Visual Cortex in Blind Used For Reading Braille (Language)


That division of labor suggests that the brain’s structure follows a predetermined, genetic blueprint. However, evidence is mounting that brain regions can take over functions they were not genetically destined to perform. In a landmark 1996 study of people blinded early in life, neuroscientists showed that the visual cortex could participate in a nonvisual function — reading Braille.
Now, a study from MIT neuroscientists shows that in individuals born blind, parts of the visual cortex are recruited for language processing. The finding suggests that the visual cortex can dramatically change its function — from visual processing to language — and it also appears to overturn the idea that language processing can only occur in highly specialized brain regions that are genetically programmed for language tasks.
“Your brain is not a prepackaged kind of thing. It doesn’t develop along a fixed trajectory, rather, it’s a self-building toolkit. The building process is profoundly influenced by the experiences you have during your development,” says Marina Bedny, an MIT postdoctoral associate in the Department of Brain and Cognitive Sciences and lead author of the study, which appears in the Proceedings of the National Academy of Sciences the week of Feb. 28. (via.)

Neural plasticity is a wonderful thing!


Brain-Derived Neurotrophic Factor & Serotonin Effects on Aging, Plasticity & More


BDNF and 5-HT: a dynamic duo in
age-related neuronal plasticity and
neurodegenerative disorders

Brain-derived neurotrophic factor (BDNF) and serotonin (5-hydroxytryptamine, 5-HT) are known to regulate synaptic plasticity, neurogenesis and neuronal survival in the adult brain. These two signals co-regulate one another such that 5-HT stimulates the expression of BDNF, and BDNF enhances the growth and survival of 5-HT neurons. Impaired 5-HT and BDNF signaling is central to depression and anxiety disorders, but could
also play important roles in the pathogenesis of several age-related disorders, including insulin resistance syndrome, Alzheimer’s disease and Huntington’s disease.
Enhancement of BDNF signaling may be a key mechanism whereby cognitive stimulation, exercise, dietary restriction and antidepressant drugs preserve brain function during aging. Behavioral and pharmacological manipulations that enhance 5-HT and BDNF signaling
could help promote healthy brain aging. [...]

By promoting neurogenesis,
synaptic plasticity and cell survival, BDNF plays a pivotal
role in the development and plasticity of the brain. During
development of the cerebral cortex and hippocampus,
BDNF induces the differentiation of neural stem cells into
neurons and promotes the survival of newly generated
neurons [1–3]. BDNF signaling at synapses enhances
long-term potentiation (LTP), a process of synaptic
strengthening associated with learning and memory;
the effect of BDNF on LTP is apparently mediated by
cAMP-response-element-binding protein (CREB), which
regulates the expression of genes involved in LTP and
memory formation [4]. Levels of BDNF are increased in
the hippocampus of rats during and after performance
of a spatial learning task (a radial-arm maze), and both
acquisition and maintenance of spatial memory are
impaired when BDNF levels are decreased using antisense
methods [5]. In rats that had previously acquired
spatial memory by extensive training, suppression of
BDNF expression impaired both reference and working
memory [5]. Another study showed that mice lacking one
copy of the BDNF gene exhibit impaired spatial learning
in the Morris water maze [6]. BDNF also plays an important
role in preventing death of neurons during development,
and promotes cell survival during stressful conditions
such as ischemia and trauma in the adult brain [7]. [...]

[A]ctivation of 5-HT1A receptors can impair learning and
memory whereas 5-HT2A and 5-HT2C receptors facilitate
memory formation [10]. [...]

5-HT can
also promote the survival of neurons in the adult brain, as
demonstrated by the abilities of a 5-HT receptor agonist
and SSRI to protect neurons against excitotoxic and
ischemic injury in animal models [12,13]. There are therefore
several commonalities of function in the CNS for
BDNF and 5-HT in terms of their effects on synaptic
plasticity, neurogenesis and cell survival. [...]

Conversely, BDNF
can stimulate the growth and sprouting of 5-HT neuron
axons innervating the cerebral cortex, thereby presumably
increasing the number of 5-HT synapses in this brain
region [14]. (via: pdf.)


Neural Plasticity and “Training” The Aging Brain


How to Train the Aging Brain – An article on neural plasticity from NY Times – “While it’s tempting to focus on the flaws in older brains, that inducement overlooks how capable they’ve become. Over the past several years, scientists have looked deeper into how brains age and confirmed that they continue to develop through and beyond middle age. [...] The brain, as it traverses middle age, gets better at recognizing the central idea, the big picture. If kept in good shape, the brain can continue to build pathways that help its owner recognize patterns and, as a consequence, see significance and even solutions much faster. [...] With a brain already full of well-connected pathways, adult learners should “jiggle their synapses a bit” by confronting thoughts that are contrary to their own. Teaching new facts should not be the focus of adult education. Instead, continued brain development and a richer form of learning may require that you “bump up against people and ideas” that are different.”

I’d argue that memorization of disconnected facts shouldn’t be the focus of youthful education pursuits, either.