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(Reference retrieved automatically from Google Scholar through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Lack of interaction between NMDA and cholecystokinin-2 receptor-mediated neurotransmission in the dorsolateral periaqueductal gray in the regulation of rat defensive behaviors

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Author(s):
Bertoglio‚ LJ ; Guimaraes‚ FS ; Zangrossi‚ H.
Total Authors: 3
Document type: Journal article
Source: Life Sciences; v. 79, n. 23, p. 2238-2244, 2006.
Abstract

Several neurotransmitters, including GABA, serotonin, glutamate, and cholecystokinin, modulate defensive behaviors in the dorsolateral periaqueductal gray (dIPAG). Although both glutamate and cholecystokinin have been shown to facilitate these behaviors, a possible interaction between them remains to be examined. The present study investigates whether activation or antagonism of N-methyl-D-aspartic acid (NMDA) glutamate and cholecystokinin 2 (CCK2) receptors located in the dlPAG would interact in animals tested in the elevated T-maze. The effect of the NMDA (50 pmol) was evaluated in rats pretreated with the CCK2 receptor antagonist LY225910 (0.05 nmol). In addition, the effect of the CCK2 receptor agonist CCK-4 (0.08 nmol) was evaluated in rats pretreated with the NNMA receptor antagonist AP-7 (1.0 nmol). Intra-dlPAG injection of NMDA increased risk assessment and inhibitory avoidance behaviors. This NNMA anxiogenic-like effect was unaltered by the pretreatment with LY225910. Similarly, the shortening of escape latencies induced by CCK-4 was unaffected by AP-7. No drug changed the general exploratory activity as assessed in the open-field. These results, showing that the activation of dIPAG NNMA or CCK2 receptors facilitate anxiety- and fear-related behaviors, further implicate glutamate and cholecystokinin-mediated neurotransmission in this midbrain area on modulation of defensive behaviors. However, the regulatory action of these two excitatory neurotransmitters seems to be exerted through independent mechanisms. (c) 2006 Elsevier Inc. All rights reserved. (AU)

FAPESP's process: 02/13197-2 - Participation of glutamate and nitric oxide on the pathophysiology of neuropsychiatry disorders
Grantee:Francisco Silveira Guimaraes
Support Opportunities: Research Projects - Thematic Grants