One area of neuroscience I’ve always been so interested by is neuroplasticity, which is the brain’s ability to structurally change throughout the lifespan. In 1948, Polish neuroscientist Jerzy Konorski[1] coined the term “neuroplasticity” to describe changes in the neuronal structure of the brain, although research into neuroplasticity didn’t begin until the 1960s. Before this, the general belief was that our brains completely stopped developing once we reached adulthood, meaning people who sustained brain injuries or stroke were deemed unable to recover.
In 1969, Raisman conducted research into neuroplasticity by inducing lesions in the brain of rats and observing the subsequent changes in the neural tissue afterwards. Raisman found that new synapses (a structure through which electrical and chemical signals can pass) formed in the brains of the rats after injury. This research demonstrated that the brain can develop new structures after damage, showing the brain can recover from traumatic injury.
A further study on rats demonstrated that rehabilitation following brain injury facilitates neuroplasticity. Rats with induced brain lesions were given growth hormone treatment and either short-term or long-term rehabilitation. The findings showed that the combination of growth hormone treatment and rehabilitation, compared to growth hormone treatment alone, resulted in improved levels of actin and nestin (proteins that facilitate cellular processes such as cell motility, muscle contraction and cell division) and significant behavioural improvement. Suggesting that hormone treatment and rehabilitation promote the production of proteins that encourage cell production and development, resulting in structural changes in the brain and improved functioning.
Further research has demonstrated that psychological stress can cause structural change in our brains. Research has looked at how the hippocampus, a structure part of the limbic system related to memory, spatial navigation, emotional regulation and response to reward, structurally changes in response to stress [2]. Chronic stress has been linked to retraction of dendrites, extensions of a nerve cell which transmit electrical signals. This retraction of dendrites leads to a reduction in the surface of neurons which reduces the number of synapses in the hippocampus. Consequently, this may cause an impaired ability to regulate emotions and impaired memory.
However, further research has demonstrated the this retraction of dendrites can be reversed once psychological stress is eliminated [3]. Additional research has shown that administering drugs that stimulate neuroplasticity can actually prevent this retraction of dendrites from occurring in the first place [4].
Additionally, beneficial practices such as meditation and exercise can cause positive structural changes in the brain. One study using fMRI neuroimaging (a scan that shows flow of oxygen in the brain) found that individuals that have regularly practised meditation over a long period of time have higher activation in numerous brain structures, including visual cortex and dorsolateral prefrontal cortex [5]. These areas of the brain are involved in monitoring and engaging attention, suggesting the effects than meditation have on brain structure improve regulating attention.
A further study used neuroimaging and memory tasks to assess the effect of exercise on neuroplasticity in older adults [6]. 24 adults over the age of 60 regularly completed Wii-Fit exercises over a 6 week period, and following this period neuroimaging showed an increased activation in the striatum (an area of the brain associated with motivation, reward and decision-making) and the posterior cingulate cortex (associated with spatial memory and emotional salience). The participants also demonstrated a significant improvement on memory tasks.
Probably the most exciting aspect of neuroplasticity is neurogenesis, the process through which new neurons are formed from neural stem cells in adults. In humans and most mammals, neurogenesis occurs throughout adulthood in two key regions of the brain; the subgranular zone, part of the hippocampus, involved in learning and the formation of memories, and the subventricular zone, a source of neural stem cells [7]. There are numerous implications of neurogenesis imperative to our neuropsychological and cognitive development. Neurogenesis in the hippocampus facilitates our ability to learn new information and form memories, and some studies have demonstrated that decreased neurogenesis in the hippocampus has been related to Alzheimer’s Disease [8], Schizophrenia [9]and Major Depressive Disorder [10].
Neuroplasticity and neurogenesis are fundamental processes influencing our ability to recover from injury, maintain and improve our cognitive function, and to learn and form memories. Recent research into neuroplasticity is shaping how we treat conditions such as brain injury, Dementia and mental disorders, making it an imperative area of neuroscience to study and research.
References:
[1] Raisman, G. (1969), Neuronal plasticity in the septal nuclei of the adult rat. Brain Research, 14(1), 25–48,.
[2] Watanabe, Y., Gould, E., & McEwen, B. S. (1992). Stress induces atrophy of apical dendrites of hippocampal CA3 pyramidal neurons. Brain Research, 588(2), 341–345.
[3] C. Sandi, H. A. Davies, M. I. Cordero, J. J. Rodriguez, V. I. Popov, and M. G. Stewart. (2003). Rapid reversal of stress induced loss of synapses in CA3 of rat hippocampus following water maze training. European Journal of Neuroscience, 17(11), 2447–2456.
[4] Y. Watanabe, E. Gould, D. C. Daniels, H. Cameron, and B. S. McEwen. (1992). Tianeptine attenuates stress-induced morphological changes in the hippocampus. European Journal of Pharmacology, 222(1), 157–162.
[5] Davidson, R. J., & Lutz, A. (2008). Buddha's Brain: Neuroplasticity and Meditation. IEEE signal processing magazine, 25(1), 176–174.
[6] Ji, L., Zhang, H., Potter, G. G., Zang, Y.-F., Steffens, D. C., Guo, H., & Wang, L. (2017). Multiple neuroimaging measures for examining exercise-induced neuroplasticity in older adults: A quasi-experimental study. Frontiers in Aging Neuroscience, 9.
[7] Ernst, A; Frisén, J (2015). Adult neurogenesis in humans- common and unique traits in mammals. PLOS Biology. 13(1).
[8]Donovan, M. H.; Yazdani, U; Norris, R. D.; Games, D; German, D. C.; Eisch, A. J. (2006). "Decreased adult hippocampal neurogenesis in the PDAPP mouse model of Alzheimer's disease". The Journal of Comparative Neurology, 495 (1), 70–83.
[9]LeStrat, Y (2009). "The role of genes involved in neuroplasticity and neurogenesis in the observation of a gene-environment interaction (GxE) in schizophrenia". Current Molecular Medicine. 9(4), 506–18.
[10]Numakawa, Tadahiro; Odaka, Haruki; Adachi, Naoki (2017). "Impact of glucocorticoid on neurogenesis". Neural Regeneration Research, 12 (7), 1028–1035.
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