Aspartic acid (580 mg/kg, SC) causes a long-lasting depression of vent
ilation in adult male, but not female rats. The purpose of these exper
iments was to determine if the aspartic acid-induced depression of ven
tilation in awake male Sprague-Dawley rats is a consequence of the rel
ease of endogenous opioids or somatostatin. These neuromodulators have
been shown to cause depression of ventilation. Pretreatment of male r
ats with the opioid antagonist naloxone (5 mg/kg) 10 min prior to aspa
rtic acid attenuated the drop of ventilation from - 138.6 +/- 26.9 ml/
min to - 63.4 +/- 16.6 ml/min (p < 0.01) by affecting both tidal volum
e and frequency of breathing. Naloxone administered prior to saline ha
d no effect on ventilation. In another experiment, cysteamine (100 mg/
kg), a somatostatin depleter, injected SC 2 h before aspartic acid adm
inistration also attenuated depression of ventilation by affecting fre
quency of breathing, Cysteamine alone, compared to saline, had no effe
ct on ventilation over 24 h. These results suggest that aspartic acid
acts by releasing endogenous opioids and somatostatin.