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PubMed1980

Chronic self-stimulation of the dentate nucleus for the relief of spasticity.

It has been assumed but not yet proved that cerebellar cortical stimulation activates the Purkinje cells, with subsequent inhibition of the deep cerebellar nuclei. However, the relatively crude, widespread excitation induced by several surface electrode arrays and the parameters of stimulation currently used, may produce other effects than selective activation of only one specific cellular type which, furthermore, seems to be rarely present in these particular patients, as demonstrated by biopsy studies prior to electrode placement. The dentate nucleus was chronically implanted with a stimulating system in a patient with spasticity due to cerebral palsy. Chronic self-stimulation induced a significant improvement in motor function, with relief of spasticity and improvement in speech, posture, balance and gait. Electrophysiological studies demonstrated a decrease in the amplitude of V1 and V2 responses and in the H/M and T/M ratios, an increase in the silent period, and marked effects in the H reflex recovery curve, as well as diminished contralateral cortical somato-sensory evoked potentials. This result seems to indicate that the clinical effects of cerebellar cortical stimulation are not due to prosthetically induced inhibition of the dentate nucleus.

Adult↗
PubMed1983

Effects of peripheral and central dopamine blockade on lateral hypothalamic self-stimulation: evidence for both reward and motor deficits.

The effects of dopamine receptor antagonists on lateral hypothalamic self-stimulation were analyzed using a reward summation function (RSF) technique. This paradigm relates running speed in a runway to the number of stimulation pulses received as a reward, and it is able to separately characterize changes in reward pulse effectiveness and motor performance. Pimozide, administered peripherally (0.125, 0.25, 0.5 mg/kg, IP), dose-dependently shifted the RSF toward higher values of number of pulses indicating reduced reward. Pimozide also reduced the asymptotic running speed of the RSF, indicating a deficit in motor performance. In a second experiment, alpha-flupenthixol infused directly into the nucleus accumbens (0.5 micrograms-0.5 micrograms, bilaterally) induced changes in the RSF similar to those obtained with peripheral neuroleptic treatment. These findings are discussed from the perspective that dopamine is involved both in the perception of reward value and in the performance of the response to obtain reward.

Animals↗
PubMed1984

Visual evoked potentials in rats selected for high or low self-stimulation.

Visual evoked potentials (VEPs) were analyzed in order to distinguish between rats from genetically high (HI) and low (LO) self-stimulation lines (LC2-HI and LC2-LO). Secondary VEP components - slow secondary negative wave (SNW) and sensory afterdischarge (SAD) - which are considered to be most sensitive indices of normal and pharmacologically-induced behavioral changes, were used for the comparison. Small, albeit statistically significant enhancement of SNW and SAD was obtained in LO rats. Unlike LO animals, HI rats gained in SNW amplitude and SAD area during repeated photic stimulation. The difference being highly significant. D,L-Amphetamine (1 mg/kg, i.p.) suppressed SAD and reduced the SNW amplitude in both HI and LO animals, although the predrug difference in their values remained practically unaltered. Apomorphine (0.25, 2.75, 5.25 mg/kg i.p.) had no measurable effect on VEP parameters even though it caused a regular picture of dose-related enhancement of locomotion and stereotypy. The effect of amphetamine can, therefore, be attributed to the activation of the norepinephrinergic system. Correspondingly, VEP variance in the two lines of rats is interpreted as related to the peculiarities of norepinephrine modulation of neocortical activity.

Amphetamine↗
PubMed1979

A reward-reduction model of depression using self stimulating rats: an appraisal.

A potential model of depression using a "reward reduction" technique with intracranial self-stimulation (ICSS) has been suggested. A number of rats with electrodes chronically implanted in the medial forebrain bundle were trained on this paradigm. The model involved the use of progressively increasing fixed ratio (IFR) schedules. Two tricyclic antidepressants, imipramine and protriptyline, were administered. Neither of these drugs resulted in the response enhancement which had been predicted. Only d-amphetamine (0.5 mg/kg) produced the predicted "antidepressant" action. It was concluded that response instability made this test difficult to operate and that even animals with adequately stable baselines did not produce a response pattern which could be categorised as specifically antidepressant.

