Abstract
Changes in the reactivating efficiency of blockade of components of the GABA-benzodiazepine-ionophore complex were analyzed in conditions of preliminary activation and inhibition of dopamine autoreceptors using (+)ZRRR and haloperidol respectively. A conditioned passive escape reflex was used, along with amnesia produced by detaining mice in the danger sector of a chamber immediately after imposition of a painful stimulus. Doses of bicuculline (1 mg/kg), picrotoxin (1 mg/kg), and flumazenil (10 mg/kg) given before testing restored performance of the conditioned response without altering the neurochemical background. Reductions and increases in dopaminergic activity during the training period prevented restoration of the conditioned passive escape response by blockade of GABAa and benzodiazepine receptors and chloride channels. It is suggested that the neurochemical mechanisms involved in restoring the damaged memory trace are based on the formation of the optimal balance in the activities of the various components of the GABA-benzodiazepine-ionophore complex and the dopaminergic system.
Similar content being viewed by others
References
N. I. Dubrovina, R. I. Parkhomenko, and R. Yu. Il'yuchenok, “GABAergic modulation of the restoration of a memory trace lost to amnesia by activation of the dopaminergic system,” Byull. Éksp. Biol. Med., No. 12, 629 (1990).
N. I. Dubrovina and R. Yu. Il'yuchenok, “The role of the dopaminergic system and the GABA-benzodiazepine-ionophore complex in the regulation of memory trace reproduction,” Fiziol. Zh., No. 3, 3 (1990).
R. Yu. Il'yuchenok, N. I. Dubrovina, and I. M. Vinnitskii, “Reproduction of a memory trace in amnesias and forgetting after changes in the activity of pre- and postsynaptic dopamine receptors,” Zh. Vyssh. Nerv. Deyat.,37, No. 6, 1148 (1987).
R. I. Kruglikov, “The neurochemical bases of learning and memory,” in: The Neurobiology of Learning and Memory [in Russian], Nauka, Moscow (1990), p. 174.
A. F. Yakimovskii and I. V. Karpova, “The effects of chronic activation and blockade of the dopaminergic and enkephalinergic systems of the neostriatum on conditioned reflex behavior and dopamine metabolism in the nigrostriatal system in rats,” Zh. Vyssh. Nerv. Deyat.,42, No. 5, 930 (1992).
G. Bartholini, B. Scatton, P. Worms, et al., “Interactions between GABA, dopamine, acetylcholine and glutamate-containing neurons in the extrapyramidal and limbic systems,” in: GABA and Basal Ganglia, G. DiChiara et al. (eds.), Raven Press, New York (1981), p. 119.
C. Baunez, A. Nieoullon, and M. Amalric, “Dopamine and complex sensorimotor integration: Further studies in a conditioned motor task in the rat,” Neurosci.,65, No. 2, 375 (1995).
D. Clark, S. Hjorth, and A. Carlsson, “Dopamine-receptor agonists: Mechanisms underlying autoreceptor selectivity. I. Review of the evidence,” J. Neural Transmis.,62, 1 (1985).
G. Di Scala and G. Sandner, “Conditioned place aversion produced by FG 7142 is attenuated by haloperidol,” Psychopharmacol.,99, 176 (1989).
P. Y. Ilyutchenok, L. V. Loskutova, A. L. Finkelberg, et al., “Neurochemical mechanisms of memory control,” Acta Physiol. Hung.,79, No. 4, 419 (1992).
G. E. Ploeger, B. M. Spruijt, and A. R. Cools, “Spatial localization in the Morris water maze in rats: Acquisition on affected by intra-accumbens of the dopaminergic antagonist haloperidol,” Behav. Neurosci.,108, No. 5, 927 (1994).
S. Retaux, M. J. Besson, and J. Penit-Soria, “Synergism between D1 and D2 dopamine receptors in the inhibition of the evoked release of [3H]GABA in the prefrontal cortex,” Neurosci.,43, 323 (1991).
F. Robustelli and M. E. Jarvik, “Retrograde amnesia from detention,” Physiol. Behav.,3, No. 4, 543 (1968).
J. Scheel-Kruger, “Dopamine-GABA interactions: Evidence that GABA transmits, modulates and mediates dopaminergic functions in the basal ganglia and limbic system,” Acta Neurol. Scand.,73, 9 (1986).
C. Spyraki and H. C. Fibiger, “A role for the mesolimbic dopamine system in the reinforcing properties of diazepam,” Psychopharmacol.,94, 133 (1988).
A. F. Steulet, R. Bernasconi, T. Leonhardt, et al., “Effects of selective dopamine D1 and D2 receptor agonists on the rate of GABA synthesis in mouse brain,” Eur. J. Pharmacol.,191, 19 (1990).
N. M. White, M. G. Packard, and J. Seamans, “Memory enhancement by post-training peripheral administration of low doses of dopamine agonists: Possible autoreceptor effect,” Behav. Neural Biol.,59, 230 (1993).
M. E. Wolf and R. H. Roth, “Autoreceptor regulation of dopamine synthesis,” Ann. N. Y. Acad. Sci.,604, 323 (1990).
L. S. Wong, G. Eschel, J. Dreher, et al., “Role of dopamine and GABA in the control of motor activity elicited from the rat nucleus accumbens,” Pharmacol. Biochem. Behav.,38, 829 (1991).
Additional information
Institute of Physiology, Siberian Division, Russian Academy of Medical Sciences, Novosibirsk. Translated from Zhurnal Vysshei Nervnoi Deyatel'nosti imeni I. P. Pavlova, Vol. 47, No. 1, pp. 117–122, January–February, 1997.
Rights and permissions
About this article
Cite this article
Dubrovina, N.I., Il'yuchenok, R.Y. Contribution of presynaptic dopaminergic receptors to the mechanism of the reactivating effects of blockade of the GABA-benzodiazepine-ionophore complex. Neurosci Behav Physiol 28, 294–298 (1998). https://doi.org/10.1007/BF02462959
Received:
Revised:
Issue Date:
DOI: https://doi.org/10.1007/BF02462959