SEARCH · PubMed Health

Results for “SELF STIMULATION”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 199 records · Page 11Linked to original sources

PubMed1984

Does naloxone suppress self-stimulation by decreasing reward or by increasing aversion?

Fifty-eight rats were implanted with electrodes in the ventrolateral midbrain central gray from which both self-stimulation reward and/or stimulation-produced analgesia can be obtained. Thirty-nine cases were positive for self-stimulation; of these, 24 also displayed significant stimulation-produced analgesia and 15 did not. Injections of the opiate receptor blocker, naloxone, suppressed self-stimulation by approximately 40% at both analgesic and non-analgesic reward sites. Since naloxone failed to act preferentially at analgesic reward sites, the hypothesis that naloxone suppresses self-stimulation primarily by antagonizing endorphin-mediated analgesia, and thereby increasing the aversive properties of the brain stimulation, was not supported. Rather, the data are consistent with the hypothesis that naloxone suppresses self-stimulation by antagonizing endorphin-mediated reward.

Animals↗

PubMed1982

Comparative effects of the ACTH 4-9 analogue (ORG 2766), ACTH 4-10 and [D-Phe7] ACTH 4-10 on medial septal self-stimulation behaviour in rats.

Experiments were performed to examine the effects of various analogues of ACTH on electrical self-stimulation behaviour elicited from the medial septal area using an ascending or descending sequence of stimulus intensities within a session. When an ascending sequence of threshold multiples was used ACTH 4-10 and the ACTH 4-9 analogue (ORG 2766) enhanced level pressing for low intensity stimulation but attenuated self-stimulation at greater current intensities. The analogue ORG 2766 appeared to be a thousand times more potent than ACTH 4-10; [D-Phe7] ACTH 4-10 inhibited the response rate at threshold level but was inactive at greater current intensities. The same effect was found following administration of ORG 2766 in a dose which was 20 times greater (1 microgram/rat) than that used in the first experiments. Lever pressing was not affected by treatment with ACTH 4-10 or ORG 2766 when a descending sequence of stimulus intensities was used within a session. Thus, ACTH-related peptides may affect motivational processes involved in self-stimulation rather than the reward of the stimulation per se. It is suggested that although ORG 2766 mimicked the action of ACTH 4-10 this synthetic peptide may have additional behavioural properties.

Adrenocorticotropic Hormone↗

PubMed1976

Differential effects of para-chlorophenylalanine on self-stimulation in caudate-putamen and lateral hypothalamus.

Rats were prepared with chronic bipolar electrodes aimed at either the caudate-putamen or lateral hypothalamus and those displaying consistent self-stimulation were given additional training at half-maximal current intensities. All subjects received an intragastric injection of para-chlorophenylalanine (400 mg/kg) and self-stimulation tests continued until pre-injection rates were re-established. Responding in both brain areas was suppressed 24 h after drug treatment. The next day, self-stimulation rates in the hypothalamus increased to 115% of pre-drug levels reaching a level of 180% by the third day of post-drug testing. In contrast, self-stimulation of sites in the neostriatum continued to decline, with minimal levels reaching 48% of control on the fourth post-drug day. Self-stimulation rates in both groups had returned to control levels by post-drug day 6. These data indicate that the role of serotonergic mechanisms in brain stimulation is locus specific, and that the specific nature of this role may be determined by interaction with other neurochemical systems. The possible interaction between dopaminergic and serotinergic mechanisms in the neostriatum is discussed as a model of self-stimulation in this region of the brain.

Animals↗

PubMed1989

Controllability of prestimulation of the medial prefrontal cortex determines the facilitation of self-stimulation and kindled seizures.

