Therefore, given that high rates of neurogenesis are present in litters of runner parents (McGreevy et al., 2019), this phenomenon is probably present from infantile stages, in which case, it might increase infantile amnesia. Likewise, they show an increase in hippocampal mitochondrial activity and the activation of certain transcription machinery genes, which could regulate the expression of proliferation-associated proteins. Then, infantile and juvenile individuals might probably have higher neurogenesis rates than the offspring of sedentary parents. ( 2019) shows that exercised male mice sire offspring with high rates of hippocampal neurogenesis Although, such high levels of neurogenesis occur in adult mice, normally the rates of proliferation decay with age (Lagace et al., 2007), an effect possibly linked to a decrease and senescence of the pool of neural stem cells (Cameron and McKay, 1999).
A massive generation of new mossy fibers from the dentate gyrus to hippocampus-CA3 modifies, or displaces previous synaptic contacts (Toni et al., 2008) and might degrade previously acquired episodic-like memories. ( 2014) probed the neurogenic hypothesis of Josselyn and Frankland ( 2012) showing that elevated neurogenesis in infantile mice is partially responsible for infantile amnesia rescuing episodic-like memories ablating neurogenesis. Interestingly NMDA receptors blockade does not disrupt neurogenesis therefore, both mechanisms that promote infant memory failure would act independently from one another (Tronel et al., 2010). However, the memory engram activation only partially rescues infantile amnesia then, the phenomenon is a combination of memory degradation and a retrieval failure (Guskjolen et al., 2018). A recent biological hypothesis suggests that a switch in maturation between NMDA subunits causes a memory retrieval failure, instead of a complete memory erasure (Travaglia et al., 2016). These comparative findings suggest that an integrative biological hypothesis to explain infantile amnesia is needed. Therefore, according to these hypotheses, infantile amnesia would be an emergent human characteristic, but comparative studies showed that infantile amnesia is present in many mammals as rats or mice (Campbell et al., 1974). Howe and Courage ( 1993) propose that the cause of Infantile amnesia is the lack of self-consciousness at early ages, while Simcock and Hayne ( 2002) propose that the absence of a complex language disables the generation of a self-narrative. ( 2019) there is an inheritance of basal neurogenesis levels, then, the extent of infantile amnesia might be inherited by an epigenetic mechanism.Īfter Freud and Brill ( 1914) mentioned the infantile amnesia, some have appeared trying to explain its origin. If the appearance of Infantile amnesia is a consequence of high levels of neurogenesis, and according to the recent study of McGreevy et al. Recently, Josselyn and Frankland ( 2012) proposed a biological hypothesis which proposes that high rates of postnatal hippocampal neurogenesis are the cause of the failure to retain infant memories. Infantile amnesia, a failure in early childhood to retain episodic memory for long periods, is a paradoxical phenomenon widely accepted as an everyday life fact, but its causes are extensively ignored.
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