Amphetamine↗
PubMed1986

Antagonism of the effects of the atypical benzodiazepine, Ro 5-4864 on intracranial self-stimulation in the rat.

The effects of Ro 5-4864 (chlordiazepam) were examined on responding for self-stimulation of the mid-lateral hypothalamus. Rewarding stimuli were delivered according to a 10-sec variable interval schedule of reinforcement. Ro 5-4864 (10-30 mg/kg, subconsulsive doses in these rats) decreased responding. This effect was antagonized by chlordiazepoxide (5-10 mg/kg) and phenobarbitone (35 mg/kg) but not by the benzodiazepine receptor antagonist Ro 15-1788 (10-20 mg/kg), the ligand for peripheral benzodiazepine receptors PK 11195 (60 mg/kg) or phenytoin (60 mg/kg). The pattern of interactions of Ro 5-4864 with these compounds differs from the pattern obtained with other procedures, and suggests that Ro 5-4864 has effects on systems unrelated to anxiety, convulsive activity or sedation.

Animals↗
PubMed1986

Hypothalamic substrates of self-stimulation in cats.

The purpose of this study was to gather anatomical data concerning sites for self-stimulation in the lateral hypothalamus in the cat. The study was conducted on 25 adult cats. In each cat, one to three monopolar stimulating electrodes were implanted bilaterally in the lateral hypothalamus in a region between sections Fr 10.0 and Fr 13.0, L 2.0 and L 5.0, and H -2.0 and H -6.0. A reference electrode was placed in the calvaria over the frontal sinus. Twenty-two of these cats learned to press a lever when each press was rewarded by a brief (0.3 s) electrical stimulus (2.0 to 7.0 V, 100/s, 1 ms duration per pulse) delivered to the hypothalamus. Postmortem anatomical analysis of the brains revealed that most of the positive rewarding sites were located in a midlateral hypothalamic zone, which included the medial forebrain bundle, and were localized to section Fr 11.5, between L 2.0 and L. 5.0, and H -3.0 and H -5.5.

Animals↗
PubMed1992

Chronic morphine fails to enhance the reward value of prefrontal cortex self-stimulation.

Dopamine (DA) plays an important role in the rewarding effects of drugs of abuse and intracranial self-stimulation (ICSS). We previously reported that ICSS derived from the prefrontal cortex appears insensitive to the reward-enhancing effects of amphetamine, a drug that increases DA release and reward at other ICSS sites. In the present study, rats with prefrontal electrodes were tested to see if morphine (7.5 or 10.0 mg/kg, IP) given once per day for 10 days enhanced prefrontal reward as assessed with the curve-shift method. Morphine initially produced sedation; however, after 3-4 days response rates increased sharply while frequency thresholds were unaffected. These results demonstrate that morphine does not enhance prefrontal ICSS reward and provide further evidence that prefrontal brain stimulation reward does not display the same characteristics as other ICSS sites.

Animals↗
PubMed1996

Shuttle-box memory facilitation by posttraining intracranial self-stimulation: differential effects in rats with high and low basic conditioning levels.

The effects of intracranial self-stimulation (ICSS) on retention (after 24 hr, 7, 15, or 60 days) of a massed 2-way active avoidance task were studied in independent groups of rats. All groups showed a higher performance on the retention session than on the acquisition one. In the control subjects, the higher retention performances were observed in the 7- and 15-day groups. However, the ICSS treatment facilitated the 24-hr retention compared with its control group, allowing the treated subjects to achieve the same level of performance on the 24-hr retention session than that achieved by the control rats at the 7-day retention test. In the 24-hr groups, the facilitatory ICSS effect was stronger in the subjects with a low level of conditioning and weaker in those with a high level. Results suggest that posttraining ICSS accelerates memory consolidation and equalizes the performance of poor and good learners.

Animals↗
PubMed1995

Self-stimulation of the MFB following parabrachial lesions.