Electrical stimulation of the medial prefrontal cortex (MPC) was administered according to the triadic design typically used to demonstrate learned helplessness. Three groups received either controllable, uncontrollable or no stimulation during the pretreatment phase. The effects of this pretreatment on the acquisition of self-stimulation at the same electrode site were investigated in the second phase of the experiment. Relative to unstimulated controls, both controllable and uncontrollable prestimulation facilitated the acquisition of self-stimulation and produced higher self-stimulation rates. In addition, compared with controllable stimulation, pretreatment with uncontrollable stimulation produced a greater facilitation in self-stimulation rate. The unambiguous demonstration of a behavioural facilitation produced by pretreatment with uncontrollable stimulation is, effectively, the inverse of the typical learned helplessness finding. It was also found, in the second phase of the experiment, that 6 of the 7 rats previously exposed to uncontrollable stimulation developed full class 5 seizures. No behavioural evidence of kindling was seen in any of the other rats or during the prestimulation procedure. These data are interpreted in terms of kindling and stress effects both proximal and distal to the site of stimulation.

Animals↗

PubMed1976

Effects of dopamine-receptor blockade on self-stimulation in the monkey.

In a dose-response experiment it was shown that intraperitoneal injections of 0.062 mg/kg, and 0.1 mg/kg of the dopamine-receptor blocking agent and neuroleptic spiroperidol severely attenuate self-stimulation in the orbitofrontal cortex, hypothalamus, and in the region of the locus coeruleus, in the rhesus monkey and in the squirrel monkey. In the rhesus monkey intracranial injections of 6 mug of spiroperidol bilaterally into the nucleus accumbens or the hypothalamus attenuated self-stimulation of the amygdala, and injections into the orbitofrontal cortex attenuated self-stimulation of the amygdala and lateral hypothalamus. Self-stimulation at other sites tested (including the region of the locus coeruleus) was much less affected by the injections, and injections into the region of the locus coeruleus were ineffective. These results together with other control experiments suggest that spiroperidol can attenuate self-stimulation in the monkey independently of any motor impairment or sedation produced, and that dopamine receptors in particular brain regions are involved in self-stimulation of particular brain sites.

Animals↗

PubMed1991

The acquisition of self-stimulation of the medical prefrontal cortex following exposure to escapable or inescapable footshock.

The effect of acute stress on the acquisition of an instrumental action reinforced by electrical stimulation of the medial prefrontal cortex (MPC) was investigated by exposing rats to either escapable, inescapable or no footshock prior to daily self-stimulation training sessions. Treatment with inescapable footshock did not affect the number of sessions required for acquisition of MPC self-stimulation but did increase the rate of responding over acquisition sessions compared with the no-shock group. When the treatment footshock was escapable, however, both a facilitation in acquisition, as indexed by a reduction in the number of sessions to criterion, and an increase in the rate of MPC self-stimulation was found. These data were interpreted as offering evidence for the operation of a dopaminergic mechanism in the acquisition of MPC self-stimulation. Further, they indicate, contrary to the reported effects of footshock on self-stimulation of other brain areas, that exposure to acute stress has a facilitatory effect on the rate of self stimulation of the MPC.

Animals↗

PubMed1993

Neuronal plasticity induced by self-stimulation rewarding experience in rats--a study on alteration in dendritic branching in pyramidal neurons of hippocampus and motor cortex.

Self-stimulation rewarding experience promoted structural changes in pyramidal neurons of the CA3 region of the hippocampus and the Vth layer of the motor cortex in adult male Wistar rats. Self-stimulation experience was allowed for 1 h daily for a duration of 10 days through bipolar electrodes placed bilaterally in lateral hypothalamus and substantia nigra--ventral tegmental area. At the end of 10 days, rats were sacrificed, and rapid Golgi examination of the CA3 hippocampal and layer V pyramidal neurons of the motor cortex was made for a grand total of 1600 neurons from 80 rats divided into 4 groups. The neurons of the self-stimulation experienced (SS) group revealed a significant (ANOVA, F-test) increase in dendritic branching in the perisomatic domains. Such changes were not observed in neurons of sham control (SH), experimenter administered stimulation (EA) and normal control (NC) groups. SS animals also showed a significant increase in the thickness of lacunosum and radiatum laminae of CA3 neurons of the hippocampus. Our results reveal that both limbic and neocortical neurons undergo changes in dendritic branching patterns due to self-stimulation rewarding experience. It is tempting to hypothesize that neuronal plasticity is the result of motivation and learning experienced by rats which underwent self-stimulation.

