Inhibition of d-amphetamine-induced locomotor activity by injection of haloperidol into the nucleus accumbens of the rat

1975 ◽  
Vol 41 (2) ◽  
pp. 87-95 ◽  
Author(s):  
A. J. J. Pijnenburg ◽  
W. M. M. Honig ◽  
J. M. Van Rossum
Keyword(s):  
Locomotor Activity ◽  
Nucleus Accumbens

scholarly journals Diazepam attenuates the effects of cocaine on locomotion, 50-kHz ultrasonic vocalizations and phasic dopamine release in the nucleus accumbens of rats

2020 ◽  
Author(s):  
William N. Sanchez ◽  
Jose A. Pochapski ◽  
Leticia F. Jessen ◽  
Marek Ellenberger ◽  
Rainer K. Schwarting ◽  
...  
Keyword(s):  
Locomotor Activity ◽  
Nucleus Accumbens ◽  
Dopamine Release ◽  
Ultrasonic Vocalizations ◽  
Control Group ◽  
List Type ◽  
Adult Rats ◽  
Fast Scan Cyclic Voltammetry ◽  
Entire Duration ◽  
Male Wistar Rats

AbstractBackground and PurposeCurrently, no effective drug exists to treat cocaine use disorders, which affect millions of people worldwide. Benzodiazepines are potential therapeutic candidates, as microdialysis and voltammetry studies have shown that they can decrease dopamine release in the nucleus accumbens of rodents. In addition, we have recently shown that diazepam blocks the increase in dopamine release and the affective marker 50-kHz ultrasonic vocalizations (USV) induced by DL-amphetamine in rats.Experimental ApproachHere we tested whether administration of 2.5 mg·kg−1 diazepam (i.p.) in adult male Wistar rats could block the effects of 20 mg·kg−1 cocaine (i.p.) on electrically evoked phasic dopamine release in the nucleus accumbens measured by fast-scan cyclic voltammetry, as well as 50-kHz USV and locomotor activity.Key ResultsCocaine injection increased evoked dopamine release up to 3-fold within 5 min and the increase was significantly higher than baseline for at least 90 min. The injection of diazepam 15 min later attenuated the cocaine effect by nearly 50% and this attenuation was maintained for at least 30 min. Stimulant drugs, natural rewards and reward predictive cues are known to evoke 50-kHz USV in adult rats. In the present study, cocaine increased the number of 50-kHz USV of the flat, step, trill, and mixed kinds by 12-fold. This effect was at maximum 5 min after cocaine injection, decreased with time and lasted at least 40 min. Diazepam significantly blocked this effect for the entire duration of the session. The distance travelled by control rats during a 40-min session of exploration in an open field was at maximum in the first 5 min and decayed progressively until the end of the session. Cocaine-treated rats travelled significantly longer distances when compared to the control group, while diazepam significantly attenuated cocaine-induced locomotion by up to 50%.Conclusions and implicationThese results suggest that the neurochemical, affective, and stimulant effects of cocaine can be mitigated by diazepam.What is already knownDiazepam decreases dopamine release in the rodent nucleus accumbens (NAc) and reduces some effects produced by DL-amphetamine.What this study addsDiazepam attenuated the increase in phasic dopamine release caused by cocaine.Diazepam blocked the effect of cocaine on 50-kHz USV and locomotor activity.Clinical significanceThis study demonstrates that diazepam can block specific effects of cocaine that likely contribute to addiction.

Alterations in amphetamine-induced locomotor activity and stereotypy after electrical stimulation of the nucleus accumbens and neostriatum

Life Sciences ◽  
1989 ◽  
Vol 44 (9) ◽  
pp. 633-641 ◽  
Author(s):  
Larry Kokkinidis ◽  
R. Duncan Kirkby ◽  
Bryon D. McCarter ◽  
Thomas B. Borowski
Keyword(s):  
Electrical Stimulation ◽  
Locomotor Activity ◽  
Nucleus Accumbens ◽  
Stimulation Of

Alterations In Glutamate Synapses In The Nucleus Accumbens Following Sensitization To Cocaine

1999 ◽  
Vol 5 (S2) ◽  
pp. 1232-1233
Author(s):  
L. B. Kozell ◽  
C. K. Meshul
Keyword(s):  
Prefrontal Cortex ◽  
Locomotor Activity ◽  
Nucleus Accumbens ◽  
Behavioral Sensitization ◽  
Neural Mechanism ◽  
Cocaine Administration ◽  
Collaborative Studies ◽  
Abundant Evidence ◽  
Dopaminergic Pathways ◽  
Intermittent Cocaine

Repeated intermittent administration of cocaine to rodents has been shown to result in behavioral sensitization, or enhanced locomotor activity. Because there are similarities between effects of intermittent cocaine use in humans and sensitization in rats, understanding the neural mechanism underlying sensitization may provide insights into mechanisms of psychopathologies in humans.There is abundant evidence that the mesolimbic dopaminergic pathways, originating in the ventral tegmental area (VTA) and terminating in both nucleus accumbens (NAc) and prefrontal cortex (PFC), are critically important for development of sensitization to the motor-stimulating effects of cocaine. Evidence also suggests that changes in glutamate (Glu) transmission in the mesolimbic DA pathways are associated with sensitization to cocaine. In recent collaborative studies, we have shown that cocaine administration transiently decreases the density of nerve terminal glutamate immunolabeling within the NAc shell following withdrawal from continuous or intermittent cocaine administration. Locomotor activity was not assessed in either of these studies.

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