PubMed Health⌕ Search

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 613 records · Page 34Linked to original sources
PubMed1990

Amphetamine affects the extinction of self-stimulation differently in prefrontal cortex and posterior hypothalamus of rats.

The effects of amphetamine on the extinction of intracranial self-stimulation (ICSS) and on postextinction ICSS performance were examined in rats implanted with electrodes either in medial prefrontal cortex (mPFC) or in the posterior hypothalamus-ventral tegmental area (PH-VTA). Lever-pressing for ICSS was allowed to stabilize in daily 15-minute sessions before each animal was exposed to 5 minutes of extinction (responding without reward). Animals were administered either 0.25 mg/kg d-amphetamine or saline before baseline, extinction and postextinction sessions. After amphetamine treatment, the number of lever presses during extinction was higher in mPFC animals and lower in PH-VTA animals compared with saline-treated controls. Rates did not change immediately after extinction but, one day later, rates had increased in all saline-treated animals (both PH-VTA and mPFC animals) and had decreased in all amphetamine-treated animals. These findings demonstrated that the effects of amphetamine on the extinction of ICSS were different in cortical and hypothalamic sites, possibly because of regional differences in stimulus-evoked reinforcement and inhibitory processes.

Animals↗
PubMed1985

The substrates for self-stimulation of the lateral hypothalamus and medial prefrontal cortex: a comparison of strength-duration characteristics.

The directly activated substrates for self-stimulation of the lateral hypothalamus (LH) and medial prefrontal cortex (MPFC) were described by comparing their strength-duration characteristics. The current required to maintain a half-maximal rate of lever pressing was traded off against the pulse duration while all other stimulation parameters were kept constant. In this manner, cathodal strength-duration curves were obtained at four LH and eight MPFC sites; anodal curves were obtained at two of the LH and six of the MPFC sites. In general, the cathodal LH curves had lower rheobases than the cathodal MPFC curves and continued to descend after the MPFC curves had levelled off. At short pulse durations, the anodal curves lay above the cathodal curves, a finding more pronounced in the LH data. The two sets of curves converged at the longer pulse durations. The differences in the strength-duration curves are consistent with the notion that different directly stimulated neurons are responsible for the rewarding effects of LH and MPFC stimulation. Anatomical and physiological properties that could account for these differences are discussed.

Animals↗
PubMed2001

Immunohistochemical characterisation of Fos-positive cells in brainstem monoaminergic nuclei following intracranial self-stimulation of the medial forebrain bundle in the rat.

Fos immunostaining was used as a marker of neuronal activity following intracranial self-stimulation (ICSS) of the medial forebrain bundle (MFB) in the rat, and was combined with immunostaining for tyrosine hydroxylase (TH), serotonin (5-HT), gamma-aminobutyric acid (GABA), or NR1 (one of the glutamate N-methyl- D-aspartate receptor subunits) for purposes of neurochemical identification. ICSS induced a significant but different degree of increase in the number of Fos-immunopositive (Fos+) cells in the six brainstem monoaminergic nuclei examined, which included the ventral tegmental area (VTA), substantia nigra pars compacta (SNc), dorsal raphe nucleus (DR), median raphe nucleus (MR), locus coeruleus (LC), and A7 noradrenaline cells. Densely labelled Fos+ cells were observed in the LC following ICSS, and many of these Fos+ cells were colocalized with TH. Similarly, many of Fos+ cells in the A7 and DR/MR were colocalized with TH and 5-HT, respectively. By contrast, a smaller number of Fos+ cells was detected in the VTA and SNc following the ICSS, and in these regions the majority of Fos+ cells were not colocalized with TH. Although results among regions quantitatively differed, the ICSS induced a significant increase in the number of double-labelled cells (GABA+/Fos+ or NR1+/Fos+) in all of the VTA, DR, and LC, in which the ICSS produced an ipsilaterally weighted increase in Fos-like immunoreactivity. These results suggest that ICSS of the MFB induces differential Fos expression within monoaminergic and GABAergic neurons in brainstem monoaminergic nuclei under modulation by glutamatergic afferents.