Animals↗

PubMed1984

Self-stimulation in the brain stem after ipsilateral precollicular decerebration.

Rats were tested for self-stimulation after unilateral removal of the entire forebrain anterior to the superior colliculus. The stimulating electrodes were situated in the peribrachial region, just lateral to the superior cerebellar peduncle. Of 27 animals tested, 8 still self-stimulated after ipsilateral decerebration. Self-stimulation was exhibited from as early as a few hours to as long as 119 days after decerebration. The results are discussed in the context of the search for neural elements that subserve reinforcing brain stimulation.

Animals↗

PubMed1984

Serotonergic mediation of habenular self-stimulation in the rat.

The possible involvement of serotonergic neurons in self-stimulation of the habenular complex was examined in 16 rats. Animals were implanted with bipolar electrodes into the habenula (Hb), lateral hypothalamus (LH), or median raphe (MR), and trained to touch a dry spout to receive electrical stimulation of the brain. Metergoline (5 mg/kg, IP), a serotonergic receptor blocking agent, produced a complete suppression of self-stimulation with Hb and MR electrodes, but significantly less suppression with LH electrodes, suggesting that the rewarding effect of habenular stimulation is mediated by serotonergic neurons. In contrast to the differential effects of metergoline, chlorpromazine (2 mg/kg, IP), a catecholamine receptor blocking agent, suppressed both Hb and LH self-stimulation in a similar manner.

Animals↗

PubMed1963

Heart rate: differential effects of hypothalamic and septal self-stimulation.

Heart rate in rats was recorded during self-stimulation with electrodes permanently implanted in both the hypothalamus and the septal region. Acceleration was observed during stimulation of the hypothalamus, and deceleration during stimulation of the septal region. In both areas self-stimulation reduced variability in heart rate.

Animals↗

PubMed1998

Electrical self-stimulation in the central amygdaloid nucleus after ibotenic acid lesion of the lateral hypothalamus.

This experiment was carried out in order to investigate the involvement of lateral hypothalamus (LH) in electrical self-stimulation of the central amygdaloid nucleus (CeA). Adult male Sprague-Dawley rats were bilaterally implanted with a guide cannula situated above each LH and with two electrodes in the CeA. Self-stimulation was subsequently obtained separately from both right and left electrodes. The LH was then lesioned unilaterally by ibotenic acid (IBO) injection. Eight days later, the effect of this unilateral lesion on self-stimulation of the ipsilateral and contralateral CeA was tested. Then the neurons of the remaining non-lesioned LH side were lesioned with IBO and self-stimulation was tested 15 days after the second lesion. Both unilateral as well as bilateral lesions of LH produced a significant decrease in CeA self-stimulation rates but had no significant effect on the reward effectiveness. The unilateral lesions did not produce any modification of the rate-intensity function in the contralateral CeA. This lesion-induced depression in performance was reversed by treatment with phenobarbital. These results provide clear evidence that the rewarding effects of CeA electrical stimulation do not result from the activation of the LH outputs and that the apparent decrease in CeA self-stimulation may result from the LH lesion-induced increase in the frequency of epileptiform manifestations that occur following amygdaloid stimulation.

Amygdala↗

PubMed1977

Specific inhibition of hypothalamic self-stimulation by selective reuptake blockade of either 5-hydroxytryptamine or noradrenaline.

The effects of two new phthalane-derived bicyclic thymoleptics on hypothalamic self-stimulation were investigated in rats. The drugs, LU 10-171 and LU 5-003 are potent and highly selective reuptake blockers of 5-hydroxytryptamine (5-HT) and noradrenaline (NA), respectively. The use of a two-way shuttle-box permitted the differentiation of specific reward modulation effects from the variety of non-specific performance changes that these drugs may produce. Selective reuptake blockade of either 5HT or NA produced a dose-dependent reduction in reward that could be clearly dissociated from any non-specific performance decrements. Besides providing direct evidence for a significant role for 5HT in the mediation of hypothalamic self-stimulation, these data show that symphy increasing transmitter availability is not a sufficient condition to enhance self-stimulation reward. It is suggested that self-stimulation is dependent on response-contingent transmitter release and that any operation that increases reward-transmitter availability in a response-independent manner should attenuate self-stimulation.

