Citation

Spiacci Junior A, Sergio TO, Ferreira da Silva GS, Glass ML, Schenberg LC, Garcia-Cairasco N, Junior HZ. Neuroscience 2015; 307: 191-198.

Affiliation

Department of Pharmacology, School of Medicine of Ribeirao Preto, University of São Paulo, Av. Bandeirantes, 3900, Ribeirão Preto, Brazil, , CEP:14049-900. Electronic address: zangross@fmrp.usp.br.

Copyright

(Copyright © 2015, International Brain Research Organization, Publisher Elsevier Publishing)

DOI

10.1016/j.neuroscience.2015.08.045

PMID

26319117

Abstract

It has been proposed that spontaneous panic attacks are the outcome of the misfiring of an evolved suffocation alarm system. Evidence gathered in the last year is suggestive that the dorsal periaqueductal gray (dPAG) in the midbrain harbors a hypoxia-sensitive suffocation alarm system. We here investigated whether facilitation of 5-HT-mediated neurotransmission within the dPAG changes panic-like defensive reactions expressed by male Wistar rats submitted to a hypoxia challenge (7% O2), as observed in other animal models of panic. Intra-dPAG injection of 5-HT (20 nmol), 8-OH-DPAT (8 nmol), a 5-HT1A receptor agonist, or DOI (16 nmol), a preferential 5-HT2A agonist, reduced the number of upward jumps directed to the border of the experimental chamber during hypoxia, interpreted as escape attempts, without affecting the rats' locomotion. These effects were similar to those caused by chronic, but not acute, intraperitoneal administration of the antidepressant fluoxetine (5 -15 mg/kg), or acute systemic administration of the benzodiazepine receptor agonist alprazolam (1 - 4 mg/kg), both drugs clinically used in the treatment of panic disorder. Our findings strengthen the view that the dPAG is a key encephalic area involved in the defensive behaviors triggered by activation of the suffocation alarm system. They also support the use of hypoxia-evoked escape as a model of respiratory-type panic attacks.

Language: en