The Link between Posttraumatic Stress Disorder and Functionality among United States Military Service Members Psychiatrically Hospitalized Following a Suicide Crisis.

Posttraumatic stress disorder (PTSD) is one of the most commonly diagnosed psychiatric disorders in the United States and has been linked to suicidal thoughts and behaviors, yet the role of a PTSD diagnosis on functional impairment among suicidal individuals remains unknown. This study examined the association between PTSD status and functional impairment among military psychiatric inpatients admitted for acute suicide risk (N = 166) with a lifetime history of at least one suicide attempt. Measures of functionality included: (1) alcohol use; (2) sleep quality; (3) social problem-solving; and (4) work and social adjustment. Thirty-eight percent of the sample met criteria for PTSD. Women were more likely than men to meet criteria for PTSD (p = 0.007), and participants who met PTSD criteria had significantly more psychiatric diagnoses (p < 0.001). Service members who met PTSD criteria reported more disturbed sleep (p = 0.003) and greater difficulties with work and social adjustment (p = 0.004) than those who did not meet PTSD criteria. However, functionality measures were not significantly associated with PTSD status after controlling for gender and psychiatric comorbidity. Gender and number of psychiatric comorbidities other than PTSD were significant predictors of PTSD in logistic regression models across four functionality measures. Future studies should assess the additive or mediating effect of psychiatric comorbidities in the association between impaired functioning and PTSD. Clinicians are encouraged to assess and address functionality during treatment with suicidal individuals, paying particular attention to individuals with multiple psychiatric diagnoses.

Synaptic Plasticity onto Dopamine Neurons Shapes Fear Learning.

Fear learning is a fundamental behavioral process that requires dopamine (DA) release. Experience-dependent synaptic plasticity occurs on DA neurons while an organism is engaged in aversive experiences. However, whether synaptic plasticity onto DA neurons is causally involved in aversion learning is unknown. Here, we show that a stress priming procedure enhances fear learning by engaging VTA synaptic plasticity. Moreover, we took advantage of the ability of the ATPase Thorase to regulate the internalization of AMPA receptors (AMPARs) in order to selectively manipulate glutamatergic synaptic plasticity on DA neurons. Genetic ablation of Thorase in DAT+ neurons produced increased AMPAR surface expression and function that lead to impaired induction of both long-term depression (LTD) and long-term potentiation (LTP). Strikingly, animals lacking Thorase in DAT+ neurons expressed greater associative learning in a fear conditioning paradigm. In conclusion, our data provide a novel, causal link between synaptic plasticity onto DA neurons and fear learning.