Animals↗
PubMed1983

Monoamines and self-stimulation of the medial prefrontal cortex in the rat.

The participation of noradrenaline (NE) and serotonine (5-HT) in self-stimulation (SS) of the medial prefrontal cortex (MPC) in the rat has been studied. Three groups of rats with bilateral electrodes implanted into the MPC were used in these experiments. In one of the groups, electrodes were also implanted into the locus coeruleus. In the first group, the rats received systemic injections of the following drugs: clonidine (alpha-agonist), phenoxybenzamine (alpha-antagonist), isoproterenol (beta-agonist) and propranolol (beta-antagonist). In the second group, p-chlorophenylalanine (a 5-HT synthesis inhibitor) was administered intragastrically and SS measured during the following 16 days. In these two groups of rats and previous to every SS session, spontaneous motor activity (SM) was measured as control for non specific effects of the drugs. In a third group of rats, lesions of the locus coeruleus were performed unilaterally and SS measured in both prefrontal cortex during the following 16 days post-lesion. SS contralateral to the lesioned side served as control for non-specific effects of the lesions. After all these treatments, SS of the MPC was not specifically affected. Our results suggest the non participation of NE and 5-HT terminals in the neural substrates underlying SS of the MPC.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

[Relationship between the frequency of self stimulation and the strength and duration of stimulation].

In experiments on thirteen rats with electrodes in the lateral hypothalamus, with a simultaneous change in current intensity I and of stimulation duration T, two variants were obtained of the empirical response surface of the self-stimulation (SS) frequency: with the maximum SS frequency, located within the surface boundaries (peak variant), and with the maximum at one of its boundaries (side variant). An equation has also been deduced on the regression of SS frequency on the parameters I and T, which quite accurately defines the experimental and rated data (R = 0.57 divided by 0.97). It has been established that current intensity has a greater effect on SS frequency as compared with the stimulation duration and that the influences of these parameters are relatively independent of one another.

Animals↗
PubMed1989

Shuttling behavior and intracranial self-stimulation reward: behavioral changes as a function of intensity and independence of on/off times.

The correlation between "on" time and "off" time in intracranial self-stimulation shuttling behavior under continuous reinforcement was examined. The results showed that if a tendency for positive trend in the data was accounted for, no consistent correlation could be found between within-trial on time and the succeeding or preceding off time either as a function of intensity or number of trials. However, mean on and off times showed a significant positive correlation at low to moderate intensities. Total charge, total time, and proportion of time on remain relatively constant over a series of trials despite significant changes in on time, off time, and crossing rate. The results indicate the importance of selecting suitable measures in the study of shuttling behavior.

Animals↗
PubMed1999

Lesions of midline midbrain structures leave medial forebrain bundle self-stimulation intact.

Previous work with psychophysically-based collision methods and pharmacological manipulation suggests a role in medial forebrain bundle (MFB) self-stimulation for neurons lying along the midline between the cerebral hemispheres, in the mid- and/or hindbrain. Also, recently-proposed models of the anatomical substrate for medial forebrain bundle stimulation reward suggest that at least part of the directly-activated axons of this substrate arise from mid- and/or hindbrain somata, bifurcate, and send bilateral projections to the MFB of each hemisphere. Branches of these axons are thought to cross the midline at some point near the ventral tegmental area. This study examines the effects on MFB stimulation reward of lesioning midbrain structures that lie along the midline between hemispheres. In 13 rats, lesions of the median raphe, the decussation of the superior cerebellar peduncle, or the interpeduncular nucleus were all ineffective in altering the stimulation frequency required to maintain half-maximal levels of operant responding for stimulation reward. These results are discussed in terms of implications for recent models of the anatomical substrate for brain stimulation reward.

