Activity-dependent Plasticity - Mechanisms Involved

Mechanisms Involved

There are a variety of mechanisms in place and being discovered from activity-dependent plasticity that work together to help the brain overcome problems and better adapt to functions. These include LTP, long-term depression (LTD), synaptic elimination, neurogenesis, and synaptogenesis. The mechanisms of activity-dependent plasticity result in membrane depolarization and calcium influx, which in turn trigger cellular changes that affect synaptic connections and gene transcription. In essence, neuronal activity helps to regulate gene expression for dendritic branching and synapse development while mutations in activity-dependent transcription-related genes can lead to neurological disorders. Each of the studies’ findings aims to help proper development of the brain while improving a wide variety of tasks such as speech, movement, comprehension, and memory. More so, the findings better explain the development induced by plasticity.

It is known that during postnatal life a critical step to nervous system development is synapse elimination. The changes in synaptic connections and strength are results from LTP and LTD and are strongly regulated by the release of brain-derived neurotrophic factor (BDNF), an activity-dependent synapse-development protein. In addition to BDNF, Nogo-66 receptors, and more specifically NgR1, are also involved in the development and regulation of neuronal structure. Damage to this receptor leads to pointless LTP and attenuation of LTD. Both situations imply that NgR1 is a regulator of synaptic plasticity. From experiments, it has been found that stimulation inducing LTD leads to a reduction in synaptic strength and loss of connections but, when coupled simultaneously with low-frequency stimulation, helps the restructuring of synaptic contacts. The implications of this finding include helping people with receptor damage and providing insight into the mechanism behind LTP.

Another mechanism that gives rise to activity-dependent plasticity includes the excitatory corticostriatal pathway that allows for the storage of adaptive motor behaviors. This pathway is also capable of adhering to long-lasting synaptic changes. The change in synaptic strength is responsible for motor learning and is dependent on the simultaneous activation of glutamatergic corticostriatal and dopaminergic nigrostriatal pathways. These are the very pathways that are affected in Parkinson's disease and the degeneration of synapses within this disorder may be responsible for the loss of cognitive abilities. Therefore, the impairment of DA/ACh-dependent learning can lead to the storage of inessential memories.