Bats are the only mammals that use highly developed laryngeal echolocation, a sensory mechanism based on the ability to emit laryngeal sounds and interpret the returning echoes to identify objects. Although this capability allows bats to orientate and hunt in complete darkness, endowing them with great survival advantages, the genetic bases underlying the evolution of bat echolocation are still largely unknown. Echolocation requires high-frequency hearing that in mammals is largely dependent on somatic electromotility of outer hair cells. Then, understanding the molecular evolution of outer hair cell genes might help to unravel the evolutionary history of echolocation. In this work, we analyzed the molecular evolution of two key outer hair cell genes: the voltage-gated potassium channel gene KCNQ4 and CHRNA10, the gene encoding the α10 nicotinic acetylcholine receptor subunit. We reconstructed the phylogeny of bats based on KCNQ4 and CHRNA10 protein and nucleotide sequences. A phylogenetic tree built using KCNQ4 amino acid sequences showed that two paraphyletic clades of laryngeal echolocating bats grouped together, with eight shared substitutions among particular lineages. In addition, our analyses indicated that two of these parallel substitutions, M388I and P406S, were probably fixed under positive selection and could have had a strong functional impact on KCNQ4. Moreover, our results indicated that KCNQ4 evolved under positive selection in the ancestral lineage leading to mammals, suggesting that this gene might have been important for the evolution of mammalian hearing. On the other hand, we found that CHRNA10, a gene that evolved adaptively in the mammalian lineage, was under strong purifying selection in bats. Thus, the CHRNA10 amino acid tree did not show echolocating bat monophyly and reproduced the bat species tree. These results suggest that only a subset of hearing genes could underlie the evolution of echolocation. The present work continues to delineate the genetic bases of echolocation and ultrasonic hearing in bats.

Exposure to a predator elicits an innate fear response and mimics several behavioral disorders related to post-traumatic stress disorder (PTSD). The protective role of an enriched condition (EC) against psychogenic stressors in various animal models has been well documented. However, this condition has not been tested in field mice in the context of PTSD. In this study, we show that field mice (Mus booduga) housed under EC exhibit predominantly proactive and less reactive behavior compared with mice housed under standard conditions (SC) during exposure to their natural predator (field rat Rattus rattus). Furthermore, we observed that EC mice displayed less anxiety-like behavior in an elevated plus maze (EPM) and light/dark-box after exposure to the predator (7 hrs/7 days). In EC mice, predator exposure elevated the level of serotonin (5-Hydroxytrypamine, [5-HT]) in the amygdala as part of the coping response. Subsequently, the serotonin transporter (SERT) and 5-HT1A receptor were up-regulated significantly, but the same did not occur in the 5-HT2C receptor, which is associated with the activation of calmodulin-dependent protein kinase-II (CaMKII) and a transcription factor cAMP response element binding protein (CREB). Our results show that predator exposure induced the activation of CaMKII/CREB, which is accompanied with increased levels of histone acetylation (H3, H4) and decreased histone deacetylases (HDAC1, 2). Subsequently, in the amygdala, the transcription of brain-derived neurotrophic factor (BDNF), neuropeptide Y (NPY) and its Y1 receptor were up-regulated, whereas the Y2 receptor was down-regulated. Therefore, EC facilitated a coping response against a fear associated cue in a PTSD animal model and reduced anxiety by differentially activating serotonergic and NPY-ergic systems.

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In this study, we examined the neuroprotective effect of standardized Bacopa monniera extract (BME: BESEB CDRI-08) against the D-galactose (D-gal)-induced brain aging in rats. Experimental groups were subjected to contextual-associative learning task. We found that the administration of BME in the D-gal-treated group attenuated contextual-associative learning deficits; the individuals showed more correct responses and retrieved the reward with less latency. Subsequent analysis showed that the BME administration significantly decreased advance glycation end product (AGE) in serum and increased the activity of antioxidant response element (ARE) and the antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and nuclear transcription factor NF-E2-related factor 2 (Nrf2), accompanied by a reduction in the level of serotonin (5-HT) in the hippocampus. The BME treatment also reversed D-gal-induced brain aging by upregulating the levels of the presynaptic proteins synaptotagmin I (SYT1) and synaptophysin (SYP) and the postsynaptic proteins Ca(2+) /calmodulin dependent protein kinase II (αCaMKII) and postsynaptic density protein-95 (PSD-95) in the hippocampus during synaptic plasticity. A significant finding is that the D-gal- + BME-treated rats exhibited more correct responses in contextual-associative learning than D-gal alone-treated rats. Our findings suggest that BME treatment attenuates D-gal-induced brain aging and regulates the level of antioxidant enzymes, Nrf2 expression, and the level of 5-HT, which was accompanied by concomitantly increased levels of synaptic proteins SYT1, SYP, αCaMKII, p-αCaMKII, and PSD-95.

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