Effects of dopamine receptor stimulants on locomotor activity of rats with electrolytic or 6-hydroxydopamine-induced lesions of the nucleus accumbens

1976 ◽  
Vol 47 (2) ◽  
pp. 195-198 ◽  
Author(s):  
G. N. Woodruff ◽  
P. H. Kelly ◽  
A. O. Elkhawad
1986 ◽  
Vol 16 (1) ◽  
pp. 37-42 ◽  
Author(s):  
R.D. Oades ◽  
K. Taghzouti ◽  
J.-M. Rivet ◽  
H. Simon ◽  
M. Le Moal

1993 ◽  
Vol 71 (5-6) ◽  
pp. 407-413 ◽  
Author(s):  
Michael Wu ◽  
Stefan M. Brudzynski ◽  
Gordon J. Mogenson

The interaction of dopamine and glutamate in the nucleus accumbens in the regulation of locomotion was investigated. Microinjection of N-methyl-D-aspartic acid (NMDA, a glutamatergic NMDA receptor agonist) or α-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA, a quisqualic receptor agonist which is a glutamatergic non-NMDA receptor agonist) into the nucleus accumbens caused a substantial increase in locomotor activity. This increase in locomotor activity was significantly reduced by prior administration of the dopamine D2 agonist quinpirole, but not the D1 agonist, SKF 38393, into the same brain sites. The reduction in locomotion produced by quinpirole was dose dependent. Eight days after the ventral tegmental area was lesioned with 6-hydroxydopamine to destroy the dopamine projection and the axon terminals of the mesolimbic dopamine neurons in nucleus accumbens, the hyperkinetic effects produced by injections of NMDA and AMPA into the nucleus accumbens were substantially reduced. These results suggested that the glutamate agonist induced locomotion is mediated by dopamine. Thus, it appears that NMDA- or AMPA-induced locomotion is due to the activation of glutamate receptors on the mesolimbic dopamine terminals in the nucleus accumbens which release dopamine and subsequently increase locomotion.Key words: nucleus accumbens, dopamine, glutamate, quinpirole, locomotion, N-methyl-D-aspartic acid, α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid.


2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Claudia Leticia Moreno Ávila ◽  
Jorge H. Limón-Pacheco ◽  
Magda Giordano ◽  
Verónica M. Rodríguez

Arsenic exposure has been associated with sensory, motor, memory, and learning alterations in humans and alterations in locomotor activity, behavioral tasks, and neurotransmitters systems in rodents. In this study, CD1 mice were exposed to 0.5 or 5.0 mg As/L of drinking water for 6 months. Locomotor activity, aggression, interspecific behavior and physical appearance, monoamines levels, and expression of the messenger for dopamine receptors D1 and D2 were assessed. Arsenic exposure produced hypoactivity at six months and other behaviors such as rearing and on-wall rearing and barbering showed both increases and decreases. No alterations on aggressive behavior or monoamines levels in striatum or frontal cortex were observed. A significant decrease in the expression of mRNA for D2 receptors was found in striatum of mice exposed to 5.0 mg As/L. This study provides evidence for the use of dopamine receptor D2 as potential target of arsenic toxicity in the dopaminergic system.


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

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