Animals↗
PubMed1983

Afferent pathways to points of self-stimulation in the medial prefrontal cortex of the rat as revealed by the horseradish peroxidase technique.

Afferent projections to points of self-stimulation (SS) in the medial prefrontal cortex (MPC) of the rat were studied using the horseradish peroxidase (HRP) technique. Intracranial microinjections of HRP (30%) were delivered at the same stereotaxic points at which the electrodes eliciting SS were located. Retrogradely transported HRP labeled neurons in different thalamic, hypothalamic, mesencephalic and pontine areas. In the thalamus, labeled neurons were found in the dorsomedial, anteromedial, anteroventral, ventral, ventromedial, posteromedial, paratenial, parafascicular nuclei and n. reuniens. Labeled neurons in mesencephalic areas were found in the n. interpeduncularis, ventral tegmental area (AVT) and substantia nigra (SN). In the pons, labeled neurons were found in the locus coeruleus and in the periaqueductal gray. Other nuclei in which labeled neurons were also found were: lateral hypothalamus (LH), periventricular gray and zona incerta (ZI). Theoretically it is possible that all these afferent areas contribute to SS of MPC. This assumption is discussed and criticized in connection with previous literature on SS. It is suggested that only specific areas and their projections are good candidates for the neural mechanisms involved in the reward produced by electrical stimulation of the prefrontal cortex.

Afferent Pathways↗
PubMed2003

Reinforcing versus anticonvulsant drugs: effects on intracranial self-stimulation rate-frequency M50 indices.

Drugs of abuse, such as amphetamine and morphine, produce reward-related shifts on intracranial self-stimulation (ICSS) thresholds. The facilitatory effects on ICSS thresholds of drugs that act through the GABAergic system, however, are reported to be attributed to their antiseizure and anticonvulsant effects, rather than their reinforcing effects. Using a rate-frequency ICSS paradigm, we examined the effects of amphetamine (a reinforcing drug of abuse that acts via the catecholaminergic system), pentobarbital (a GABA(A) receptor agonist and reinforcing barbiturate with anticonvulsant properties), and gabapentin (a nonspecific GABAergic agonist and anticonvulsant with low abuse potential) on ICSS M(50) indices. All three doses of amphetamine (0.5, 1.0, and 2.0 mg/kg) and pentobarbital (2.5, 5.0, and 10.0 mg/kg) significantly lowered rate-frequency M(50) values. Gabapentin, on the other hand, significantly raised rate-frequency M(50) values, albeit only at the highest dose administered (30 mg/kg). Our results indicate that shifts in ICSS M(50) values produced by pentobarbital are associated with the reinforcing, not the anticonvulsant, effect of pentobarbital. These results are consistent with the view that there is a common system underlying the reinforcing effects of drugs and ICSS reinforcement, and suggest that the reinforcing and anticonvulsant effects of GABA agonists are dissociable.

Acetates↗
PubMed1984

Visual evoked potentials and nociceptive thresholds in high and low self-stimulators.

Tail flick latencies (TFL) were examined in order to distinguish between rats from genetically high (HI) and low (LO) self-stimulation lines (LC2-HI and LC2-LO). In addition, slow secondary negative wave (SNW) of the visual evoked potential, which is considered to be a sensitive index of normal and pharmacologically-induced behavioral arousal, was analysed. Small, albeit statistically significant enhancement of SNW was obtained in LO rats. Unlike LO animals, HI rats gained in SNW amplitude during repeated photic stimulation. The difference between the lines was highly significant. TFL assessment yielded slightly reduced (NS) values for HI rats. However, when TFL and SNW data were compared it appeared that TFL vary as a function of SNW amplitude in LO but not in HI rats, (r = 0.9). SNW may be employed as a predictor of the nociceptive threshold in rats.

Animals↗
PubMed1994

Kindled epileptic seizures, postictal refractoriness, status epilepticus, and electrical self-stimulation.

