NPY is inversely related to PTSD symptomology, with low NPY correlating specifically to the presence of intrusion symptoms (Sah et al., 2014). Higher NPY is predicative of PTSD symptom improvement and shows a positive association with coping following a traumatic event (Yehuda et al., 2006). Aberrant NPY and norepinephrine

function have been linked in PTSD. Yohimbine, an antagonist of the presynaptic α2-adrenergic receptor that increases norepinephrine levels, elicits panic attacks and exacerbates the core symptoms of PTSD (Bremner et al., 1997). Yohimbine has also been shown to stimulate increases in plasma NPY and levels of the norepinephrine metabolite MHPG (3-methyl-4-hydroxy-phenyl-glycol) in healthy Z-VAD-FMK nmr subjects. However, yohimbine-stimulated increases in NPY are significantly blunted in persons with PTSD (Rasmusson and

et al, 2000a and Rasmusson and et al, 1998). Additionally, baseline concentrations of plasma NPY correlated negatively to yohimbine-induced increases in MHPG in the same study (Rasmusson et al., 2000). This correlation suggests that low basal levels of NPY were associated with an exaggerated increase in MHPG following yohimbine (Rasmusson et al., 2000). Both basal and yohimbine-stimulated levels of NPY were negatively correlated Paclitaxel to scores on a combat-exposure scale, indicating that greater combat exposure was associated with blunted levels of NPY (Rasmusson et al., 2000). whatever Pathological

responses to stress manifest in behaviors that include enhanced anxiety, arousal, and fear. In this section, we review the findings in animal models utilized to examine these three behavioral responses, as well as the effects of NPY in rodent models of PTSD and depression-like behavior. Examples provided in the text are summarized in Table 1. Genetic rodent models and pharmacological studies have provided insight into the anxiolytic properties of NPY in multiple paradigms of anxiety-like behavior (Kask and et al, 2002 and Sajdyk et al., 2004). NPY deficiency is associated with an anxiogenic phenotype in rodents (Bannon et al., 2000), and highly anxious rats are more sensitive to the anxiolytic actions of NPY (Sudakov et al., 2001). Intracerebroventricular (i.c.v.) administration of NPY decreases anxiety-like behavior in the elevated plus maze, Vogel’s drinking conflict test (Broqua and et al, 1995 and Heilig and et al, 1989), and other operant conflict tasks (Britton and et al, 1997 and Heilig and et al, 1992). Site specific-studies have revealed the amygdala, locus coeruleus, lateral septum, and hippocampus as regions that are involved in the anxiolytic properties of NPY (Lin and et al, 2010, Thorsell and et al, 2000, Primeaux and et al, 2005, Sajdyk et al., 1999, Heilig and et al, 1993, Kask et al., 1998a, Kask et al., 1998b, Kask et al., 1998c and Trent and Menard, 2011).