The naked mole‐rat (Heterocephalus glaber) has fascinated zoologists for at least half a century. It has also generated considerable biomedical interest not only because of its extraordinary longevity, but also because of unusual protective features (e.g. its tolerance of variable oxygen availability), which may be pertinent to several human disease states, including ischemia/reperfusion injury and neurodegeneration. A recent article entitled ‘Surprisingly long survival of premature conclusions about naked mole‐rat biology’ described 28 ‘myths’ which, those authors claimed, are a ‘perpetuation of beautiful, but falsified, hypotheses’ and impede our understanding of this enigmatic mammal. Here, we re‐examine each of these ‘myths’ based on evidence published in the scientific literature. Following Braude et al., we argue that these ‘myths’ fall into four main categories: (i) ‘myths’ that would be better described as oversimplifications, some of which persist solely in the popular press; (ii) ‘myths’ that are based on incomplete understanding, where more evidence is clearly needed; (iii) ‘myths’ where the accumulation of evidence over the years has led to a revision in interpretation, but where there is no significant disagreement among scientists currently working in the field; (iv) ‘myths’ where there is a genuine difference in opinion among active researchers, based on alternative interpretations of the available evidence. The term ‘myth’ is particularly inappropriate when applied to competing, evidence‐based hypotheses, which form part of the normal evolution of scientific knowledge. Here, we provide a comprehensive critical review of naked mole‐rat biology and attempt to clarify some of these misconceptions.

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The ability to remember conspecifics is critical for adaptive cognitive functioning and social communication, and impairments of this ability are hallmarks of autism spectrum disorders (ASDs). Although hippocampal ventral CA1 (vCA1) neurons are known to store social memories, how their activities are coordinated remains unclear. Here we show that vCA1 social memory neurons, characterized by enhanced activity in response to memorized individuals, were preferentially reactivated during sharp-wave ripples (SPW-Rs). Spike sequences of these social replays reflected the temporal orders of neuronal activities within theta cycles during social experiences. In ASD model Shank3 knockout mice, the proportion of social memory neurons was reduced, and neuronal ensemble spike sequences during SPW-Rs were disrupted, which correlated with impaired discriminatory social behavior. These results suggest that SPW-R-mediated sequential reactivation of neuronal ensembles is a canonical mechanism for coordinating hippocampus-dependent social memories and its disruption underlie the pathophysiology of social memory defects associated with ASD.

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The host microbial community is thought to have an important role in the host endocrine system and behavioral phenotype. We investigated chronological changes of levels of gonadal hormones and corticosterone in the feces of 4‐ to 8‐week‐old female germ‐free (GF) mice, and conducted odor preference test at 8 weeks of age. We further evaluated the developmental impact of the microbial community by analyzing 4‐week‐old GF mice orally administered the fecal microbiota of specific pathogen‐free (SPF) mice or guinea pigs (GF‐SPF mice or GF‐Guinea pig mice). The fecal estradiol, progesterone, and corticosterone levels of GF mice were lower than those of SPF mice. Furthermore, the increased levels in GF mice were suggested to be caused by colonization of microbiota of SPF mice or guinea pigs. However, the degree of recovery of progesterone and corticosterone by microbiota of guinea pigs was lower than that by SPF mice. In odor preference tests, interestingly, female GF mice preferred female odors to male odors, although this preference was not seen in other mice. These findings suggested that the microbial community plays an important role in the development of the host endocrine system for gonadal hormones and corticosterone, and odor preference in mice.