A single stimulus applied once daily to the limbic system commonly leads to convulsive seizures yet seizures are relatively infrequent during intracranial self-stimulation (ICSS), a procedure that involves many hundreds of similar stimuli. The present study examined the possible role of electrode site, interstimulus interval, afterdischarge and reinforcement thresholds and postictal refractoriness in accounting for this paradox. Electrode location was an overriding factor: seizures were never seen with hypothalamic implants posterior to the level of the ventromedial nucleus but were elicited by the majority of more rostral reward sites. Frequent repeated stimulation by ICSS did not in itself prevent subsequent kindling or reverse the effects of earlier kindling; on the contrary, seizures induced by ICSS showed a progressive increase in severity similar to the progression produced by conventional kindling. Individual convulsive seizures, as in previous studies, conferred transient protection against further seizures whether from ICSS or from kindling. More prolonged protection occassionally developed after repeated convulsive seizures: protection was accompanied by continuous EEG slow-waves corresponding in presentation to clinical petit mal status. Prolonged resistance to seizures has also been reported after tonic-clonic status epilepticus causing temporal lobe damage. The relative infrequency of seizures during ICSS ordinarily appears to depend on the siting of the electrodes, on distinct short- and long-term postictal refractory states, and on the rat learning to restrict stimulus input to subseizural levels.

Animals↗
PubMed1993

Effects of intracranial self-stimulation on selected physiological variables in rats.

The purpose of this investigation was to characterize selected metabolic, cardiovascular, and hormonal responses to reinforcing intracranial self-stimulation (ICSS) of the ventral tegmental area (VTA) in rats. Twenty male Sprague-Dawley rats were stereotaxically implanted with bipolar electrodes aimed at the VTA of the brain. Rats were trained to lever-press for ICSS for 1 wk. While they adapted to the experimental environment by sitting in a metabolic operant chamber, they were connected to the electrode cable but did not lever-press. All animals were instrumented with arterial catheters. Rats receiving contingent stimulation (C-St; n = 10) performed 30 min of lever pressing in the metabolic operant chamber for reinforcing brain stimulation. Oxygen consumption (VO2), heart rate (HR), mean arterial pressure (MAP), and rectal temperature (Trec) increased with the onset and continuation of contingent brain stimulation over 30 min (P < 0.05). In addition, plasma norepinephrine (NE), epinephrine (Epi), and corticosterone increased significantly above resting values in C-St rats (P < 0.05). Five animals received investigator-delivered reinforcing brain stimulation (noncontingent stimulation; NC-St), with MAP, HR, VO2, NE, and Epi increasing significantly above resting values (P < 0.05). Trec and corticosterone were not responsive to noncontingent brain stimulation. With the exception of HR, nonstimulated controls (n = 5) did not experience increases above resting values in any of the variables measured. The responses suggest that contingent brain stimulation reward elicits heightened sympathetic arousal.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1970

Temporal summation and refractoriness in hypothalamic reward neurons as measured by self-stimulation behavior.

A neurophysiological technique of double-pulse stimulation has been applied to freely moving rats with chronic indwelling electrodes in the hypothalamic reward area. Self-stimulation thresholds, measured as a function of the interpulse interval, generated curves with time constants characteristic of refractory periods and temporal synaptic summation. The results indicate a way of studying central neuronal processes for which the overt behavior of the animal is the dependent variable.

Animals↗
PubMed2000

Acute opioid but not benzodiazepine dependence in rats responding for intracranial self-stimulation.

