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Mathematical principles of reinforcement (MPR; Killeen, 1994) is a quantitative model of operant behavior that contains 3 parameters representing motor capacity (δ), motivation (a), and short term memory (λ). The present study applied MPR to characterize the effects of bilateral infusions of 6-OHDA into the substantia nigra pars compacta in the rat, a model of Parkinson's disease. Rats were trained to lever press under a 5-component fixed ratio (5,15,30,60, and 100) schedule of food reinforcement. Rats were tested for 15 days prior to dopamine lesions and again for 15 days postlesion. To characterize functional loss relative to lesion size, rats were grouped according to the extent and the degree of lateralization of their dopamine loss. Response rates decreased as a function of dopamine depletion, primarily at intermediate ratios. MPR accounted for 98% of variance in preand post-lesion response rates. Consistent with reported disruptions in motor behavior induced by dopaminergic lesions, estimates of δ increased when dopamine was severely depleted. There was no support for different estimates of a based on pre-and post-lesion performance of any lesion group, suggesting that dopamine loss has negligible effects on incentive motivation. The present study demonstrates the usefulness of combining operant techniques with a theoretical model to better understand the effects of a neurochemical manipulation.

Objectives:Frailty is associated with cognitive decline in older adults. However, the mechanisms explaining this relationship are poorly understood. We hypothesized that sleep quality may mediate the relationship between frailty and cognition.Participants:154 participants aged between 50-90 years (mean = 69.1 years, SD = 9.2 years) from the McKnight Brain Registry were included.Measurements:Participants underwent a full neuropsychological evaluation, frailty and subjective sleep quality assessments. Direct relationships between frailty and cognitive function were assessed using linear regression models. Statistical mediation of these relationships by sleep quality was assessed using nonparametric bootstrapping procedures.Results:Frailty severity predicted weaker executive function (B = −2.77, β = −0.30, 95% CI = −4.05 – −1.29) and processing speed (B = −1.57, β = −0.17, 95% CI = −3.10 – −0.16). Poor sleep quality predicted poorer executive function (B = −0.47, β = −0.21, 95% CI = −0.79 – −0.08), processing speed (B = −0.64, β = −0.28, 95% CI = −0.98 – −0.31), learning (B = −0.42, β = −0.19, 95% CI = −0.76 – −0.05) and delayed recall (B = −0.41, β = −0.16, 95% CI = −0.80 – −0.31). Poor sleep quality mediated the relationships between frailty severity and executive function (B = −0.66, β = −0.07, 95% CI = −1.48 – −0.39), learning (B = −0.85, β = −0.07, 95% CI = −1.85 – −0.12), delayed recall (B = −0.47, β = −0.08, 95% CI = −2.12 – −0.39) and processing speed (B = −0.90, β = −0.09, 95% CI = −1.85 – −0.20).Conclusions:Relationships between frailty severity and several cognitive outcomes were significantly mediated by poor sleep quality. Interventions to improve sleep quality may be promising avenues to prevent cognitive decline in frail older adults.

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Self-medication theory posits that some trauma survivors use alcohol to cope with posttraumatic stress disorder (PTSD) symptoms, but the role of negative posttraumatic cognitions in this relationship is not well defined. We examined associations among PTSD symptoms, posttraumatic cognitions, and alcohol intoxication frequency in 290 men who have sex with men (MSM), who reported a history of childhood sexual abuse (CSA). Using a bootstrap approach, we examined the indirect effects of PTSD symptoms on alcohol intoxication frequency through posttraumatic cognitions regarding the self, world, and self-blame. In separate regression models, higher levels of PTSD symptoms and posttraumatic cognitions were each associated with more frequent intoxication, accounting for 2.6% and 5.2% of the variance above demographics, respectively. When examined simultaneously, posttraumatic cognitions remained significantly correlated with intoxication frequency whereas PTSD symptoms did not. Men reporting elevated posttraumatic cognitions faced increased odds for current alcohol dependence, odds ratio (OR) = 2.19, 95% CI [1.13, 4.22], compared with men reporting low posttraumatic cognitions, independent of current PTSD diagnosis. A higher level of PTSD symptom severity was indirectly associated with more frequent alcohol intoxication through cognitions about the self and world; the indirect to total effect ratios were 0.74 and 0.35, respectively. Negative posttraumatic cognitions pertaining to individuals' self-perceptions and appraisals of the world as dangerous may play a role in self-medication with alcohol among MSM with a history of CSA. Interventions targeting these cognitions may offer potential for reducing alcohol misuse in this population, with possible broader implications for HIV-infection risk.