Animals↗

PubMed1998

Long-lasting structural changes in CA3 hippocampal and layer V motor cortical pyramidal neurons associated with self-stimulation rewarding experience: a quantitative Golgi study.

Self-stimulation (SS) rewarding experience induced structural changes in CA3 hippocampal and layer V motor cortical pyramidal neurons in adult male Wistar rats has been demonstrated. In the present study, whether these structural changes are transient or of a permanent nature was evaluated. Self-stimulation experience was provided for 1 h daily over a period of 10 days through bilaterally implanted bipolar electrodes in the lateral hypothalamus and the substantia nigra-ventral tegmental area. Following 10 days of SS experience, the rats were sacrificed after an interval of 30 and 60 days for the quantitative analysis of the dendritic morphology in Golgi stained CA3 hippocampal and layer V motor cortical pyramidal neurons. The results revealed a significant increase in the dendritic branching points and intersections in apical and basal dendrites in both types of neurons in 30 days post-SS group compared to sham control. The total number of apical and basal dendrites were significantly increased in both 30 and 60 days post-SS groups of rats. This study suggests that SS experience induced structural changes are sustainable, even in the absence of rewarding experience.

Analysis of Variance↗

PubMed1978

Electrical self-stimulation of the brain: a model for the behavioral evaluation of toxic agents.

Rats implanted chronically with electrodes in the posterior lateral hypothalamus were trained to press levers in order to stimulate the brain electrically. Brief exposures to low oxygen concentrations reduced the lever pressing rate proportionately with the reduction in inspired oxygen. Similar reductions in self-stimulation rates could be observed in animals exposed to carbon monoxide or the organic solvent, trichloroethylene. Prolonged exposures of animals to hypoxia in chambers where self-stimulation rates as well as food and water intake via lever pressing were monitored, indicated that as oxygen concentration declined self-stimulation rates showed a marked increase for 12 hr followed by a decline. Food and water intake were depressed. This increase in self-stimulation was only observed at low (20 degrees C) ambient temperatures and was accompanied by central depletion of norepinephine. At high (30 degrees C) ambient temperatures, self-stimulation was depressed by hypoxia. The data show the importance of comparing acute with chronic exposure to toxic agents, as well as the influence of environmental temperature in influencing behavioral events. In addition, the data indicate that the self-stimulation technique offers unique advantages over behavior maintained by food or water reinforcers in evaluating toxic compounds.

Animals↗

PubMed1985

Effects of morphine and naloxone on thresholds of ventral tegmental electrical self-stimulation.

The involvement of opioid systems in self-stimulation reward was investigated by studying the effects of the opioid antagonist naloxone (10 mg/kg s.c.) and graded doses of morphine (0.3-5.0 mg/kg s.c.) on intracranial electrical self-stimulation (ICSS) in rats with electrodes in the ventral tegmental area. Lever pressing for ICSS was analyzed using three different procedures: determination of response rate i.e. the number of responses to high and threshold currents, measuring threshold current when response rate was kept low and relatively constant, determination of 'behavioural' threshold using a two-lever procedure in which a response on one lever resulted in a reset of the decreasing current to a high current contingent on a response to the other lever. It was found that low doses of morphine increased the response rate of ICSS behaviour and decreased the threshold whereas the higher doses decreased the response rate but also decreased the threshold current when measured with a rate insensitive procedure. Naloxone raised the threshold for ICSS and caused a corresponding decrease of response rate. In a second series of experiments in which the behaviour of rats which had been tested in one procedure was analysed using one of the other methods, it was observed that naloxone caused smaller changes, while the effects of morphine were at least comparable to those observed in the first series of experiments. The present data suggest that response rate insensitive procedures to analyse ICSS should be preferred to response rate sensitive ones, especially when the interaction of depressant drugs such as morphine with reward mechanisms is investigated.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Two substrates for medial forebrain bundle self-stimulation: myelinated axons and dopamine axons.

