Brain is modulated by neuronal plasticity during postnatal development

Abstract

Neuroplasticity is referred to the ability of the nervous system to change its structure or functions as a result of former stimuli. It is a plausible mechanism underlying a dynamic brain through adaptation processes of neural structure and activity patterns. Nevertheless, it is still unclear how the plastic neural systems achieve and maintain their equilibrium. Additionally, the alterations of balanced brain dynamics under different plasticity rules have not been explored either. Therefore, the present article primarily aims to review recent research studies regarding homosynaptic and heterosynaptic neuroplasticity characterized by the manipulation of excitatory and inhibitory synaptic inputs. Moreover, it attempts to understand different mechanisms related to the main forms of synaptic plasticity at the excitatory and inhibitory synapses during the brain development processes. Hence, this study comprised surveying those articles published since 1988 and available through PubMed, Google Scholar and science direct databases on a keyword-based search paradigm. All in all, the study results presented extensive and corroborative pieces of evidence for the main types of plasticity, including the long-term potentiation (LTP) and long-term depression (LTD) of the excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs).

Increased glutamate and glutamine levels and their relationship to astrocytes and dopaminergic transmissions in the brains of adults with autism

“…In the brain, assemblies of excitatory and inhibitory neurons are involved in learning and memory and the balance between their activities is critically significant for their network development 5 . One of the plausible theories for the pathophysiology of autism is the excitation-inhibition (E/I) imbalance theory 6 .…”

Effects of chronic fluoxetine treatment on anxiety- and depressive-like behaviors in adolescent rodents – systematic review and meta-analysis

“…It has been postulated that the therapeutic effects of fluoxetine may be rather mediated by its influence on neuroplasticity by affecting gene expression, inducing epigenetic changes and modifying synaptic transmission through, e.g., synaptic remodeling or long-term potentiation/depression [11,13]. In the context of pharmacotherapy of young patients it is worth emphasising that the developing brain has broad ability and sensitivity to neuroplastic changes [14]. Fluoxetine is considered the first-choice drug in the pharmacotherapy of MDD and anxiety disorders in children and adolescents.…”

Overexpression of the schizophrenia risk gene C4 in PV cells drives sex-dependent behavioral deficits and circuit dysfunction

“…During development, neuronal networks are far from static; an ever-dynamic landscape, synaptic connections are constantly being formed, lost, strengthened, or weakened across development (151)(152)(153). The fundamental unit of this plasticity is the information transferred from the presynaptic partner to its postsynaptic partner(s), the efficacy or existence of this connection being largely an activity-dependent factor (152,154).…”