Microbial life in slow and stopped lanes.

Microbes in nature often lack nutrients and face extreme or widely fluctuating temperatures, unlike microbes in growth-optimized settings in laboratories that much of the literature examines. Slowed or suspended lives are the norm for microbes. Studying them is important for understanding the consequences of climate change and for addressing fundamental questions about life: are there limits to how slowly a cell's life can progress, and how long cells can remain viable without self-replicating? Recent studies began addressing these questions with single-cell-level measurements and mathematical models. Emerging principles that govern slowed or suspended lives of cells - including lives of dormant spores and microbes at extreme temperatures - are re-defining discrete cellular states as continuums and revealing intracellular dynamics at new timescales. Nearly inactive, lifeless-appearing microbes are transforming our understanding of life.

Prefrontal cortex nicotinic receptor inhibition by methyllycaconitine impaired cocaine-associated memory acquisition and retrieval.

Cocaine administration has been shown to induce plastic changes in the medial prefrontal cortex (mPFC), which could represent a mechanism by which cocaine facilitates the association between cocaine rewarding effects with contextual cues. Nicotinic acetylcholine receptors (nAChRs) in the mPFC have critical roles in cognitive function including attention and memory and are key players in plasticity processes. However, whether nAChRs in the mPFC are required for the acquisition and maintenance of cocaine-associated memories is still unknown. To assess this question, we used the conditioning place preference (CPP) model to study the effect of intra-mPFC infusion of methyllycaconitine, a selective antagonist of α7 nAChRs, on the acquisition, consolidation and expression of cocaine-associated memory in adult rats. Our findings reveal that mPFC α7 nAChRs activation is necessary for the acquisition and retrieval, but not consolidation, of cocaine induced CPP. Moreover, cocaine-induced sensitization during CPP conditioning sessions was abolished by methyllycaconitine infusion in the mPFC. Together, these results identify mPFC α7 nAChRs as critical players involved in both acquiring and retrieving cocaine-associated memories. Considering that drug seeking often depends on the association between drug-paired cues and the rewarding effects of the drug, α7 nAChRs in the mPFC could be considered as potential targets for the prevention or treatment of cocaine use disorder.