The presence of new neurons in the adult hippocampus indicates that this structure incorporates new neurons into its circuitry and uses them for some function related to learning and/or related thought processes. Their generation depends on a variety of factors ranging from age to aerobic exercise to sexual behavior to alcohol consumption. However, most of the cells will die unless the animal engages in some kind of effortful learning experience when the cells are about one week of age. If learning does occur, the new cells become incorporated into brain circuits used for learning. In turn, some processes of learning and mental activity appear to depend on their presence. In this review, we discuss the now rather extensive literature showing that new neurons are kept alive by effortful learning, a process that involves concentration in the present moment of experience over some extended period of time. As these thought processes occur, endogenous patterns of rhythmic electrophysiological activity engage the new cells with cell networks that already exist in the hippocampus and at efferent locations. Concurrent and synchronous activity provides a mechanism whereby the new neurons become integrated with the other neurons. This integration allows the present experience to become integrated with memories from the recent past in order to learn and predict when events will occur in the near future. In this way, neurogenesis and learning interact to maintain a fit brain.

Chemotherapy, especially if prolonged, disrupts attention, working memory and speed of processing in humans. Most cancer drugs that cross the blood–brain barrier also decrease adult neurogenesis. Because new neurons are generated in the hippocampus, this decrease may contribute to the deficits in working memory and related thought processes. The neurophysiological mechanisms that underlie these deficits are generally unknown. A possible mediator is hippocampal oscillatory activity within the theta range (3–12 Hz). Theta activity predicts and promotes efficient learning in healthy animals and humans. Here, we hypothesized that chemotherapy disrupts learning via decreases in hippocampal adult neurogenesis and theta activity. Temozolomide was administered to adult male Sprague–Dawley rats in a cyclic manner for several weeks. Treatment was followed by training with different types of eyeblink classical conditioning, a form of associative learning. Chemotherapy reduced both neurogenesis and endogenous theta activity, as well as disrupted learning and related theta-band responses to the conditioned stimulus. The detrimental effects of temozolomide only occurred after several weeks of treatment, and only on a task that requires the association of events across a temporal gap and not during training with temporally overlapping stimuli. Chemotherapy did not disrupt the memory for previously learned associations, a memory independent of (new neurons in) the hippocampus. In conclusion, prolonged systemic chemotherapy is associated with a decrease in hippocampal adult neurogenesis and theta activity that may explain the selective deficits in processes of learning that describe the ‘chemobrain’.

Learning increases the number of immature neurons that survive and mature in the adult hippocampus (Gould et al., 1999). One week old cells are more likely to survive in response to learning than cells in animals that are exposed to training but do not learn (Shors, 2009). Because neurogenesis is an ongoing and overlapping process, it is possible that learning differentially affects new cells as a function of their maturity. To address this issue, we examined the effects of associative learning on the survival of cells at different stages of development. Training did not alter the number of cells that were produced and present during the training experience. Cells that were 1-2 weeks of age at the time of training remained in the hippocampus several weeks later but cells that were young or older did not. In contrast, cells that were produced during training were less likely to survive when compared to cells in untrained animals. Additionally, the number of cells that were generated after learning in trained animals was not different from untrained animals. Finally, survival was not increased if the association was reacquired and expressed when the cells were about one week old. Together, these results indicate that new neurons are rescued from death by initial acquisition, not the expression or reacquisition, of an associative memory and only during a critical period. Overall, these results suggest the presence of a feedback system, which controls how many new neurons become incorporated into the adult brain in response to learning.

Among ED patients with possible ACS, the modified HEART score, original EDACS, and simplified EDACS all predicted a low risk of 60-day MACE with improved accuracy using a cTnI cutoff below the 99th percentile. The original EDACS identified the most low-risk patients, and thus may be the preferred risk score.

Drinking alcohol in moderation is often considered a health-conscious behavior, associated with improved cardiovascular and brain health. However, “moderate” amounts of alcohol include drinking 3-4 alcohol beverages in a day, which is closer to binge drinking and may do more harm than good. Here we examined how daily drinking of moderate-high alcohol alters the production of new neurons in the adult hippocampus. Male and female adult Sprague-Dawley rats were provided free access to a liquid replacement diet that was supplemented with either 4 % ethanol or Maltodextrin for a period of two weeks. Proliferating cells were labeled with 5-bromo-2-deoxyuridine (BrdU) and the number of BrdU-positive cells in the hippocampus was assessed after the final day of drinking. A subset of rats was also exposed to a motor skill or associative learning task to examine the functional effects of alcohol consumption. The drinking regime resulted in an average blood alcohol concentration of approximately 0.08 %, which is comparable to the human legal driving limit in many countries. This level of intoxication did not impair motor skill learning or function in either sex, nor did the alcohol consumption disrupt associative learning two days after drinking. Therefore, moderate alcohol consumption did not disrupt basic sensory, motor or learning processes. However, the number of cells produced in the dentate gyrus of the hippocampus was reduced by nearly 40 %. Thus, even moderate consumption of alcohol for a relatively short period of time can have profound effects on structural plasticity in the adult brain.