Neuroplasticity and Depressive Disorder
Depressive disorder is associated with decreased neuroplasticity and decreased concentration of glutamate , which is a neurotransmitter of arousal.
Some monoamines act on secondary messengers – mitogen- activated protein kinase , contribute to the normalization of neuroplasticity and glutamate content . Some drugs cause an increase in glutamate secretion, act on synapsogenesis, and improve mood (eg ketamine). But the effect is short-lived.
Electroconvulsive therapy and antidepressants at the cellular level cause an increase in the expression of neuroprotective proteins – the neurotrophic factor BDNF, which promotes neuronal life and regulates synaptic connections.
In experiments on rats, electroconvulsive therapy and antidepressants increase the secretion of neurons in the dentate gyrus of the hippocampus and reduce the effects of the action of the hypothalamic-pituitary-adrenal axis in depression.
In post-traumatic stress disorder, antidepressants restore the limbic system and the hippocampus .
But in Russian medicine, these changes are not taken into account by clinicians, like the content of glutamate and the processes of neuroplasticity in depression.
Prolonged stress reduces the volume of the hippocampus, the number of neurons, and leads to neuronal atrophy.