Strategies and Tools for Enhancing Positive Neural Plasticity
As we age, our brain becomes more selective or resistant to change. Because of this resistance to change, assuming that anything we experience will cause significant alterations or modifications in our brain is incorrect. That is not to say that change or neural plasticity does not occur. There are many cases of neural plasticity in adult brains. For instance, there is considerable neurogenesis or axon sprouting in the months and years after a stroke (Taupin et al., 2006). Stress, drugs, and environmental stimulation can also alter neuroplasticity for better or worse (Fuchs et al., 2014). The adult brain though less malleable than a child’s, is still flexible. And this flexibility spawns a new thought on how we can strategically influence brain structures to be more susceptible to positive change and contribute to higher brain functioning.
The first step to neuroplasticity in adults is neuronal activation generated through focus or engagement. As a result, the ERK pathway and transcription factor CREB is triggered, inducing NMDAR signal transduction (glutamate receptor) and BDNF expression (3, 4, 5). In turn, neuroplasticity involved in memory processes, emotional regulation, neuronal development, and refinement of synaptic connection can be prompted (Krapivinsky et al., 2003). However, whether or not significant change occurs depends on repetition, novelty, engagement, and timing of engagement. Such as how often is the task being performed? How novel is the information? How focused are you during the learning session? And at what time of day are you performing this bout of activity or learning?
In addition, a critical component of neural plasticity is the activation of the neuromodulation network. Work from Jun Kang and Elvire Vaucher found that if you induced visual stimulation and injected acetylcholine in the basal forebrain of rats, you could significantly improve Long term potentiation from neuroplasticity during 6 hours. A recent study found that administering a cholinergic transmission enhancer in healthy adults undergoing highly demanding perceptual-cognitive tasks can increase learning speed. These findings suggest the importance of choline (precursor to acetylcholine) and the receptors it binds to for enhancing neuroplasticity (Chamoun et al., 2017).
An exciting study published in the same year looking at neural plasticity dynamics found that pairing sensory stimulation with activation of an area of the basal forebrain called the nucleus basalis affected a rapid reduction of synaptic inhibition and a significant increase in excitation. These changes remained for hours after a few minutes of stimulation (Froemke et al., 2017). Considering that the nucleus basalis is one of the largest reservoirs of cholinergic neurons suggests that the excitation of acetylcholine in this brain region could predispose for a much higher affinity for change and long-term potentiation than neutral acetylcholine release.
Noradrenaline also has an important role to play in neural plasticity. Noradrenaline or norepinephrine is primarily synthesized in neurons deep into the brain stem called the locus coeruleus (Tully et al., 2010). When excited, norepinephrine travels along the axon throughout various brain regions, including the amygdala, brain stem, spinal cord, cerebellum, hypothalamus, and hippocampus, and binds to G-coupled adrenergic receptors (Tully et al., 2010). Studies have consistently found that upregulation of norepinephrine during memory consolidation or directly afterward could enhance memory performance (11, 12). More so, blocking adrenergic receptors in the amygdala prevents the increase in memory performance (13).
A fascinating study showed that increased norepinephrine during emotional arousal could lower the threshold for memory formation (Hu et al., 2007), which means that changing functional connectivity in the amygdala and hippocampus could create stronger neural connectivity between structures important for long-term memory storage, learning, and emotion. This idea of cross-wiring for enhanced cognition and memory has been a crucial field of study in neuroscience. And now more than ever, scientists are beginning to unravel the importance of neuromodulators, particularly acetylcholine, norepinephrine, and dopamine, for neural plasticity.
To recap, some neuroplasticity is caused by triggering the ERK pathway and transcription factor CREB, which affect neurotrophic factors and glutamate receptors. Other processes include acetylcholine upregulation in the nucleus basalis and norepinephrine release from the locus coeruleus. These excitatory changes can affect cognition, retention, and memory by enhancing the brain's neural functioning and neural plasticity. In light of this, how can we use this information to enhance learning, retention, and positive neural plasticity?
Strategies and Tools for Enhancing Neural Plasticity Before Learning
When it comes to finding the best time of day for learning and how long you should be engaged in learning varies. What chronotype are you (take this quiz)? Are you more likely to wake up closer to six or nine? Are you required to wake up at six, or do you prefer to wake up at this time? If you gravitate to waking up around 7-8, the best time to begin the first learning session is around 9-11. Cortisol, a hormone produced in the adrenals, usually peaks 2 hours after waking. Research shows that this hormone modulates neuronal activity in the hippocampus (Haley et al., 2005). Though the cortisol-learning model offers valuable insight, it is important to consider individual variance, including how much sleep and morning sunlight you get.
