dopamine receptor agonists and operant behavior

Doneuron doneuron at aol.com
Sun Sep 17 11:37:05 EST 1995


  The effects that you are getting with the low dose of quinpirole and the
cessation of spontaneous activity is the result of quinpirole's effects on
the cell bodies of the dopamine neurons in the ventral tegmentum
projecting to the terminal regions in the nuc accumbens.  Quinpirole is
very effective at shutting down these cells via activation of D2/D3
impulse-regulating autoreceptors and tis effect is not D1 dependant
because there is no D1/D2 coupling on the cell bodies regulating impulse. 
It is not surprising that when the DA cells stop firing that the rat
ceases to locomote or show a reaction because the release of DA in the
terminal regions in the Nuc Acc and striatum has been shut down.  No DA no
movement. At higher doses it is possible that direct activation of the
D2/D3 receptors in the striatum become activated directly by quin causing
sniffing stereotypies. 
     Raclopride likely blocks the postsynaptic receptors in the striatum
and decreases activity directly via binding D2 receptors,  however it is
also possible that it decreases the firing rate of DA cells in the VTA via
long-loop feedback pathways from the nuc acc.  which would transiently
increase DA firing rate and soon lead to a state of depolarization block. 
In this state the cells become over depolarized and sodium channels cannot
be released from inhibition and all firing ceases.  This state is
typically seen following chronic treatment with D2 antagonists.  For more
information on this I would look do a search for the following names in
the DA field.  Francis J. White, L. Chiodo, or B.S. Bunny from 1983 to
present.  



More information about the Neur-sci mailing list