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PubMedDate not supplied

Behavioral measures of conduction velocity and refractory period for reward-relevant axons in the anterior LH and VTA.

Psychophysical techniques were used to estimate the conduction velocities and refractory periods of reward-relevant fibers in the anterior lateral hypothalamus (ALH) and ventral tegmental area (VTA). Six male rats of the Long-Evans strain served as subjects. Stimulation consisted of trains of pulse pairs delivered to the ALH and VTA; each stimulation site received one pulse from each pair. Collision of antidromic and orthodromic action potentials along the same reward-relevant axons was inferred from a decrease in the effectiveness of the stimulation at short intra-pair intervals. Significant collision-like effects were obtained for 5 of the 6 subjects, supporting the notion that reward-relevant neurons directly link the ALH and VTA. Estimates of the slowest conduction velocities ranged from 0.4 to 5.5 m/s. Refractory period estimates, obtained by delivering the trains of pulse pairs to a single stimulation site, ranged from 0.5 to 5.4 ms. The overlap between these psychophysical estimates and the electrophysiological estimates obtained in the accompanying paper is consistent with the notion that reward-relevant MFB fibers arise in one or several rostral MFB nuclei.

Action Potentials↗
PubMed1976

Dose-dependent dual effect of morphine on electrophysiologic correlates of positive reinforcement (reward contingent positive variation: RCPV) in the cat.

In cats trained to press a lever for milk reward, the postreinforcement EEG synchronization (PRS) and the associated epicortical steady potential shift, known as "Reward Contingent Positive Variation (RCPV) restricted to the occipital cortex, were studied prior to and after administration of morphine sulfate. Contrary to what has ordinarily been described as a typical feline response to morphine, such as restlessness, aggressiveness, rage, and exaggerated startle reaction to environmental stimuli, associated with an increased tonus of the brainstem-hypothalamic arousal system and desynchronized EEG patterns, doses of 0.1-0.4 mg/kg, IM, caused a strong monophasic enhancement of the PRS-RCPV phenomenon. Doses of 0.6-1.0 mg/kg, IM, had clearly a biphasic action: the initial enhancement of the PRS-RCPV responses was followed by their strong suppression. Chlorpromazine (0.1-1.6 mg/kg, i.e.) promptly restored the EEG responses. During the peak effect of the enhancing doses of morphine, the reward-related EEG phenomena also occurred prior to or after the nonrewarded bar press when the animals licked the empty cup. This dissociation of the PRS-RCPV from consumption was much more conspicuous in animals whose control frequency of the PRS oscillations was higher, and after morphine showed more significant slowing. Despite the strong facilitation of the PRS-RCPV in the presence of light, morphine, in contrast to LSD-25, was not able to restore the reward-induced phenomena in the dark.

Animals↗
PubMed1981

Disruption of autoshaped responding to a single of brain-stimulation reward by neuroleptic drugs.

Repeated pairing of the onset of a stationary light (CS) that signalled electrical stimulation of brain-stimulation reward sites in the mesencephalon (US) resulted in autoshaped approach behavior to the CS. After acquisition of approach to the CS two groups of rats were injected with either pimozide (0.15, 0.50, or 1.0 mg/kg) or haloperidol (0.05, 0.10, or 0.15 mg/kg) prior to test sessions consisting of 30 CS-US pairings. Both neuroleptic drugs caused a significant dose-related attenuation of the autoshaped CS-approach. A within-session analysis of responding after treatment with the high dose of each drug indicated that most responses occurred in the first 10 trials, a result that appears to rule out a direct effect of the drugs on sensory processes and orientation. The effect of repeated testing with pimozide (1.0 mg/kg) or haloperidol (0.15 mg/kg) was compared to three sessions with CS alone (extinction). Autoshaped CS-approaches declined gradually over the three extinction sessions, in contrast to the immediate and sustained disruption of approaching during the three drug sessions. These data suggest that neuroleptic-induced suppression of autoshaped CS-approach with brain-stimulation reward cannot be attributed solely to a block of reward processes. It is suggested that neuroleptic drugs disrupt neural mechanisms by which signals of impending reward release pre-organized response patterns.

Animals↗
PubMed1986

Effects of pimozide on positive and negative incentive contrast with rewarding brain stimulation.