The directly activated substrates for medial forebrain bundle (MFB) self-stimulation are primarily low threshold, myelinated axons with absolute refractory periods of 0.4 to 1.2 msec, conduction velocities of 1 to 8 m/sec and current-distance constants of 1000 to 3000 microA/mm2. When small electrode tips or high currents are used, however, a second population of long refractory period (1.2 to 5 msec) axons is added. The excitability properties of this second population are almost identical with those of dopamine (DA) axons. Furthermore, the long-refractory period effects of MFB self-stimulation are reduced, but not completely blocked, by peripheral injections of alpha-flupenthixol, suggesting that dopamine axons make small contributions to MFB self-stimulation when small tips are used. Collision data, strength-duration data and refractory period data in various self-stimulation experiments are compared. Asymmetric collision effects, recently observed in cortical and striatal sites mediating electrically evoked turning, may help determine where synapses are located in circuits mediating electrically evoked behaviors. A neural model of symmetric, asymmetric and mixed collision is proposed.

Animals↗

PubMed1989

The appetite suppressant, d-fenfluramine, decreases self-stimulation at a feeding site in the lateral hypothalamus.

In prior studies rats showed a relative shift from self-stimulation to escape (i.e., from reward to aversion) following a large meal, obesity or anorectic doses of insulin. Racemic fenfluramine, on the other hand, decreased both self-stimulation and escape suggesting it had a general behavior suppressant property. To avoid the depressive, antidopaminergic effects of the l-isomer, this study tested the d-isomer which is primarily serotonergic. Rats were screened for stimulation-induced feeding and then trained to self-stimulate with one lever in 5-min periods that alternated with 5-min periods of automatic stimulation from which the animal could escape with a different lever. d-Fenfluramine (1.5-4.5 mg/kg IP) caused a dose-related decrease in self-stimulation. Stimulation-escape was relatively unaffected. This is interpreted as a decrease in feeding reward due to d-fenfluramine.

Animals↗

PubMed1993

Activation of single neurons in the rat nucleus accumbens during self-stimulation of the ventral tegmental area.

Single neurons (n = 76) were recorded in the nucleus accumbens septi (NAS) of rats self-stimulating the ipsilateral medial forebrain bundle (MFB) at the level of the ventral tegmental area (VTA). Responses evoked by rewarding trains of stimulus pulses fell into five categories. The first category (40% of the sample) was characterized by a single discharge at invariant latency in response to individual pulses of the train, and hence was termed "tightly time locked" (TTL). Two TTL neurons were collision tested, and both showed collision, suggesting that self-stimulation of the VTA may involve antidromic, and thus direct, activation of a substantial number of NAS axons. The second category (26%) was characterized by discharges that varied in latency from pulse to pulse and hence was termed "loosely time locked" (LTL). Responses of the remainder of the sample showed no coupling to individual pulses but were categorized based on general firing patterns during the train: excited (7%), inhibited (4%), and no change (23%). Irrespective of category, immediately after the self-stimulation session, the likelihood of evoked discharge at monosynaptic latency by single pulse stimulation of the ipsilateral fimbria was reduced (relative to pre-session level), concurrent with elevations in mean firing rate and motor activity. NAS neurons thus exhibit vigorous activation, apparently both antidromically and orthodromically, in response to VTA self-stimulation. The responses of certain LTL and TTL neurons increased as a function of pulse number in the train, suggestive of integrative mechanisms important for brain stimulation reward. Conduction velocities of directly activated (TTL) axons (0.41-0.65 m/sec) were slower than those previously reported for first-stage, reward-relevant axons. Nonetheless, an implication of direct activation of NAS (and other MFB) axons is that rewarding stimulation triggers action potentials that could invade all axonal branches, including those between the stimulation site and the soma, and send synaptic signals to target neurons. Such signals from NAS neurons could contribute to the increased motor behavior accompanying MFB self-stimulation, and/or could interact with dopamine-mediated signals projected to the NAS from reward circuitry.

Animals↗