Effects of a Systemic AMPA/KA and NMDA Receptor Blockade on Pavlovian-instrumental Transfer

Overview

Journal Psychopharmacology (Berl)

Specialty Pharmacology

Date 2005 Jul 8

PMID 16001115

Citations 9

Authors

Anja Murschall

Wolfgang Hauber

Affiliations

Soon will be listed here.

Abstract

Rationale: Pavlovian stimuli can markedly elevate instrumental responding directed toward a common reward, an effect known as pavlovian-instrumental transfer (PIT). PIT critically depends on the amygdala and nucleus accumbens (ACB); however, little is known yet about its neurochemical basis.

Objective: Here we examined the role of ionotropic glutamate receptors in PIT.

Methods: The effects of a systemic blockade of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate/kainate (AMPA/KA) and N-methyl-D: -aspartate (NMDA) receptors on PIT and locomotor activity were investigated in rats.

Results: The competitive AMPA/KA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione disodium salt (CNQX) (1.5 mg/kg i.p.) did not alter the overall rate of lever pressing and left PIT intact, i.e. presentation of a pavlovian stimulus significantly enhanced instrumental responding. Furthermore, CNQX did not affect horizontal and vertical activity in an open field. The non-competitive NMDA receptor antagonist (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine hydrogen maleate (dizocilpine) (0.08 mg/kg i.p.) elevated the overall rate of lever pressing but did not affect PIT. In addition, dizocilpine increased horizontal and decreased vertical activity in an open field.

Conclusions: Previous studies imply that the training protocol used here induced a general, not outcome-specific, form of PIT which is mediated by the central nucleus of the amygdala (CeN) through modulation of mesoaccumbens dopamine transmission. Thus, we suggest that an AMPA/KA and NMDA receptor blockade did not affect PIT here because the general motivational influence of pavlovian stimuli to induce PIT is conveyed by GABAergic projections from the CeN to midbrain dopaminergic neurons.

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