Positive and negative contrast effects with brain-stimulation reward were inferred from significant differences in rate/intensity curves obtained by ascending, random and descending orders of current presentation. The neuroleptic drug pimozide caused a dose-related attenuation of both positive and negative contrast. A dose of 0.1 mg/kg blocked positive contrast obtained by comparing ascending and random rate/intensity curves. Negative contrast and threshold current intensities for brain-stimulation reward at sites in the ventral tegmental area were unaffected by the low dose (0.1 mg/kg) of pimozide. Higher doses of pimozide (0.25, 0.4 mg/kg) blocked both positive and negative contrast effects, and caused a significant elevation in threshold current intensities under the random order condition. Two doses (0.25, 0.4 mg/kg) of pimozide were associated with performance deficits as the response rates at the maximum current intensities were attenuated significantly with each order of current presentation. These demonstrations of both positive and negative contrast are consistent with the theoretical position linking brain-stimulation reward to incentive motivation. Furthermore the effects of the dopamine receptor antagonist pimozide are consistent with a role for dopamine in brain-stimulation reward and also raise the possibility of dopaminergic involvement in incentive contrast phenomena.

Analysis of Variance↗
PubMed1988

Haloperidol blocks the response-reinstating effects of food reward: a methodology for separating neuroleptic effects on reinforcement and motor processes.

To test the hypothesis that dopamine antagonist drugs attenuate the reinforcing properties of food, rats previously trained to traverse a straight runway for food reward subsequently underwent extinction sessions. After running speeds had substantially decreased, rats received a single food-rewarded trial either in the presence or absence of haloperidol (0, 0.15 or 0.30 mg/kg IP). Twenty-four hours later, animals were tested for reinstatement of the running response during a drug-free test trial. Animals that were nondrugged during the food-rewarded trial showed increases in running speed on the test trial relative to extinction baseline speeds. In contrast, animals under the influence of haloperidol during the food-rewarded trial failed to show test day increases in running speed. Additional control groups ruled out the possibility that the haloperidol results were due to either motor or state-dependent learning effects. The findings support the view that dopamine systems play a role in the neural substrates underlying food reinforcement. In addition, the study demonstrates a simple and effective methodology for separating neuroleptic effects on motor and reinforcement processes.

Animals↗
PubMed1988

The reinforcing properties of the mixed agonist-antagonist buprenorphine as assessed by brain-stimulation reward.

The effect of buprenorphine on the threshold for rewarding brain stimulation to the medial forebrain bundle-lateral hypothalamus was determined in rats using a rate-independent psychophysical method. Increased sensitivity to rewarding brain stimulation (i.e., lowering of the reward threshold) was used as the measure of a drug's reinforcing action. Buprenorphine (SC) produced a significant dose-dependent lowering of the reward threshold, with effective doses varying from 0.004-0.06 mg/kg. These results are consistent with buprenorphine's euphoria producing effects in humans and its ability to sustain self-administration in animals and suggest that buprenorphine may have abuse potential.

Animals↗
PubMed1990

Evidence for the rewarding effects of ethanol using the conditioned place preference method.

Rats were tested for the rewarding effects of ethanol using a place preference conditioning procedure. After receiving a total of 15 daily conditioning trials under 1.0 g/kg ethanol (IP), a significant place preference was produced. Subjects conditioned using saline or 0.5 g/kg ethanol showed no changes in place preference. This study suggests that failures to demonstrate rewarding effects from ethanol with the conditioned place preference method may be due to an insufficient number of conditioning trials or to an inadequate exposure to the drug. The fact that place preference conditioning was effective in demonstrating ethanol reward while other methods have been equivocal suggests that this method may be a valuable technique for studying the mechanisms of ethanol reward.

Animals↗
PubMed1990

Acute and chronic desipramine treatment effects on rewarding electrical stimulation of the lateral hypothalamus.

Two weeks of chronic desipramine HCl (DMI) (10 mg/kg, IP) treatment did not alter reward or motor/performance components of intracranial self-stimulation (ICSS) as assessed with the rate-frequency method. Acute DMI treatment produced an ICSS reward decrement relative to saline control treatment, which was similar in size on Day 1 and Day 15 of chronic testing. The failure to find a chronic DMI effect on ICSS reward suggests that ICSS in normal rats may not be a valid animal model of depression. A better paradigm may be to test the ability of antidepressants to reverse a chronic reduction in ICSS reward function that is first produced by some other method.

Animals↗
PubMed1994

Effects of cocaine and GBR-12909 on brain stimulation reward.

Cocaine and GBR-12909, two dopamine reuptake blockers, were administered in a multiple current rate-frequency curve-shift test of intracranial self-stimulation (ICSS) reward in rats with medial forebrain bundle (MFB) electrodes. Acute injections of cocaine (0, 5, 15, 30 mg/kg, IP) increased ICSS reward at all currents (501, 316, 200 microAmps) as measured by decrease half-maximal frequency threshold. Cocaine also increased operant motor performance but only at the low current. In addition, cocaine increased dynamic interval at the highest dose at all currents. Similar treatment with GBR-12909 (0, 5, 10, 20 mg/kg, IP) significantly increased ICSS reward (decreased threshold) especially at the medium dose in all currents and had no significant effects on operant motor performance or dynamic interval. The major novel finding of the present study is that the rewarding effects of both drugs was not dependent on the choice of stimulation current, which is discussed as simplifying future psychophysical testing of psychostimulant drugs in the ICSS rate-frequency curve-shift paradigm.

