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

Nitric oxide modulates dopaminergic regulation of prepulse inhibition in the basolateial amygdala

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Author(s):
Salum, C. [1, 2] ; Issy, A. C. [2] ; Brandao, M. L. [3, 4] ; Guimaraes, F. S. [5] ; Del Bel, E. A. [2]
Total Authors: 5
Affiliation:
[1] Univ Fed ABC, Ctr Matemat Computacao & Cognicao, Nucleo Cognicao & Sistemas Complexos, BR-09090400 Sao Paulo - Brazil
[2] Univ Sao Paulo, Dept Morfol Estomatol & Fisiol, Fac Odontol Ribeirao Preto, Sao Paulo - Brazil
[3] Inst Neurociencias & Comportamento INEC, Sao Paulo - Brazil
[4] Univ Sao Paulo, Fac Filosofia Ciencias & Letras Ribeirao Pret, Lab Psicobiol, Sao Paulo - Brazil
[5] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Farmacol, Sao Paulo - Brazil
Total Affiliations: 5
Document type: Journal article
Source: JOURNAL OF PSYCHOPHARMACOLOGY; v. 25, n. 12, p. 1639-1648, DEC 2011.
Web of Science Citations: 9
Abstract

Systemic injection of the nitric oxide (NO) synthase inhibitor N(G)-nitro-L-arginine (LNO) prevents the disruptive effect of amphetamine (Amph) on prepulse inhibition (PPI), a sensorimotor gating model in which the amplitude of the acoustic startle response (ASR) to a startling sound (pulse) is reduced when preceded immediately by a weaker stimulus (preputse). Given that dopamine (DA) projections to the basolaterat amygdala (BLA) are involved in the control of information processing, our aim was to investigate if intra-BLA administration of LNO would modify the disruption caused by the DA agonists, Amph, apomorphine (Apo) and quinpirole (QNP), on PPI. Male Wistar rats received bilateral intra-BLA microinjections (0.2 mu l/min/side) of combined treatments (saline or LNO 11 mu g followed by saline, QNP 3 mu g, Apo 10 mu g or Amph 30 fig). PPI was disrupted by intra-BLA Apo, QNP or Amph but not by LNO. Prior bilateral intra-BLA injection of LNO prevented the Apo- and QNP-induced disruption of PPI but did not affect that caused by Amph. APO- or QNP-induced increases in ASR to prepulse + pulse were also restored by LNO. Since local inhibition of NO formation affected the effects of direct, but not indirect. DA agonists, the results suggest that this modulation is not occurring at the level of DA release but may involve complex interactions with other neurotransmitter systems. (AU)