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Effects of medial amygdala inactivation on a panic-related behavior.
Behav Brain Res. 2006 Sep 25; 172(2):316-23.BB

Abstract

In the last years, the role played by the medial nucleus of the amygdala (MeA) in the modulation of fear- and anxiety-related behaviors has been increasingly investigated. This nucleus plays an important role in the processing of predator odor-induced defensive reactions, i.e. freezing and risk-assessment behaviors. Immunohistochemical evidence also indicates that the MeA may be involved in the regulation of escape, a defensive behavior related to panic attacks. In this study, we further addressed this question by investigating the effects of the reversible inactivation of the nucleus on escape behavior generated in male Wistar rats by two different aversive stimuli, electrical stimulation of the dorsal periaqueductal gray matter (dPAG) and exposure to one of the open arms of the elevated T-maze. Results showed that intra-MeA administration of either the reversible sodium channel blocker lidocaine (34 nmol/0.2 microl) or the GABA(A) receptor agonist muscimol (0.22 nmol/0.2 microl) raised the threshold of aversive electrical stimulation, increasing the amount of current that applied to the dPAG evokes escape, an antiaversive effect. Local microinjection of muscimol (0.22 nmol/0.2 microl) inhibited escape behavior in the elevated T-maze, also suggesting an antiaversive effect. In this latter test, muscimol did not affect inhibitory avoidance, a behavior associated with generalized anxiety disorder. Muscimol effect in the elevated T-maze was independent of changes in general exploratory activity as measured in an open-field. Taken together, our data corroborate previous evidences suggesting that the MeA is involved in the modulation of escape. Dysfunction of this regulatory mechanism may be of relevance in the genesis/maintenance of panic disorder.

Authors+Show Affiliations

Laboratório de Psicofarmacologia, FFCLRP, Universidade de São Paulo, 14040-901 Ribeirão Preto, Brazil.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

16806522

Citation

Herdade, Karina Costa Paes, et al. "Effects of Medial Amygdala Inactivation On a Panic-related Behavior." Behavioural Brain Research, vol. 172, no. 2, 2006, pp. 316-23.
Herdade KC, Strauss CV, Zangrossi Júnior H, et al. Effects of medial amygdala inactivation on a panic-related behavior. Behav Brain Res. 2006;172(2):316-23.
Herdade, K. C., Strauss, C. V., Zangrossi Júnior, H., & Viana, M. B. (2006). Effects of medial amygdala inactivation on a panic-related behavior. Behavioural Brain Research, 172(2), 316-23.
Herdade KC, et al. Effects of Medial Amygdala Inactivation On a Panic-related Behavior. Behav Brain Res. 2006 Sep 25;172(2):316-23. PubMed PMID: 16806522.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of medial amygdala inactivation on a panic-related behavior. AU - Herdade,Karina Costa Paes, AU - Strauss,Christiana Villela de Andrade, AU - Zangrossi Júnior,Hélio, AU - Viana,Milena de Barros, Y1 - 2006/06/27/ PY - 2006/03/24/received PY - 2006/05/15/revised PY - 2006/05/17/accepted PY - 2006/6/30/pubmed PY - 2006/12/29/medline PY - 2006/6/30/entrez SP - 316 EP - 23 JF - Behavioural brain research JO - Behav Brain Res VL - 172 IS - 2 N2 - In the last years, the role played by the medial nucleus of the amygdala (MeA) in the modulation of fear- and anxiety-related behaviors has been increasingly investigated. This nucleus plays an important role in the processing of predator odor-induced defensive reactions, i.e. freezing and risk-assessment behaviors. Immunohistochemical evidence also indicates that the MeA may be involved in the regulation of escape, a defensive behavior related to panic attacks. In this study, we further addressed this question by investigating the effects of the reversible inactivation of the nucleus on escape behavior generated in male Wistar rats by two different aversive stimuli, electrical stimulation of the dorsal periaqueductal gray matter (dPAG) and exposure to one of the open arms of the elevated T-maze. Results showed that intra-MeA administration of either the reversible sodium channel blocker lidocaine (34 nmol/0.2 microl) or the GABA(A) receptor agonist muscimol (0.22 nmol/0.2 microl) raised the threshold of aversive electrical stimulation, increasing the amount of current that applied to the dPAG evokes escape, an antiaversive effect. Local microinjection of muscimol (0.22 nmol/0.2 microl) inhibited escape behavior in the elevated T-maze, also suggesting an antiaversive effect. In this latter test, muscimol did not affect inhibitory avoidance, a behavior associated with generalized anxiety disorder. Muscimol effect in the elevated T-maze was independent of changes in general exploratory activity as measured in an open-field. Taken together, our data corroborate previous evidences suggesting that the MeA is involved in the modulation of escape. Dysfunction of this regulatory mechanism may be of relevance in the genesis/maintenance of panic disorder. SN - 0166-4328 UR - https://www.unboundmedicine.com/medline/citation/16806522/Effects_of_medial_amygdala_inactivation_on_a_panic_related_behavior_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0166-4328(06)00292-0 DB - PRIME DP - Unbound Medicine ER -