Corticotropin releasing factor in neuroplasticity

Abstract

Stress is among the strongest signals promoting neuroplasticity: Stress signals, indicating real or perceived danger, lead to alterations of neuronal function and often structure, designed to adapt to the changed conditions and promote survival. Corticotropin releasing factor (CRF) is expressed and released in several types of neuronal populations that are involved in cognition, emotion and the regulation of autonomic and endocrine function. CRF expressing neurons undergo functional and structural plasticity during stress and, in addition, the peptide acts via specific receptors to promote plasticity of target neurons.

Keywords: CRF; Epigenetics; Hippocampus; Hypothalamus; Memory; Neuropeptide; Plasticity; Stress; Synapse.

Figure 1. The long-term consequences of early-life stress may result from two alternative processes

(A) Chronic early-life stress (ES) may exert its long-term effects on hippocampal structure and function by interfering with hippocampal maturation during a vulnerable / critical developmental period; this possibility predicts that whereas interventions within the critical window will be effective (blue box), interventions initiated later in life will be ineffective (purple box). (B) Alternatively, ES may set in motion molecular cascades that progress over time to lead to functional / structural deficits apparent during middle age. This possibility predicts that therapeutic interventions initiated during young adulthood (blue box) will ameliorate the cognitive deficits.