The Impact of PTSD on Veterans’ Family Relationships: Mechanisms of Distress and Available Treatments

When veterans return home from war with PTSD, the disorder can have detrimental effects on their close family relationships. Researchers have proposed different mechanisms underlying the distress experienced by partners and children of veterans with PTSD in the hopes that these mechanisms can be targeted in treatment. The purpose of this project is to review and synthesize the current literature on these mechanisms of distress, as well as the treatments that have been designed to address them. This review examines several key factors that account for veterans’ relationship distress, including the important factors of intimacy and aggression. Due to the emotional numbing symptoms of PTSD, veterans have a difficult time experiencing emotions and communicating them to their partners, which can hinder the development of intimacy in the relationship. Through an increased propensity to perceive threat and a loss of self-monitoring, the hyperarousal symptoms of PTSD can lead to intimate partner aggression. A number of couple-based treatments have been developed for veterans with PTSD and their partners, referred to as Behavioral Conjoint Therapies. These interventions are currently only in their pilot stages, but address some of the key mechanisms of distress for veterans and their partners, including intimacy and communication

Alien Registration- De Lamotte, Antonia D. (Saint Agatha, Aroostook County)

https://digitalmaine.com/alien_docs/33221/thumbnail.jp

TRPV1-expressing primary afferents generate behavioral responses to pruritogens via multiple mechanisms

The mechanisms that generate itch are poorly understood at both the molecular and cellular levels despite its clinical importance. To explore the peripheral neuronal mechanisms underlying itch, we assessed the behavioral responses (scratching) produced by s.c. injection of various pruritogens in PLCβ3- or TRPV1-deficient mice. We provide evidence that at least 3 different molecular pathways contribute to the transduction of itch responses to different pruritogens: 1) histamine requires the function of both PLCβ3 and the TRPV1 channel; 2) serotonin, or a selective agonist, α-methyl-serotonin (α-Me-5-HT), requires the presence of PLCβ3 but not TRPV1, and 3) endothelin-1 (ET-1) does not require either PLCβ3 or TRPV1. To determine whether the activity of these molecules is represented in a particular subpopulation of sensory neurons, we examined the behavioral consequences of selectively eliminating 2 nonoverlapping subsets of nociceptors. The genetic ablation of MrgprD^+ neurons that represent ≈90% of cutaneous nonpeptidergic neurons did not affect the scratching responses to a number of pruritogens. In contrast, chemical ablation of the central branch of TRPV1+ nociceptors led to a significant behavioral deficit for pruritogens, including α-Me-5-HT and ET-1, that is, the TRPV1-expressing nociceptor was required, whether or not TRPV1 itself was essential. Thus, TRPV1 neurons are equipped with multiple signaling mechanisms that respond to different pruritogens. Some of these require TRPV1 function; others use alternate signal transduction pathways