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Articles in PresS, published online ahead of print November 15, 2002
J Appl Physiol, 10.1152/jap.00740.2002
Submitted on August 9, 2002
Accepted on November 4, 2002
1 Department of Physiological Sciences, University of Florida College of Veterinary Medicine, Gainesville, Florida, USA
* To whom correspondence should be addressed. E-mail: davenportp{at}mail.vetmed.ufl.edu.
The neural substrates mediating autonomic components of the behavioral defense response have been shown to reside in the periaqueductal gray (PAG). The cardiovascular components of the behavioral defense response have been well described and are tonically suppressed by GABAergic input. The ventilatory response associated with disinhibition of the dPAG neurons is unknown. In urethane anesthetized, spontaneously breathing rats, electrical stimulation of the dorsal PAG (dPAG) was shown to decrease the expiration time (Te) and increase respiratory frequency, with no change in time of inspiration (Ti). Baseline and the change in diaphragm EMG also increased, resulting in an increase in neural minute activity. Microinjection of bicuculline methobromide, a GABAA receptor antagonist, into the dPAG produced a similar response, which was dose dependent. Disinhibition of the dPAG also produced a decrease in Ti. These results suggest that GABAA mediated suppression of dPAG neurons plays a role in the respiratory component of behavioral defense responses. The respiratory change is due in part to a change in brainstem respiratory timing and phasic inspiratory output. In addition, there is an increase in tonic diaphragm activity.
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