Engagement With Online Sexual Trauma-Related Content Among Women Who Have Experienced Sexual Trauma.

Sleep exists in all animals with nervous systems () and may even have evolved in ancestral animals who lacked true tissues, considering parazoans express circadian and synaptic transmission genes (; ). Conserved sleep-regulatory molecules are found even in primitive animals with radially arranged nerve nets, like hydra () and jellyfish (), suggesting that this mysterious behavioral state evolved once, prior to the appearance of the bilaterians. Thus, conserved mechanisms may regulate sleep across phylogeny (; ), despite dramatic differences in nervous system complexity. Invertebrate models have emerged as powerful tools for sleep gene discovery and mechanistic dissection. The nematode has a 302-cell, fully mapped nervous system (; ) and displays sleep controlled by conserved genes (). Stress-induced sleep (SIS) is a particularly intriguing model for sleep gene identification, considering its experimental reproducibility, and control by just 2 interneurons, ALA () and RIS (). SIS provides restorative functions required for recovery following injury or infection, akin to sickness sleep of mammals (). Extreme temperatures, ethanol, pore-forming toxins, hyperosmotic conditions (), wounding (), exposure to the bacterial toxin indole (), viral infection (), and ultraviolet (UV) irradiation () can lead to SIS. Noxious stimuli can damage tissues differently, but a common behavioral program occurs: (i) avoidance and escape; (ii) sleep, and (iii) arousal. The timing and amount (i.e. maintenance) of sleep depends on the extent of cellular damage (); thus, temporal dynamics can vary. Numerous signaling mechanisms must coordinate the opposing states of sleep and arousal. Some of the most critical molecules of sleep regulation are epidermal growth factors (EGF) coded by (), which are shed from damaged tissues to activate EGF receptors, coded by , on the surface of the ALA (), and RIS (). Wounding of skin promotes ALA and RIS activation by as well as by the upregulation and release of antimicrobial peptides (; ). ALA and RIS activation leads to the secretion of a collection of neuropeptides required for sleep behaviors like movement, feeding, and defecation quiescence. These include , , , and , expressed in the ALA (; ; ), and in the RIS (; ). Upon secretion, these peptides may function to inhibit wake and motor interneurons (; ) and cholinergic motor neurons (), via inhibitory G-protein coupled receptors (GPCRs) (; ). Despite the identification of neuropeptides, only a small subset of GPCRs has been implicated in sleep regulation. The GPCR functions as a receptor on the RIS, which provides an autocrine feedback mechanism to regulate sleep duration, as well as a receptor on excitatory cholinergic neurons (), and a receptor on wake interneurons (). The orphaned GPCR is required for sleep in the ADL sensory neurons and may play a broader timing role for SIS. Overexpression of by multicopy arrays causes a profound shift in the timing of sleep initiation, in that it occurs early when arousal and escape should dominate. Additionally, is required for heat and blue light avoidance behaviors, as well as general arousal (). Thus, may regulate the timing of ALA and RIS activation, together with other unknown pathways, to coordinate the broader stress response.