Learning is a complicated process that involves storage and retrieval of information inside the brain. Without long-term storage, the process of learning would be impossible as all the learned information would be lost after a short period, as it happens in simple organisms that lack nervous systems. There are two types of memory, which are declarative memory (memories of facts, people, and events that a person can verbalize or declare) and non-declarative memory (memories for behaviors) (Garrett & Hough, 2018). Understanding the neurological processes behind learning is of extreme importance for understanding how brain damage affects memory and learning ability.
Learning is a form of neuroplasticity, which is a process of remodeling neural connections. According to Hebb rule, “if an axon of a presynaptic neuron is active while the postsynaptic neuron is firing, the synapse between them will be strengthened” (Garrett & Hough, 2018, p. 546). Long-term potentiation (LTP) is a continuous strengthening of synapses due to simultaneous activation of presynaptic neurons and postsynaptic neurons. LTP is known to occur mostly in the hippocampus; however, it can also happen in visual, auditory, and motor cortex (Garrett & Hough, 2018). LTP is induced by a cascade of events at the synapse, where neurotransmitter (glutamate) activates AMPA receptors by the first few pulses of stimulation depolarizing the membrane and dislodging the magnesium ions (Garrett & Hough, 2018). As a result, an influx of calcium ions. Within 45-60 minutes, an increased amount of dendritic spines in post-synaptic neurons bridge the synaptic cleft and make the synapse more sensitive (Garrett & Hough, 2018). This process, together with neurogenesis, supports learning.
Learning impairment can be a result of various events, such as trauma, stroke, and electric stimulation. Chen et al. (2018) conducted an experimental study on rats to understand how electroconvulsive shock (ECS) can cause learning impairment. Previous research demonstrated that ECS could cause an antidepressant effect in rats with depression-like behavior; however, there was an important side effect of learning impairment, and the mechanisms of the impact were unknown (Chen et al., 2018). Therefore, Chen et al. (2018) created an electrophysiological experiment to detect synaptic plasticity in LTP, long-term depression (LTD), depotentiation, and post-tetanic potentiation (PTP). The results revealed that ECS caused a lower magnitude in LTD and PTP, which is a signal of their impairment, and high magnitude in LTP, which is a signal of its enhancement (Chen et al., 2018). These changes demonstrate how ECS causes learning impairment.
The study by Chen et al. (2018) provides significant insights into the causes of learning impairments and the ways they can be addressed. In particular, the study revealed that acute strong enough stress, such as electronic stimulation with ECS, could cause severe learning disabilities, while milder stressors induce less LTP impairment and LTD enhancement. At the same time, the anesthetics, such as propofol, thiopental, can mitigate learning impairment, which is vital knowledge for treating patients with learning disabilities.
In summary, learning is a process characterized by storage and retrieval information. Learning causes neuroplastic changes as the brain rearranges neural connections. The postsynaptic changes include LTP and LTD, while the presynaptic changes are the PTP. Brain damages occur in various circumstances, including trauma, stroke, and electric stimulation. Learning problems after electrical stimulation is caused by LTP and PTP impairment and LTD enhancement. The effect of ETC can be mitigated using anesthetics.
References
Chen, Q., Ren, L., Min, S., Hao, X., Chen, H., & Deng, J. (2018). Changes in synaptic plasticity are associated with electroconvulsive shock-induced learning and memory impairment in rats with depression-like behavior. Neuropsychiatric Disease and Treatment, 14, 1737-1746.
Garrett, B., & Hough, G. (2018). Brain and behavior: An introduction to behavioral neuroscience (5th ed.). Los Angeles, CA: SAGE Publications, Inc.