Pharmacologic evidence for nociception resulting from noncontingent “rewarding” brain stimulation

Pollock, Jondavid; Kornetsky, Conan

doi:10.1016/0031-9384(90)90091-h

Cited by 7 publications

(2 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The electrical impulses that rats learn to self stimulate are brief (usually lasting less than one second) and stimulate neuronal activity (Wise et al, 1992). Previous evidence indicates that only the initial onset of brain stimulation is reinforcing (Pollock and Kornetsky, 1990). In contrast, in the present experiments high frequency DBS was administered continuously throughout the reinstatement session in order to suppress neuronal activity.…”

Section: Discussionmentioning

confidence: 99%

Deep Brain Stimulation of the Nucleus Accumbens Shell Attenuates Cocaine Priming-Induced Reinstatement of Drug Seeking in Rats: Figure 1.

Vassoler¹,

Schmidt²,

Gerard³

et al. 2008

J. Neurosci.

173

134

View full text Add to dashboard Cite

Increasing evidence suggests that deep brain stimulation (DBS), which is currently being used as a therapy for neurological diseases, may be effective in the treatment of psychiatric disorders as well. Here, we examined the influence of DBS of the nucleus accumbens shell on cocaine priming-induced reinstatement of drug seeking, an animal model of relapse. Rats were allowed to self-administer cocaine (0.25 mg, i.v.) 2 h daily for 21 d and then cocaine-seeking behavior was extinguished by replacing cocaine with saline. During the reinstatement phase, DBS was administered bilaterally to the nucleus accumbens shell through bipolar stainless steel electrodes. Biphasic symmetrical pulses were delivered at a frequency of 160 Hz and a current intensity of 150 A. DBS began immediately after a priming injection of cocaine (0, 5, 10, or 20 mg/kg, i.p.) and continued throughout each 2 h reinstatement session. Results indicated that only the higher doses of cocaine (10 and 20 mg/kg) produced robust and reliable reinstatement of cocaine seeking. DBS of the nucleus accumbens shell significantly attenuated the reinstatement of drug seeking precipitated by these higher cocaine doses. Additional experiments indicated that this DBS effect was both anatomically and reinforcer specific. Thus, DBS of the dorsal striatum had no influence on cocaine reinstatement and DBS of the accumbens shell did not affect the reinstatement of food seeking. Together, these results suggest that DBS of the nucleus accumbens shell may be a potential therapeutic option in the treatment of severe cocaine addiction.

show abstract

Section: Discussionmentioning

confidence: 99%

Deep Brain Stimulation of the Nucleus Accumbens Shell Attenuates Cocaine Priming-Induced Reinstatement of Drug Seeking in Rats: Figure 1.

Vassoler¹,

Schmidt²,

Gerard³

et al. 2008

J. Neurosci.

173

134

View full text Add to dashboard Cite

show abstract

“…These observations raised the argument of whether experimenter-administered ICS is aversive or whether rats are attempting to regulate their brain stimulation. Recently Pollock and Kornetsky (1990), using pharmacological probes, inferred that rats worked to terminate medial forebrain bundle ICS due to the nociceptive properties of the noncontingent stimulation. In contrast, although some rats have been shown to prefer a signaled or response-contingent ICS over unsignaled or noncontingent ICS (Cantor and Lolordo, 1970;Tsang and Stutz, 19841, others prefer noncontingent ICS over no stimulation (Cantor and Lolordo, 1972), arguing that noncontingent stimulation may not only be nonaversive, it may indeed have positive reinforcing properties.…”

Section: Introductionmentioning

confidence: 99%

Ventral tegmental self‐stimulation selectively induces opioid peptide release in rat CNS

Stein

1993

Synapse

View full text Add to dashboard Cite

Intracranial self-stimulation (ICS) is thought to activate neuronal systems involved in processing natural reinforcing agents. Metabolic mapping studies have previously demonstrated a subset of CNS structures specifically engaged by ICS in animals receiving stimulation actively vs. passively. Since opiates are known to enhance ICS behavior and presumably its reinforcing properties, the current study addressed the question of the role of opioid peptides as mediators of ICS. Rats were trained on a fixed ration (FR) 20 schedule of responding maintained by ICS. Following response stabilization, rats were assigned either to an active or a corresponding yoked stimulation group at 1 of 2 schedules of reinforcement (i.e., FR1-YFR1, FR20-YFR20, or sedentary control), and opioid peptide release was inferred from in vivo receptor occupancy. Autoradiographic analyses identified 3 groups of structures. Treatment-induced alterations in occupancy were seen in the medial dorsal nucleus of the thalamus, basolateral amygdala, ventral pallidum, medial habenula, dorsal raphe, posterior hypothalamus, substantia nigra pars compacta, agranular preinsular cortex, and zona incerta. Depending upon the structure, peptide release was dependent upon stimulus contingency (active vs. yoked) and/or schedule (FR1 vs. FR20). Evidence for ICS-induced inhibition of peptide release was found in the habenula and preinsular cortex. Nine additional structures, all components of, or receiving projections from, the limbic system, revealed complex interactions between ICS treatment and the electrode side. Finally, a widespread ipsilateral increase in receptor binding was seen rostrally from the cingulate, olfactory tubercle, and nucleus accumbens, along the lateral hypothalamus and hippocampus, and extending caudally to the substantia nigra and ventral tegmentum. These later effects appear to be related to stimulation-induced changes in blood flow and subsequent ligant presentation increases. Collectively, these data point towards the ability of rewarding brain stimulation to activate discrete neuronal opioid systems contingent upon specific behavioral as well as stimulus conditions.

show abstract

Animal Studies in Deep Brain Stimulation Research

Feenstra

Denys

2012

Deep Brain Stimulation

View full text Add to dashboard Cite

Pharmacologic evidence for nociception resulting from noncontingent “rewarding” brain stimulation

Cited by 7 publications

References 19 publications

Deep Brain Stimulation of the Nucleus Accumbens Shell Attenuates Cocaine Priming-Induced Reinstatement of Drug Seeking in Rats: Figure 1.

Deep Brain Stimulation of the Nucleus Accumbens Shell Attenuates Cocaine Priming-Induced Reinstatement of Drug Seeking in Rats: Figure 1.

Ventral tegmental self‐stimulation selectively induces opioid peptide release in rat CNS

Animal Studies in Deep Brain Stimulation Research

Contact Info

Product

Resources

About