Animals↗
PubMed1994

Bromocriptine, a D2 receptor agonist, lowers the threshold for rewarding brain stimulation.

Drug-induced lowering of brain stimulation reward threshold can serve as a model for the pharmacological activation of reward pathways. Here, the effects of bromocriptine, a direct D2 dopamine receptor agonist, on reward thresholds were investigated. Bromocriptine administration resulted in the significant lowering of threshold levels in all test animals, suggesting that this agent can activate the same reward processes as do abused substances such as cocaine and morphine.

Animals↗
PubMed1996

Measurement issues in curve-shift analysis of apomorphine effects on rewarding brain stimulation.

The direct dopamine agonist apomorphine has been reported to reduce the rewarding efficacy of lateral hypothalamic (LH) self-stimulation. This effect has been claimed to support the notion that dopamine mediates the rewarding effects of LH self-stimulation. Using a standard rate-frequency curve-shift paradigm with ascending order of frequency presentation, we also found that apomorphine (0.1-0.8 mg/kg, SC) appeared to decrease LH self-stimulation reward. These apparent rightward curve shifts were exacerbated by shortening the test duration, which also produced a number of sessions in which the subjects did not respond at all. When the presentation order of stimulation frequencies was reversed, apomorphine did not produce large reward decreases. These results suggest that the previously reported effects of apomorphine on LH self-stimulation were the result of artifact, perhaps related to apomorphine-induced stereotypical behavior combined with rapid pharmacological recovery.

Animals↗
PubMed1996

Locating reward cue at response manipulandum (CAM) induces symptoms of drug abuse.

Appetitive instrumental discrimination learning procedures provide for CAM (cue and manipulandum) when the reward cue (discriminative stimulus positively correlated with positive reinforcement) is located at the response manipulandum (object that when contacted or manipulated defines the performance of the instrumental response). Evidence reviewed shows that CAM induces excessive and compulsive instrumental responding relative to otherwise comparable non-CAM control procedures. In humans, symptoms of drug abuse are particularly likely when the drug-taking implement (response manipulandum at which instrumental drug-taking is directed) is also predictive of the drug's rewarding effects (reward cue). Evidence that the predictive relationship between a drug-taking implement and drug reward relates to drug abuse is reviewed, and implications for treatment and prevention are considered. CAM is related to neurobiological models of drug abuse that emphasize the role of the neurotransmitter dopamine (DA). CAM produces convergence of DA-mediated responding for conditioned reinforcement with DA mediation of psychomotor activation and incentive-motivational processes to yield reflexive cue-directed responding not observed in non-CAM controls.

Animals↗
PubMed1994

Automating the generation and collection of rate-frequency functions in a curve-shift brain stimulation reward paradigm.

The electrical self-stimulation paradigm has proven to be very useful in research aimed at delineating the neural substrates involved in reward-related learning. Of the procedures currently employed the curve-shift method is among the more useful since it distinguishes between treatment effects on reward and performance. This method involves generating and plotting rate-frequency functions and quantifying the effects of experimental manipulations on reward by measuring the degree of lateral shift in these functions. We have designed a computerized system that automatically generates and collects descending rate-frequency functions from self-stimulating rats. The 3 main units of this system consisted of a 6809 micro-controller, a programmable timer logic board and a constant current source. The micro-controller and programmable timer operated on custom written software that monitored lever pressing in the operant chambers and controlled stimulation parameters to generate and record rate-frequency functions. The present report describes this system and presents some typical data collected from rats self-stimulating on ventral tegmental electrodes before and after the administration of intra-accumbens vehicle (0.5 microliter distilled H2O), (+)-amphetamine (20.0 micrograms/0.5 microliter), quinpirole (10.0 micrograms/0.5 microliter) and systemic quinpirole (1.0 mg/kg), all dopamine agonists. Stimulation consisting of 300-ms trains of cathodal rectangular pulses (0.1 ms) was available in 50-s trials. The number of pulses per train was decreased logarithmically from a value that sustained maximal responding to one that would not sustain responding. Self-stimulation thresholds were obtained by fitting the Gompertz growth model to the data and calculating the point of maximal acceleration of the sigmoidal curve. It was found that the present system generated and collected rate-frequency functions similar to those that have been obtained manually in previous experiments. The data showed that the system was sensitive to both central and systemic pharmacological manipulations by producing lateral and vertical shifts of the rate-frequency functions, indications of reward and motor effects, respectively. It was concluded that the present design was useful in conducting entire self-stimulation sessions that required minimal monitoring by the experimenter.

