The midbrain periaqueductal gray (PAG) organizes basic survival behavior, which includes respiration. How the PAG controls respiration is not known. We studied the PAG control of respiration by injecting D,L-homocysteic acid in the PAG in unanesthetized precollicularly decerebrated cats. Injections in different parts of the PAG caused different respiratory effects. Stimulation in the dorsomedial PAG induced slow and deep breathing and dyspnea. Stimulation in the dorsolateral PAG resulted in active breathing and tachypnea consistent with the respiratory changes during fright and flight. Stimulation in the medial part of lateral PAG caused inspiratory apneusis. Stimulation in lateral parts of the lateral and ventrolateral PAG produced respiratory changes associated with vocalization (mews, alternating mews and hisses, or hisses). D,L-Homocysteic acid injections in the caudal ventrolateral PAG induced irregular breathing. These results demonstrate that the PAG exerts a strong influence on respiration, suggesting that it serves as the behavioral modulator of breathing.

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1. The time dependence of the increase in amplitude (facilitation) of a second end-plate potential (e.p.p.) elicited within 10-100 msec of a preceding e.p.p. was examined at neuromuscular junctions in sartorius muscles of toads. Facilitation was defined by two characteristics, initial facilitation and the time constant of its exponential decay. 2. The time constant of decay of facilitation was longer at lower temperatures and the Q10 was 4'3 in the range 10-250 C. There was no significant effect of temperature on initial facilitation. 3. Ouabain (104-10-3 M), lithium substitution for sodium, sodium azide (5 mM) and N-ethylmaleimide (NEM, 0.1 mm) initially had no effect on initial facilitation or the decay of facilitation. After some time, they all caused a longer time constant of decay of facilitation and a depression of initial facilitation. 4. It was concluded that the decay of facilitation is not directly dependent on active transport of sodium ions, calcium efflux, ATP-dependent movements of calcium or mitochondrial uptake of calcium following an action potential. 5. Ouabain, lithium, sodium azide, and NEM all caused an increase in transmitter release. This effect, and the late effects on facilitation, were thought to be due to an increase in intracellular calcium concentration in nerve terminals. 6. No relationship was found between the quantal content of e.p.p.s (range, 0.8-100) and initial facilitation, or the time constant of decay of facilitation. 7. Substitution of strontium for calcium ions caused a marked pro-longation of the time constant of decay of facilitation, and a depression of initial facilitation. 8. The results were consistent with the hypothesis that the time 27 PH Y 239 RON J. BALNAVE AND PETER W. GAGE constant of decay of facilitation is related to the rate of disappearance of an ' active' complex of calcium (CaA) which, of itself, is not sufficient for transmitter release. It is suggested that an action potential produces CaA which decays with the time constant of facilitation and CaS, a short-life complex of calcium which decays with the time constant of the phasic release of transmitter. The release of transmitter is proportional to some function of [CaA] and [CaS].