Fewer cells were labeled following a second binge.

<p>Cells generated 7 days after the first binge were labeled with IdU, while cells generated 7 days after the second binge were labeled with CldU. In both sedentary (S2) and exercised (E2) Two Binge animals, there were significantly fewer CldU+ cells, compared with IdU+ cells. *p<0.05</p

Exercise enhanced survival of cells generated post-binge.

<p>Sedentary single Binge animals had significantly more IdU+ cells (A; scale bar = 100 µm) 35 days post-binge (B). Sedentary Two Binge animals showed a non-significant increase. In all groups, exercise significantly increased the number of IdU+ cells. Within binged animals, there was a significant positive correlation between number of IdU+ cells and volume of the DG (C) and between number of IdU+ cells and number of granule neurons (D). * p<0.05</p

After a second binge, animals acted less intoxicated, but experienced more severe withdrawal.

<p>In this figure, “Single Binge” indicates data from animals that underwent one binge combined with the first binge data from animals that underwent 2 binges (“Two Binge”). During the second binge, animals took longer to act intoxicated (A), despite initially receiving more ethanol (B) and having blood ethanol concentrations that were similar to Single Binge (C). Following a second binge, withdrawal symptoms were significantly increased overall (D). *p<0.05; † p<0.05 significant main effect of Binge.</p

Experimental design and time course of events.

<p>Animals underwent either 0 (control diet), 1 or 2 binges. Beginning 7 days after the last binge, half the animals in each group exercised for 28 days (groups E0, E1, E2). In order to label cells generated in response to the first binge, all animals received IdU 7 days after the last dose of ethanol. In order to label cells generated in response to the second binge, animals in the Two Binge groups (S2 and E2) received CldU 7 days after the end of the second binge. All animals were sacrificed 35 days after the last binge.</p

A stressful spatial navigation task differentially affected protein expression in the dorsal and ventral subregions.

<p>Expression of mature BDNF was not significantly changed by RAWM exposure in either the dorsal or ventral dentate gyrus (A). In contrast, proBDNF was significantly increased in the dorsal dentate, and significantly decreased in the ventral (C). PSD-95 was unchanged in the dorsal, but significantly increased in the ventral dentate (C). * significantly different from control.</p

Stress most severely affected neurogenesis in the ventral dentate gyrus.

<p>Compared with controls, rats in the CUS group showed decreased proliferation (A), survival (B) and neuronal differentiation (C) in the dentate gyrus. This effect was most pronounced in the ventral, compared to the dorsal, sub-region († indicates significant difference between subregions). * significantly different from control.</p

CUS facilitated long-term spatial memory in the RAWM.

<p>Escape latencies did not differ between control and stressed animals during the acquisition trials (1–12), or on the short-term memory trial (30 min) (A). However, stressed animals took significantly less time to locate the hidden platform on the long-term memory trial (24 hrs). A similar pattern was seen for errors made during search (B). * significantly different from control.</p

CUS and learning were both stressful.

<p>Animals that underwent CUS did not gain weight over the 2-week period of stressor exposure, whereas control animals did (A). Exposure to the CUS paradigm raised corticosterone levels, as did learning in the RAWM (B). Note, however, that learning did not further elevate corticosterone in stressed animals. *significantly different from baseline, † significantly different from Post CUS control.</p

Table_2_Olfactory Memory Impairment Differs by Sex in a Rodent Model of Pediatric Radiotherapy.pdf

<p>Although an effective treatment for pediatric brain tumors, cranial radiation therapy (CRT) damages surrounding healthy tissue, thereby disrupting brain development. Animal models of pediatric CRT have primarily relied on visual tasks to assess cognitive impairment. Moreover, there has been a lack of sex comparisons as most research on the cognitive effects of pediatric CRT does not include females. Therefore, we utilized olfaction, an ethologically relevant sensory modality, to assess cognitive impairment in an animal model of CRT that included both male and female mice. Specifically, we used the novel odor recognition (NOdorR) task with social odors to test recognition memory, a cognitive parameter that has been associated with olfactory neurogenesis, a form of cellular plasticity damaged by CRT. In addition to odor recognition memory, olfactory ability or discrimination of non-social and social odors were assessed both acutely and 3 months after CRT. Magnetic resonance imaging (MRI) and histology were performed after behavioral testing to assess long-term damage by CRT. Long-term but not acute radiation-induced impairment in odor recognition memory was observed, consistent with delayed onset of cognitive impairment in human patients. Males showed greater exploration of social odors than females, but general exploration was not affected by irradiation. However, irradiated males had impaired odor recognition memory in adulthood, compared to non-irradiated males (or simply male controls). Female olfactory recognition memory, in contrast, was dependent on estrus stage. CRT damage was demonstrated by (1) histological evaluation of olfactory neurogenesis, which suggested a reduction in CRT versus control, and (2) imaging analyses which showed that the majority of brain regions were reduced in volume by CRT. Specifically, two regions involved in social odor processing (amygdala and piriform cortex) were damaged by cranial irradiation in males but not females, paralleling olfactory recognition findings.</p