In neuroscience, homeostatic plasticity refers to the capacity of neurons to regulate their own excitability relative to network activity.
At the same time, neurons need to have flexibility to adapt to changes and make connections to cope with the ever-changing environment of a developing nervous system.
This process involves various mechanisms, such as quantal size adjustment, differential expression of presynaptic proteins, and modification of vesicle recycling.
Homeostatic postsynaptic plasticity is crucial for maintaining consistent levels of synaptic activity in neurons, which are formed at specific synapses in the brain.
Additionally, changes in the expression and location of neurotransmitter receptors can impact synaptic transmission when specific signaling pathways are activated.
This process involves alterations in the excitability or firing characteristics of individual neurons, rather than primarily adjusting synaptic strength.
Neurons can upregulate the expression of sodium channels to maintain firing rates and increase excitability in case of a drop in synaptic activity.
Synaptic scaling is a homeostatic mechanism that allows neurons to modulate the strength of all synapses to maintain stable activity levels within a specific range.
Homeostatic plasticity in neocortical circuits has been studied in depth by Gina G. Turrigiano and Sacha Nelson of Brandeis University, who first observed compensatory changes in excitatory postsynaptic currents (mEPSCs) after chronic activity manipulations.
[8] Another type of neuroplasticity that, as the name suggests, involves the actual structure of the brain changing as a result of learning, as opposed to just synapses.
In this context, neuronal properties are modulated in response to environmental changes in order to maintain an appropriate and balanced neural output.
In these disorders, neurons ability to maintain stability in response to changes in activity levels or external stimuli is often altered.
In an epileptic brain, homeostatic plasticity mechanisms may become dysregulated leading to episodes of highly synchronized neuronal firing and seizure activity.
Deficits in homeostatic plasticity contribute to cognitive decline and memory impairment which are characteristic symptoms of Alzheimer's disease.
Alterations in synaptic strength and connectivity potentially due to dysregulation in homeostatic mechanisms may lead to the symptoms observed in schizophrenic patients.