RATIONALE: Four-hour pretreatment with a single dose of morphine or related opioids sensitizes rats responding for intracranial self-stimulation (ICSS) to the rate-decreasing effect of naltrexone, indicative of antagonist-precipitated withdrawal from acute opioid dependence. OBJECTIVES: To determine whether sensitization to naltrexone could be observed in morphine-pretreated rats responding under a progressive ratio (PR) schedule of ICSS and to determine whether acute pretreatment with benzodiazepines produces similar sensitization to flumazenil. METHODS: Rats with an electrode in the medial forebrain bundle were trained to respond under an ICSS PR schedule, in which the number of responses required for a 250-ms stimulus started at one, then increased gradually. If no responding occurred for 30 s, the response requirement reverted to a single response and the break point was operationally defined. RESULTS: Pretreatment (4-h) with 3.0 mg/kg or 5.6 mg/kg morphine reduced the ED25 values of naltrexone for decreasing response rate from 18+/-6.7 mg/kg to 0.021+/-0.006 mg/kg and 0.006+/-0.001 mg/kg, respectively. Changes in break point usually paralleled changes in response rate. In contrast, 4- to 24-h pretreatment with the benzodiazepines chlordiazepoxide (30 mg/kg and 100 mg/kg) or diazepam (3.0 mg/kg and 10 mg/kg), behaviorally-active doses, did not significantly alter sensitivity to the effects of flumazenil (1.0-30 mg/kg). CONCLUSIONS: These results show that PR ICSS provides a stable behavioral baseline for testing drugs in rats and extend to this procedure the generality of the phenomenon of acute opioid dependence. There was no comparable evidence of acute benzodiazepine dependence, suggesting that there are differences in the ways that opioid and benzodiazepine agonists initiate the adaptive changes that underlie the state of physical dependence.

Animals↗
PubMed1975

Effects of amphetamine isomers and neuroleptics on self-stimulation from the nucleus accumbens and dorsal noradrenergic bundle.

In an attempt to examine the possible role of noradrenergic (NA) and dopaminergic (DA) systems in intracranial self-stimulation (ICS), the rate-increasing effects of D- and L-amphetamine on ICS were determined in rats with nucleus accumbens electrodes (DA placement) or dorsal NA bundle electrodes (NA placement). The D-isomer produced a significantly greater increase in ICS than did the L-isomer in animals with dorsal NA bundle electrodes. In contrast, the amphetamine isomers were equipotent in facilitating ICS in animals with nucleus accumbens electrodes. These data, together with previous observations, suggest that there exists a correlation between equipotential effects of D- and L-amphetamine and DA electrode placements on the one hand, and prepotent effects of D-amphetamine and NA electrode placements on the other. Pimozide and haloperidol, which in low doses are thought to specifically block DA receptors, decreased ICS obtained from both DA and NA electrode placements. It is suggested that neuroleptic drugs may produce a general disruption of operant behavior and that the decrease in ICS produced by these agents does not therefore necessarily implicate dopaminergic mechanisms in the neurochemistry of reward.

Amphetamine↗
PubMed1999

Dissociation of dopamine release in the nucleus accumbens from intracranial self-stimulation.

Mesolimbic dopamine-releasing neurons appear to be important in the brain reward system. One behavioural paradigm that supports this hypothesis is intracranial self-stimulation (ICS), during which animals repeatedly press a lever to stimulate their own dopamine-releasing neurons electrically. Here we study dopamine release from dopamine terminals in the nucleus accumbens core and shell in the brain by using rapid-responding voltammetric microsensors during electrical stimulation of dopamine cell bodies in the ventral tegmental area/substantia nigra brain regions. In rats in which stimulating electrode placement failed to elicit dopamine release in the nucleus accumbens, ICS behaviour was not learned. In contrast, ICS was acquired when stimulus trains evoked extracellular dopamine in either the core or the shell of the nucleus accumbens. In animals that could learn ICS, experimenter-delivered stimulation always elicited dopamine release. In contrast, extracellular dopamine was rarely observed during ICS itself. Thus, although activation of mesolimbic dopamine-releasing neurons seems to be a necessary condition for ICS, evoked dopamine release is actually diminished during ICS. Dopamine may therefore be a neural substrate for novelty or reward expectation rather than reward itself.

Animals↗