Amplifiers, Electronic↗
PubMed1986

Neural basis of psychomotor stimulant and opiate reward: evidence suggesting the involvement of a common dopaminergic system.

Data are reviewed that suggest a common neural system may be involved in the rewarding properties of psychomotor stimulant and opiate drugs. This neural system corresponds to elements in the ventral tegmental dopamine system with cell bodies in the ventral tegmentum and axon terminals in the nucleus accumbens. Several lines of evidence have shown that psychomotor stimulant reward involves a drug action in the nucleus accumbens and that opiate reward involves a drug action in the ventral tegmentum. Activation of the ventral tegmental system at either synaptic element can produce reinforcement by an enhancement of dopaminergic neurotransmission in the nucleus accumbens. Although additional brain systems may be involved in the rewarding actions of these compounds, their ability to activate the ventral tegmental dopamine system appears to make an important contribution to their net reinforcing impact.

Animals↗
PubMed1993

Electrical stimulation of reward sites in the ventral tegmental area increases dopamine transmission in the nucleus accumbens of the rat.

In vivo microdialysis with HPLC-ED was used to measure dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) in the nucleus accumbens of the rat, prior, during, and after 15-min periods of electrical brain stimulation at sites in the ventral tegmental area (VTA) that supported intracranial self-stimulation (ICSS). In the first experiment, both ICSS and yoked stimulation of the VTA evoked significant increases in extracellular concentrations of DA, its metabolites, and 5-HIAA. Comparable results from ICSS and yoked groups were interpreted as evidence that the rewarding properties of VTA stimulation were a causal factor in the elevated DA transmission in the nucleus accumbens, rather than intense operant behavior. Further evidence for this hypothesis came from a second set of data in which changes in extracellular DA levels during the measurement of rate/intensity functions for ICSS were positively correlated. 5-HIAA concentrations also increased during ICSS but these changes were not correlated with either ICSS rate or current intensity, suggesting that changes in serotonin metabolism were unlikely to subserve brain stimulation reward in the VTA. These results add to the growing body of evidence linking changes in extracellular DA in the mesolimbic DA system with both brain stimulation reward and the conditioned and unconditioned rewarding effects of biologically relevant stimuli.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1995

Interaction of CCKB receptors with amphetamine in responding for conditioned rewards.

Cholecystokinin (CCK) has been localized in the nucleus accumbens (NAC) where it may interact with dopamine neurotransmission. NAC dopamine is involved in the control over behavior produced by conditioned rewards. The present experiment tested the whether blockade of endogenous CCKB receptors with L-365,260 (0.1 mg/kg, IP) potentiates bar pressing for stimuli previously associated with food reward. Intra-accumbens amphetamine (20 micrograms) facilitated bar pressing for conditioned rewards. Systemic administration of L-365,260 potentiated this amphetamine response but produced no effect on responding when administered alone. These findings suggest that endogenous CCKB mechanisms may normally inhibit DA function in reward-related behaviors.

Animals↗
PubMedDate not supplied

Age-related learning and memory deficits in odor-reward association in rats.

In these experiments, potential cognitive deficits in aged rats were studied using an odor-reward association task. Aged Fischer 344 rats first performed to an odor-reward association task. After five daily sessions of 60 trials, the aged rats were globally impaired in comparison to the control rats. However, considering individual performance, 40% of the aged population performed as well as the control animals. These aged rats were then tested for retention at various times. They demonstrated an increased rate of forgetting which was confirmed by a final reversal experiment. The other group of aged rats remained severely impaired and unable to make the odor-reward association correctly until the inter-trial interval was decreased from 15 to 5 s. When they were submitted to a task requiring the learning and retention of 7 new odor pairs, these aged rats again performed poorly. A subsequent reversal session confirmed the rapid forgetting phenomenon for this aged group, even when the odor-reward associations were in fact made.

Aging↗
PubMed1996

PD-135158, a CCKB receptor antagonist, microinjected into the nucleus accumbens and the expression of conditioned rewarded behavior.

Cholecystokinin (CCK) has been localized in the nucleus accumbens (NAC) where it may interact with dopamine neurotransmission. NAC dopamine is involved in the control over behavior produced by conditioned rewards. The present experiment examines whether the blockade of CCKB receptors in the NAC with microinjection of PD-135158 (10 micrograms in 0.5 microliter) potentiates bar-pressing for stimuli previously associated with food reward. Intra-NAC microinjections of amphetamine (10 micrograms in 0.5 microliter) increased the number of bar presses for conditioned reward presentation. Furthermore, similar administration of PD-135158 produced no significant effect on responding when administered alone but potentiated the level of amphetamine responding. These findings suggest that endogenous CCKB mechanisms in the NAC may normally inhibit dopamine function in reward-related behaviors.

Animals↗