It has been reported previously that the parabrachial region supports robust self-stimulation. In the present study, we determined whether lesions of the parabrachial nucleus (PBN) influence the rewarding effect of medial forebrain bundle (MFB) stimulation. In 10 rats, stimulation electrodes were aimed at the lateral hypothalamus and/or ventral tegmental area and a lesioning electrode aimed at the PBN. Rate-frequency curves were collected at each of three stimulation currents at each electrode, before and after lesioning. Four rats showed virtually no change in the frequency required to sustain half-maximal performance following lesioning, and two showed some postlesion decreases. Only two rats showed substantial postlesion increases in required frequency; the lesions in these subjects damaged the region ventral to the superior cerebellar peduncle, just caudal to the decussation of the peduncle, but spared the PBN. Thus, the reward effectiveness of MFB stimulation does not appear to be altered substantially following PBN lesions but may decrease following damage to the neighboring pedunculopontine region.

Animals↗
PubMed1987

Behavioral determination of refractory periods of the brainstem substrates of self-stimulation.

The objective of this study was to estimate the refractory periods of the brainstem neurons responsible for self-stimulation behavior in the rat. In a first experiment, we tested the robustness of the double pulse technique used to estimate the refractory periods of reward-relevant neurons. We obtained estimates of the relative T-pulse effectiveness at a wide range of stimulation frequencies. The results of this experiment suggest that the refractory period estimates obtained with the behavioral version of the double pulse technique are not dependent on the arbitrary choice of the stimulation frequency. However, the use of stimulation frequencies higher than 100 Hz should preferably be avoided. In a second experiment, we applied the double pulse technique using C-pulse intensity higher than T-pulse intensity to estimate the refractory periods of the brainstem reward-relevant neurons. Using moveable electrodes, we tested 9 metencephalic and 7 mesencephalic sites in 4 animals. In the metencephalon, the most excitable reward-relevant neurons have absolute refractory periods of less than 0.6 and 0.8 ms and have a supernormal period that occurs at least between 5 and 10 ms after the initial excitation. The mesencephalic reward-relevant neurons were found to have more heterogeneous physiological characteristics. The most excitable cells in the mesencephalon have absolute refractory periods of less than 0.4 ms and have a supernormal period occurring as soon as 2.4 ms after the initial excitation. At some mesencephalic sites, we observed first an abrupt initial recovery followed by a plateau, followed by a renewed and continuous recovery, a pattern that was never observed in the metencephalon. The hypothesis of the contribution of two distinct sub-populations of reward-relevant neurons is proposed and the implication of monoaminergic pathways in reward is discussed.

Animals↗
PubMedDate not supplied

[Temporal organization of the excitation summation effect during interaction between self-stimulation zones].

The analysis has been conducted of changes of histograms of pressing and pauses duration at self-stimulation (SS) of certain cerebral zones under the influence of motivational and reinforcing stimulations of other cerebral zones, performed at different phases of SS: in the moment of pedal pressing; 0.1; 0.3; 0.5; 0.7 s from the beginning of the pedal pressing and in the moment of its releasing. In the case of delay of motivational stimulation from the moment of pedal pressing a gradual reduction has been observed of relative duration of pressings (sign of rewarding SS effect) and pauses (sign of driving SS effect). Motivational stimulation performed at the moment of pedal release, elicited the greatest inhibitory effect. Reduction of SS-frequency was accompanied by the appearance of consummatory reactions. Delay of the reinforcing stimulation reduced the efficiency of its intensifying influences on the rewarding SS effect (expression of summation effect) and enhanced its influence on the driving effect. The common character has been shown of motivational and disrupting mechanisms of SS, on the one hand, and rewarding mechanisms--on the other hand.

Animals↗
PubMedDate not supplied

[Avoidance mechanisms during self stimulation].

Increased negative discordance of the dominating mode of the pressing duration histogram (PDH), which correlates with the growth of fixed bursts of stimulation is accompanied by a progressive decrease in the reinforcing properties of self-stimulation (SS), avoidance of the pedal and at the same time by a change of behavioral grooming reactions in the intervals between SS for search and consummatory reactions. Hunger considerably shortens the preferable duration of pressing or leads to the appearance of an additional mode on the PDH. With the change of the dominating PDH mode from positive discordance to a negative one, brain stimulation acquires aversive properties which are apparently due to the activation of the mechanisms of specific motivations.

Animals↗
PubMed1986

Compulsive thalamic self-stimulation: a case with metabolic, electrophysiologic and behavioral correlates.

