Mechanisms of neuroplasticity

Neuroplasticity refers to the capacity that neural systems have to adapt to experience. Lived experience shapes our biology in meaningful ways that helps us adapt to that experience so that we are better prepared next time it, or something similar, happens. Neuroplasticity serves evolution by helping us adapt to our environment, even picking the best strategy for reproduction within that environment so that our genetic line will be continued. Mechanisms of neuroplasticity have been selected by evolution because they are survival positive. In my next 4 blogs I introduce four mechanisms of neuroplasticity: epigenetics, neurogenesis, synaptic plasticity and white matter plasticity.


Epigenetics literally means ‘above the gene’ and epigenetics is a field of study that examines experiences that result in changes to gene expression. One way this occurs is by small chemical groups becoming attached either to the DNA itself or to the core proteins that the DNA coils around. These small chemical groups make the gene itself more or less accessible. Lived experience cannot add or take away genes but the addition of these small chemical groups acts as a volume control over the gene. The gene may literally be silenced (inaccessible) so it is no longer transcribed at all or it may be turned up, or turned down. Turning a ‘the volume’ of a gene up or down really means regulating the rate of transcription of the gene, i.e. how many copies are made of the gene; copies that can then be made into protein. The epigenetic marks on genes may persist from anything from moments to a lifetime and as the pattern of epigenetic marks is copied alongside the DNA it may persist into the next generation. The experiences that leave marks on your genes to help you adapt and survive in your environment may be inherited by your children, because nature assumes that your children going to face similar challenges in a similar environment to the ones you have faced and gives them a head start.

A seminal paper in the epigenetics field published in 2004 showed how the stress axis of rat pups is epigenetically programmed by the type of care they get from their mothers. Rat pups that had high levels of licking and grooming from their mother had lower levels of DNA methylation at the glucocorticoid receptor gene promoter (Weaver et al. 2004). What this means is that the rat pups that had high levels of licking and grooming, which in the rat world counts as good mothering, also had their glucocorticoid receptor gene’s volume turned up. This in turn led to the rats growing up to have a lot of glucocorticoid receptors, which both mediate the effects of the stress axis via corticosterone (in humans it is cortisol) and importantly, means that stress response can be efficiently turned off once it has done its job. The converse was also true. Rat pups that had low levels of licking and grooming, equating to less sensitive and attentive mothering, had a more methylated glucocorticoid receptor gene promoter, so had fewer glucocorticoid receptors, meaning that their stress response would persist for longer because they have fewer glucocorticoid receptors available to turn it off.

The experience of lots of licking and grooming is adaptive for the rat pups because they have lots of glucocorticoid receptors so their stress response is more efficiently terminated and this is okay because they have a sensitive, attentive and available mother to help them both to survive and to recover from any threat. The experience of low levels of licking and grooming is also adaptive because the stress response itself helps the rat pups survive. The stress response is not so readily turned off so the survival advantage conferred by the activated stress system persists and this perhaps can compensate for these rat pups not having a sensitive attentive mother available to help them survive and recover from any threat.

Rachel Yehuda studies the intergenerational effects of trauma, including how a mother’s experience of trauma leading to a diagnosis of PTSD may transfer to her children as an increased risk for PTSD (Yehuda et al. 2008). This doesn’t sound adaptive at all until you consider that the symptoms of PTSD, including anxiety, hypervigilance and insomnia are all adaptive strategies to try and remain safe in case something else traumatic occurs. Nature perhaps assumes that the mother’s children will be born into an environment that is dangerous and so prepares these children for survival in advance, by enhancing the expression of genes that contribute to these feelings of anxiety and hyper-vigilant behaviours. It is, after all the paranoid rabbit that survives. The intergenerational transmission of stress is fully discussed in a recent review by Yehuda and Bowers in Neuropsychopharmacology which is freely available (Bowers and Yehuda 2016).

Next time…neurogenesis and why chickadees, tits and squirrels have higher rates of neurogenesis in the autumn.