Gender gaps in exam scores or final grades are common in introductory college science and engineering classrooms, with women underperforming relative to men with the same admission test scores or college grade point averages. After failing to close a historically documented gender gap in a large introductory biology course using interventions targeted at training a growth mindset, we implemented interventions designed to reduce student test anxiety. We combined evidence-based exercises based on expressive writing and on reappraising physiological arousal. We also used a valid measure to quantify test anxiety at the start and end of the course. This instrument measures an individual’s self-declared or perceived test anxiety—also called trait anxiety—but not the immediate or “state” anxiety experienced during an actual exam. Consistent with previous reports in the literature, we found that women in this population declared much higher test anxiety than men and that students who declared higher test anxiety had lower exam scores than students who declared lower test anxiety. Although the test anxiety interventions had no impact on the level of self-declared trait anxiety, they did significantly increase student exam performance. The treatment benefits occurred in both men and women. These data suggest that 1) a combination of interventions based on expressive writing and reappraising physiological arousal can be a relatively easy manner to boost exam performance in a large-enrollment science, technology, engineering, and mathematics (STEM) course and encourage emotion regulation; 2) women are more willing than men to declare that they are anxious about exams, but men and women may actually experience the same level of anxiety during the exam itself; and 3) women are underperforming in STEM courses for reasons other than gender-based differences in mindset or test anxiety.
Real world memories are formed in a particular context and are not acquired or recalled in isolation. Time is a key variable in the organization of memories, since events experienced close in time are more likely to be meaningfully associated, while those experienced with a longer interval are not. How does the brain segregate events that are temporally distinct? Here, we report that a delayed (12-24h) increase in the expression of the C-C chemokine receptor type 5 (CCR5), an immune receptor well known as a co-receptor for HIV infection, following the formation of a contextual memory, determines the duration of the temporal window for associating or linking that memory with subsequent memories. This delayed CCR5 expression in mouse dorsal CA1 (dCA1) neurons results in a decrease in neuronal excitability, which in turn negatively regulates neuronal memory allocation, thus reducing the overlap between dCA1 memory ensembles. Lowering this overlap affects the ability of one memory to trigger the recall of the other, thus closing the temporal window for memory linking. Remarkably, our findings also show that an age-related increase in CCL5/CCR5 expression leads to impairments in memory linking in aged mice, which could be reversed with a CCR5 knockout and an FDA approved drug that inhibits this receptor, a result with significant clinical implications. All together the findings reported here provide the first insights into the molecular and cellular mechanisms that shape the temporal window for memory linking.
Although mGluR5-antagonists prevent fear and anxiety, little is known about how the same receptor in the amygdala gives rise to both. Combining in vitro and in vivo activation of mGluR5 in rats, we identify specific changes in intrinsic excitability and synaptic plasticity in basolateral amygdala neurons that give rise to temporally distinct and mutually exclusive effects on fear-related behaviors. The immediate impact of mGluR5 activation is to produce anxiety manifested as indiscriminate fear of both tone and context. Surprisingly, this state does not interfere with the proper encoding of tone-shock associations that eventually lead to enhanced cue-specific fear. These results provide a new framework for dissecting the functional impact of amygdalar mGluR-plasticity on fear versus anxiety in health and disease.DOI:
http://dx.doi.org/10.7554/eLife.25665.001
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