Abstract
The circuit structure and function underlying post-coital male behaviors remain poorly understood. Using mutant analysis, laser ablation, optogenetics, and Ca2+ imaging, we observed that following C. elegans male copulation, the duration of post-coital lethargy is coupled to cellular events involved in ejaculation. We show that the SPV and SPD spicule-associated sensory neurons and the spicule socket neuronal support cells function with intromission circuit components, including the cholinergic SPC and PCB and the glutamatergic PCA sensory-motor neurons, to coordinate sex muscle contractions with initiation and continuation of sperm movement. Our observations suggest that the SPV and SPD and their associated dopamine-containing socket cells sense the intrauterine environment through cellular endings exposed at the spicule tips and regulate both sperm release into the hermaphrodite and the recovery from post-coital lethargy.
Highlights
Persistence in performing a goal-orientated behavior must be balanced by behavioral termination cues once the task is completed
We report that acetylcholine, dopamine, and glutamate secreting cells are stimulated upon successful intromission and promote sperm movement and release
Successful copulation is followed by a period of reduced mating drive and ability Similar to other species, C. elegans males exhibit a period of reduced activity following ejaculation (Barfield and Geyer, 1972; Oomura et al, 1983; Ureshi et al, 2002)
Summary
Persistence in performing a goal-orientated behavior must be balanced by behavioral termination cues once the task is completed. Sexual disinterest and inability following mating are described in two ways: the refractory period, defined by the short term duration between consecutive ejaculations (Levin, 2009), and sexual satiation or exhaustion, a period of time following repeated copulations where the male rats require 6–14 days to regain sexual potency (Beach and Jordan, 1956). While the behavioral phenomenon has been described, little is understood about the molecular and cellular mechanisms controlling both satiation and the refractory period. Neurotransmitters and hormones such as serotonin and prolactin may extend the period of inactivity, while others such as dopamine and norepinephrine may shorten it (McIntosh and Barfield, 1984a, 1984b, 1984c; Buvat et al, 1985; Marson and McKenna, 1992). The basic structure and function of mating circuits that exhibit a period of inactivity are still being elucidated (Levin, 2009; Turley and Rowland, 2013)
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