A 48-year-old woman with a stimulating electrode implanted in the right thalamic nucleus ventralis posterolateralis developed compulsive self-stimulation associated with erotic sensations and changes in autonomic and neurologic function. Stimulation effects were evaluated by neuropsychologic testing, endocrine studies, positron emission tomographic measurements of regional cerebral metabolic rate for glucose, EEG and evoked potentials. During stimulation, vital signs and pupillary diameter increased and a left hemiparesis and left hemisensory loss developed. Verbal functions deteriorated and visuospatial processing improved. Plasma growth hormone concentrations decreased, and adrenocorticotrophic hormone and cortisol levels rose. With stimulation, glucose metabolism increased in both thalami and both hemispheres, reversing baseline right-sided hypometabolism and right-left asymmetries. EEG and both somatosensory and brain-stem auditory evoked potentials remained unchanged during stimulation, while visual evoked potentials revealed evidence of anterior visual pathway dysfunction in the left eye. This case establishes the potential for addiction to deep brain stimulation and demonstrates that widespread behavioral and physiological changes, with concomitant alteration in the regional cerebral metabolic rate for glucose, may accompany unilateral thalamic stimulation.

Brain↗
PubMed1977

Effects of lesions of various medial forebrain bundle components on lateral hypothalamic self-stimulation.

Unilateral lesions of various medial forebrain bundle components were assessed for their effects on lateral hypothalamic self-stimulation. Damage of areas containig nigrostriatal dopaminergic or ascending noradrenergic neurons had negligible effects on bar pressing, tail moving and alley running for hypothalamic stimulation. Lesions which appeared to destroy most or all of the catecholaminergic fibers in the posterior medial forebrain bundle virtually eliminated reinforced bar pressing and tail moving, but only partially suppressed alley running. The results suggest that brain stimulation reinforcement of the bar press and tail movement tasks depends upon the integrity of neural tissue in the area of the catecholaminergic pathways of the medial forebrain bundle, but not upon specific dopaminergic or noradrenergic systems. The data further suggest that the reinforcement of alley running is at least partially mediated by different neural tissue (possibly non-catecholaminergic) at the level of the posterior medial forebrain bundle lesions.

Animals↗
PubMed1975

Hypothalamic self-stimulation in rats following immunosympathectomy or central nerve growth factor antiserum injection.

In Experiment 1, immunosympathectomized rats self-stimulated at a much lower rate on high variable ratio schedules of reinforcement than injected controls. No differences were found for responding on continuous reinforcement or low variable ratio reinforcement schedules. In Experiment 2, a similar reduction in varialbe ratio response rate was found for subjects centrally injected with nerve growth factor-antiserum relative to controls. The results suggest a reduction in central catecholamine levels as a result of antiserum treatment.

Animals↗
PubMed1975

Effects of heroin on lever pressing for intracranial self-stimulation, food and water in the rat.

Male rats maintained with continuous access to levers for intracranial self-stimulation (ICSS), water, and food were subjected to five consecutive daily injections of heroin (5 mg/kg). Rates of lever pressing for ICSS were increased in 8 rats, 2--6 hrs after administration of heroin. Rates of lever pressing for water and food were not significantly changes during this period. Naloxone (5 mg/kg) pretreatment attenuated by 82% the facilitative effect of heroin on ICSS. A second group of 8 rats maintained at reduced ICSS rates failed to show an increase in lever pressing for ICSS with heroin. The facilitative effect of heroin described in this study is consistent with previously reported studies describing the effects of morphine on ICSS.

Animals↗
PubMed1981

Increase in mesolimbic electrical self-stimulation after chronic haloperidol: reversal by L-DOPA or lithium.

After chronic neuroleptic drug treatment, an increase in electrical intracranial self-stimulation (ICSS) rate is seen from electrodes in the A10 dopaminergic nucleus. This increase, which persists for approximately 3 weeks following drug withdrawal, is believed to represent a behavioral manifestation of drug-induced dopaminergic synaptic supersensitivity. Chronic L-DOPA caused a partial reversal of haloperidol-induced ICSS increase. Lithium carbonate, given concurrently with the haloperidol, partially prevented the development of ICSS supersensitivity. It is concluded that dopaminergic synaptic sensitivity has a two-way modulatory capability.

Animals↗