The quality of sleep the previous night has countless times been shown to affect the quality of cognition the following day (16). Sunlight in the morning could also prime the body for a day of alertness and concentration (17). Whether you sleep poorly, view little sunlight, drink alcohol and caffeine, or tend to sleep in later, could all contribute to cortisol secretion and other neuromodulators highly relevant for cognition.
Once you find the earliest optimal time for learning, you should treat this moment of the day as sacred. If this is 10 for you, then shut off any other distractions from 10-12. Dr. Andrew Hubermann, a world-renowned scientist, claims that by aligning your ultradian rhythms with a focused learning session, you could optimize for learning and neural plasticity (Learn more on ultradian cycles here). The idea is to get in tune with the ebb and flow of energy (90-120 min.) in your natural day-to-day ultradian cycle. Methods of discovering what time of day that might be could be gathered by a continuous heart rate monitor: a higher heart rate might indicate increased alertness. Also, valuable data includes perceived energy or writing fluency. For example, if your writing is consistently quicker and more fluid at 11 than 1, then 10-12 is when you are most alert and focused.
Proceeding the learning session, you should take a 90-120 minute break or engage in less demanding work. Repeat one more at another energy cycle. Repeat two at the most. Following this rule is about being productive and tapping into when you are most focused and primed for neural plasticity.
Strategies and Tools for Enhancing Neural Plasticity During and after Learning
Put away all distractions. If you live in a noisy space and are extoreceptively dominant or get distracted easily from the external environment, then put on headphones and listen to some light music. However, If you are interoceptively dominant or more viscerally in tune, music may add another layer of distraction, but this is only sometimes the case. You have to find this out for yourself. For example, music or light classical adds no added benefit when I am engaged in a 90-120 minute learning session alone. However, when I am in a disrupted environment putting on headphones is a game changer.
Besides avoiding distractions, sipping on a caffeinated beverage while or after engaging in cognitively demanding work is usually the best for honing concentration. Caffeine binds to the A2A receptors on the shell of the nucleus accumbens, which indirectly affects many neurotransmitter secretions, including epinephrine. As discussed earlier, epinephrine is a pivotal neuromodulator for enhancing learning and memory. Taking caffeine while you are working can increase alertness. By taking it afterward, you can increase the consolidation or retention of the material you were engaged in. A study found that injecting rats with epinephrine immediately after a learning event enhanced memory in a dose-dependent manner, meaning the administration of epinephrine too much or too late (4 hrs) did not affect memory positively (Liang et al., 2021). These findings suggest that a small to moderate increase in epinephrine, such as with caffeine or cold exposure after a medium to short learning session, may be most beneficial.
Cold exposure causes a significant increase in epinephrine, dopamine, and norepinephrine in the brain and body. A study found that when a group of men was immersed in water for an hour at 32, 20, and 14 degrees Celsius, the coldest water group had a 350% increase in metabolic rate, a 530% increase in noradrenaline, and a 250% increase in dopamine. In contrast, the other groups had small or insignificant changes (19). Taking an ice bath for 5-10 minutes after a learning session instead of sitting at 57 degrees Fahrenheit for one hour may elicit similar neural benefits.
At this point, we talked about chronotypes, cortisol, sunlight, ultradian rhythms, avoiding distractions, music, caffeine, and cold thermogenesis for enhancing neural plasticity. Other strategies can be implemented, like optimizing nutrition by taking Omega 3’s, Creatine, Choline, Alpha GPC, Lions Mane, and/or Electrolytes (particularly magnesium and sodium). If you want to know more about why these supplements benefit the brain, click on this article. Click here to learn more about which magnesium is right for you.
At the beginning of the article, we discussed the importance of acetylcholine or the activation of the cholinergic receptors for neural plasticity. Nicotine activates the acetylcholine receptors by mimicking the action of acetylcholine (20). Taking a tolerable dose of nicotine (gum or patch) during work can stimulate cognition and neural plasticity via cholinergic projection between the basal forebrain and cerebral cortex (Zhang et al., 2017). Moreover, by increasing the density of nicotinic cholinergic receptors, nicotine indirectly augments acetylcholine, epinephrine, dopamine, glutamate, and serotonin, making it a potent drug for learning and memory (22).
Most importantly, even when implementing the tools and strategies mentioned for increasing neural plasticity, it is unlikely that positive change will occur if you are not willing to put in the work. Positive change results from increasing pathways and neuromodulators that might incline the body to change AND by engaging in novelty, short-term stress, or focused attention on a given task to induce directional or controlled change. Half without the other will not instigate as much positive functional connectivity as having both halves in place. You may find that some interventions work better than others as you get better at implementing these strategies. This is good! You can start implementing your strategy for enhancing cognition, learning, and memory by learning what works best.
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