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Testosterone Increase Hypercapnic Ventilatory Response of Adult Male Rats Subjected to Panic Attack Model
Author(s) -
Lopes Luana,
Gulemetova Roumiana,
Kinkead Richard
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.860.5
Subject(s) - testosterone (patch) , sexual dimorphism , medicine , respiratory system , panic , fight or flight response , endocrinology , plethysmograph , hormone , physiology , psychology , biology , anxiety , psychiatry , biochemistry , gene
Panic attacks occur when the brain wrongly detects a lack of air triggering a false suffocation alarm system. Panic disorder (PD) patients exhibit greater CO 2 chemo‐sensitivity and an increasedventilatory response to CO 2 compared to normal individuals. Interestingly, the prevalence of PD is ~3 times greater in women than men.
Neonatal Maternal Separation (NMS) is a form of stress that disrupts respiratory control development in a sex‐specific fashion. We showed that NMS augments the ventilatory response to CO 2 in females but not males. These results brought us to propose that testosterone prevents NMS‐induced enhancement of the ventilatory response to CO 2 . Pups subjected to NMS were placed in an incubator for 3 h/day from postnatal day 3 to 12. Control pups remained undisturbed. Rats were reared until adulthood, and the ventilatory response to CO 2 was measured by whole‐body plethysmography (FICO 2 = 0.10, for 10 min). We used gonadectomy to evaluate the effects of reducing testosterone on the hypercapnic response.
By comparison with sham‐operated animals, gonadectomy augmented the hypercapnic ventilatory response of control rats; an opposite (albeit modest) effect was observed in NMS rats.
While these results do not support our initial hypothesis, they highlight the importance of testosterone in regulating the CO 2 ‐related respiratory drive in normal rats. Further experiments (hormone measurements) will help elucidate the mechanisms underlying the sexual dimorphism of stress‐related respiratory disorder such as PD. Supported by: Canadian Institutes of Health Research.