#Thalamic amplification of #cortical connectivity sustains attentional control
http://www.nature.com/nature/journal/vaop/ncurrent/full/nature22073.html
Consistent with this notion, broadly enhancing prefrontal cortex (PFC) excitability diminishes rule specificity and behavioural performance, whereas enhancing mediodorsal excitability improves both. Overall, our results define a previously unknown principle in neuroscience; thalamic control of functional cortical connectivity. This function, which is dissociable from categorical information relay, indicates that the thalamus has a much broader role in cognition than previously thought.
http://www.nature.com/nature/journal/vaop/ncurrent/full/nature22073.html
Consistent with this notion, broadly enhancing prefrontal cortex (PFC) excitability diminishes rule specificity and behavioural performance, whereas enhancing mediodorsal excitability improves both. Overall, our results define a previously unknown principle in neuroscience; thalamic control of functional cortical connectivity. This function, which is dissociable from categorical information relay, indicates that the thalamus has a much broader role in cognition than previously thought.
The Role of Aging, Drug Dependence, and Hepatitis #C Comorbidity in #Alcoholism #Cortical Compromise
https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2674964
Given the high drug-dependence incidence (54.5%) in the alcoholism group, analysis examined drug subgroups (cocaine, cannabis, amphetamines, opiates) compared with drug-dependence–free alcoholism and control groups. Although the alcohol plus cocaine (t = −2.310, P = .04) and alcohol plus opiate (t = −2.424, P = .04) groups had smaller frontal volumes than the drug-dependence–free alcoholism group, deficits in precentral (t = −2.575, P = .01), supplementary motor (t = −2.532, P = .01), and medial (t = −2.800, P = .01) volumes endured in drug-dependence–free participants with alcoholism compared with control participants. Those with HCV infection had greater deficits than those without HCV infection in frontal (t = 3.468, P = .01), precentral (t = 2.513, P = .03), superior (t = 2.533, P = .03), and orbital (t = 2.506, P = .03) volumes, yet total frontal (t = 2.660, P = .02), insular (t = 3.526, P = .003), parietal (t = 2.414, P = .03), temporal (t = 3.221, P = .005), and precentral (t = 3.180, P = .01) volume deficits persisted in the uninfected participants with alcoholism compared with control participants with known HCV status.
Conclusions and Relevance Drug dependence and HCV infection compounded deleterious effects of alcohol dependence on frontal cortical volumes but could not account for the frontally distributed volume deficits in the drug-free participants with alcoholism. We speculate that age-alcohol interactions notable in frontal cortex put older adults at heightened risk for age-associated neurocompromise even if alcohol misuse is initiated later in life
https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2674964
Given the high drug-dependence incidence (54.5%) in the alcoholism group, analysis examined drug subgroups (cocaine, cannabis, amphetamines, opiates) compared with drug-dependence–free alcoholism and control groups. Although the alcohol plus cocaine (t = −2.310, P = .04) and alcohol plus opiate (t = −2.424, P = .04) groups had smaller frontal volumes than the drug-dependence–free alcoholism group, deficits in precentral (t = −2.575, P = .01), supplementary motor (t = −2.532, P = .01), and medial (t = −2.800, P = .01) volumes endured in drug-dependence–free participants with alcoholism compared with control participants. Those with HCV infection had greater deficits than those without HCV infection in frontal (t = 3.468, P = .01), precentral (t = 2.513, P = .03), superior (t = 2.533, P = .03), and orbital (t = 2.506, P = .03) volumes, yet total frontal (t = 2.660, P = .02), insular (t = 3.526, P = .003), parietal (t = 2.414, P = .03), temporal (t = 3.221, P = .005), and precentral (t = 3.180, P = .01) volume deficits persisted in the uninfected participants with alcoholism compared with control participants with known HCV status.
Conclusions and Relevance Drug dependence and HCV infection compounded deleterious effects of alcohol dependence on frontal cortical volumes but could not account for the frontally distributed volume deficits in the drug-free participants with alcoholism. We speculate that age-alcohol interactions notable in frontal cortex put older adults at heightened risk for age-associated neurocompromise even if alcohol misuse is initiated later in life