Factors Associated with Cigarette Smoking in Homeless Adults: Findings From an Outpatient Counseling Clinic.

BACKGROUND: Those who are homeless are 4 times more likely to smoke cigarettes than the general population in the United States. Though research has investigated smoking risk factors among homeless individuals, further investigation is needed to understand factors that can be addressed by smoking cessation programs. This study seeks to understand characteristics associated with cigarette use in clients of the counseling clinic at a Midwest homeless shelter, including whether homeless individuals who smoke demonstrate lower self-efficacy, greater social isolation, poorer perception of therapy, and greater levels of chronic homelessness than nonsmokers. METHODS: From 2014 through 2019, clients of the counseling clinic were invited to contribute to a data bank. Logistic regression was performed to determine predictors of smoking status. RESULTS: No association was identified between smoking status and self-efficacy, social isolation, perception of therapy, or chronic homelessness. Compared to those without a high school degree, odds of being a smoker were 95% lower for those with a high school degree or equivalent and 93% lower for those with more than a high school education. Those with 3 or more episodes of prior substance abuse treatment were more likely to be smokers. CONCLUSION: This study demonstrates that cigarette use among the homeless population is associated with low education level and prior substance abuse treatment. Smoking cessation programs would benefit from tailoring information to the education level of their audience. Further study could determine whether use of other substances may contribute to cigarette use in the homeless population and how this may be addressed by smoking cessation programs.

Infralimbic cortex pyramidal neuron GIRK signaling contributes to regulation of cognitive flexibility but not affect-related behavior in male mice.

Dysfunction of the infralimbic cortical (ILC) region of the medial prefrontal cortex (mPFC) is thought to be an underlying factor in both affect- and cognition-related behavioral deficits that co-occur across neuropsychiatric disorders. Increasing evidence highlights pathological imbalances in prefrontal pyramidal neuron excitability and associated aberrant firing as an underlying factor in this dysfunction. G protein-gated inwardly rectifying K+ (GIRK/Kir3) channels mediate excitability of mPFC pyramidal neurons, however the functional role of these channels in ILC-dependent regulation of behavior and pyramidal neuron excitation is unknown. The present study used a viral-cre approach in male mice harboring a 'floxed' version of the kcnj3 (Girk1) gene, to disrupt GIRK1-containing channel expression in pyramidal neurons within the ILC. Loss of GIRK1-dependent signaling increased excitability and spike firing of pyramidal neurons but did not alter affective behavior measured in an elevated plus maze, forced swim test, or progressive ratio test of motivation. Alternatively, ablation of GIRK1 impaired performance in an operant-based attentional set-shifting task designed to assess cognitive flexibility. These data highlight a unique role for GIRK1 signaling in ILC pyramidal neurons in the regulation of strategy shifting but not affect and suggest that these channels may represent a therapeutic target for treatment of cognitive deficits in neuropsychiatric disease.

Suppression of pyramidal neuron G protein-gated inwardly rectifying K+ channel signaling impairs prelimbic cortical function and underlies stress-induced deficits in cognitive flexibility in male, but not female, mice.

Imbalance in prefrontal cortical (PFC) pyramidal neuron excitation:inhibition is thought to underlie symptomologies shared across stress-related disorders and neuropsychiatric disease, including dysregulation of emotion and cognitive function. G protein-gated inwardly rectifying K+ (GIRK/Kir3) channels mediate excitability of medial PFC pyramidal neurons, however, the functional role of these channels in mPFC-dependent regulation of affect, cognition, and cortical dynamics is unknown. We used a viral-cre approach in male and female mice harboring a "floxed" version of the kcnj3 (Girk1) gene, to disrupt GIRK1-containing channel expression in pyramidal neurons within the prelimbic cortex (PrL). In males, loss of pyramidal GIRK1-dependent signaling differentially impacted measures of affect and impaired working memory and cognitive flexibility. Unexpectedly, ablation of PrL GIRK1-dependent signaling did not impact affect or cognition in female mice. Additional studies used a model of chronic unpredictable stress (CUS) to determine the impact on PrL GIRK-dependent signaling and cognitive function. CUS exposure in male mice produced deficits in cognition that paralleled a reduction in PrL pyramidal GIRK-dependent signaling akin to viral approaches whereas CUS exposure in female mice did not alter cognitive flexibility performance. Stress-induced behavioral deficits in male mice were rescued by systemic injection of a novel, GIRK1-selective agonist, ML297. In conclusion, GIRK1-dependent signaling in male mice, but not females, is critical for maintaining optimal PrL function and behavioral control. Disruption of this inhibition may underlie stress-related dysfunction of the PrL and represent a therapeutic target for treating stress-induced deficits in affect regulation and impaired cognition that reduce quality of life.