while d-amphetamine (1.4 or 5.4 microM/kg, SC) decreased the EC50 values. In the second experiment, animals were subjected to a subthreshold current intensity for 30 min. The intensity was set to produce a response of 15% or less of maximal, shaping response rate for the respective animals. Of these 22 animals, 10 responded with a stimulation, while the ICSS response was inhibited in the others. We did not, however, get consistent results in all rats tested. In summary, this study shows that (+)-AJ76 appears to lack positive reinforcing properties comparable to those produced by classical stimulants such as d-amphetamine.

Animals↗

PubMed1977

Effects of dopamine supersensitivity on lateral hypothalamic self-stimulation in rats.

Dopamine (DA) receptor supersensitivity was demonstrated by potentiated d-amphetamine stereotype after a three-day treatment regimen in which the DA receptor blocker pimozide (4.0 mg/kg) was administered twice daily. Similarly-induced DA supersensitivity produced a significant increase in the rate of lever-pressing for lateral hypothalamic (LH) intracranial self-stimulation (ICSS) and a significant decrease in ICSS thresholds. No change from pretreatment baselines was observed in vehicle-treated control animals. Following three-day treatment with the noradrenaline--(NA) and DA-receptor blocker, haloperidol (4.0 mg/kg twice daily), a single injection of the alpha-adrenergic agonist clonidine (0.15 mg/kg) caused increased running behavior. In contrast clonidine decreased running in rats pretreated with chronic pimozide or vehicle. These results indicate an increase in the sensitivity of central NA receptors following chronic haloperidol but not chronic pimozide. Taken together, these findings were interpreted as a potentiation in the reinforcing properties of LH-ICSS after chronic pimozide treatments due to increases in the sensitivity of DA and not NA receptors.

Animals↗

PubMed1997

NMDA receptor antagonists prevent conditioned activation of intracranial self-stimulation in rats.

Rats with bipolar electrodes implanted unilaterally into the ventral tegmental area were trained to lever-press for response contingent electrical stimulation (continuous reinforcement). After preliminary lever-press training, two types of daily sessions were held on 10 consecutive days: type T+, during which current intensity was set at the Threshold level and each response was accompanied by the visual signal (stimulus lights above the lever briefly went off); and type ST-, during which current was set at the SubThreshold level and there were no visual stimuli. On day 11, combination of the subthreshold current intensities and stimulus lights previously associated with the threshold stimulation (session type ST+) resulted in significantly elevated response rates compared to the performance under the subthreshold current without visual stimuli (session type ST-). This effect was dose dependently blocked by competitive NMDA receptor antagonist (+/-)-CPP ((+/-)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid) and CGS 19755 (cis-4-(phosphonomethyl) piperidine-2-carboxylic acid). The present findings suggest that the activation of intracranial self-stimulation induced by a conditioned visual stimulus is dependent on the NMDA receptor functioning.

Animals↗

PubMed2004

The basolateral complex of the amygdala mediates the modulation of intracranial self-stimulation threshold by drug-associated cues.

Learning and memory appear to be critical aspects of drug abuse; presumably playing an especially important role in craving and relapse. Thus, understanding the interaction of learning- and memory-related brain areas with the classical reward circuitry is of importance. Toward this goal, the effect of drug-associated contextual cues on intracranial self-stimulation (ICSS) behaviour was assessed in rats. We used a method that allows the establishment of baseline behaviour, the pairing of drug exposure with unique cues, and testing the effect of cue exposure within the same apparatus. ICSS thresholds were decreased by morphine (5 mg/kg, i.p.) or cocaine (10 mg/kg, i.p.) during five days of paired drug-cue training sessions. Subsequent presentation of the drug-associated cues decreased thresholds in the absence of drug. Cues associated with saline had no effect. These results suggest a Pavlovian conditioning phenomenon in which the functioning of brain reward circuitry is modulated by drug-associated cues. In a second experiment, we tested the hypothesis that the mechanism by which conditioning affects ICSS thresholds may include the basolateral complex of the amygdala (BLC) due to its known role in conditioning and anatomical linkage with classical reward circuitry. Lesions of the BLC abolished the ability of cocaine-associated cues to lower ICSS threshold. Lesions did not alter response capability or the unconditioned effect of cocaine. We conclude that the BLC is necessary for cues associated with previous drug exposure to modulate activity within or downstream from the classical reward circuitry of the medial forebrain bundle.

Amygdala↗

PubMedDate not supplied

Striatal dopaminergic modulation of lateral hypothalamic self-stimulation.

The bilateral application of crystalline 6-hydroxydopamine to the ventral anterior head of the corpus striatum of rats severely suppressed responding for electrical stimulation of the lateral hypothalamus. This suppression lasted for days or weeks, after other behavioral deficits in food and water intake and activity had recovered. Application of crystalline dopamine through the same cannulas temporarily reversed the impairment. Applications of crystalline dopamine to the same striatal region of untreated rats were more effective in enhancing self-stimulation than similar applications of norepinephrine.

Animals↗

PubMed1985

Reward, performance, and the response strength method in self-stimulating rats: validation and neuroleptics.

The response strength method consists of exposing the subject to a series of variable interval schedules of reinforcement at differing densities. Response rate is plotted against obtained reinforcement rate for each schedule. The data conform to a negatively accelerated curve that is fit well by an analytical representation which contains two parameters. The values of these parameters are obtained from the fitted curve, and are suggested to independently reflect reinforcement and performance functions. In a first experiment, two manipulations were conducted that validated these suggestions. First, lowering the frequency of brain stimulation pulses induced a relatively selective shift in the reinforcement parameter. Second, increasing the force required to press the lever primarily altered the performance parameter. In a second experiment, the effects of neuroleptic administration on these two parameters were noted and compared to the results of the first experiment. In general, neuroleptics were seen to produce both reward and motor/performance impairments in self-stimulating rats.

Animals↗

PubMed1981

Differential effects of drug treatments on nose-poke and bar-press self-stimulation.

To assess the possibility of dissociating drug-induced gross performance deficits from effects on brain stimulation reward, the nose-poke and bar-press operants were systematically compared. Pentobarbital and methocarbamol (a muscle relaxant) reduced bar-pressing more strongly than nose-poking. In contrast, clonidine and haloperidol, which disrupt noradrenergic and dopaminergic neurotransmission respectively, had no differential effect on these operants. The nose-poke operant appears less vulnerable to drug-induced gross motor impairment and may be more suitable for pharmacological studies of self-stimulation.

Animals↗