Activity-dependent Plasticity - Structures and Pathways Involved

Structures and Pathways Involved

Nearly every cortex and region within the brain is involved in its plasticity feature since most regions are capable of adopting other regions’ functions based on relative use and the “rewiring” of the topographic map. The reorganization of sensory and motor maps involves a variety of pathways and cellular structures related to relative activity.

More important than structures and regions are the subunits involved in these changes: AMPA and NMDA receptors are capable of altering long and short-term potentiation between neurons. NMDA receptors can detect local activity due to activation and therefore modify signaling in the post-synaptic cell. The increased activity and coordination between pre- and post-synaptic receptors leads to more permanent changes and therefore result in changes in plasticity. Hebb’s postulate addresses this fact by stating that synaptic terminals are strengthened by correlated activity and will therefore sprout new branches. However, terminals that experience weakened and minimal activity will eventually lose their synaptic connection and deteriorate.

A major target of all molecular signaling is the inhibitory connections made by GABAergic neurons. These receptors exist at postsynaptic sites and along with the regulation of local inhibitory synapses have been found to be very sensitive to critical period alterations. Any alteration to the receptors leads to changed concentrations of calcium in the affected cells and can ultimately influence dendritic and axonal branching. This concentration change is the result of many kinases being activated, the byproduct of which may enhance specific gene expression.

In addition, it has been identified that the wg postsynaptic pathway, which is responsible for the coding and production of many molecules for development events, can be bidirectionally stimulated and is responsible for the downstream alteration of the postsynaptic neuron. When the wg presynaptic pathway is activated, however, it alters cytoskeletal structure through transcription and translation.

Cell adhesion molecules (CAMs) are also important in plasticity as they help coordinate the signaling across the synapse. More specifically, integrins, which are receptors for extracellular matrix proteins and involved with CAMs, are explicitly incorporated in synapse maturation and memory formation. They play a crucial role in the feedback regulation of excitatory synaptic strength, or long-term potentiation (LTP), and help to control synaptic strength by regulating AMPA receptors, which result in quick, short synaptic currents. But, it is the metabotropic glutamate receptor 1 (mGlu1) that has been discovered to be required for activity-dependent synaptic plasticity in associative learning.

Activity-dependent plasticity is even seen in the primary visual cortex, a region of the brain that processes visual stimuli and is capable of modifying the experienced stimuli based on active sensing and arousal states. It is known that synaptic communication trends between excited and depressed states relative to the light/dark cycle. By experimentation on Long Evans rats, it was found that visual experience during vigilant states leads to increased responsiveness and plastic changes in the visual cortex. More so, depressed states were found to negatively alter the stimulus so the reaction was not as energetic. This experiment proves that even the visual cortex is capable of achieving activity-dependent plasticity as it is reliant on both visual exploration and the arousal state of the animal.