Corticotropin-Releasing Factor Induces Functional And Structural Synaptic Remodelling In Acute Stress

Abstract

Biological responses to internal and external stress factors involve highly conserved mechanisms, using a tightly coordinated interplay of many factors. Corticotropin-releasing factor (CRF) plays a central role in organizing these lifesaving physiological responses to stress. We show that CRF rapidly and reversibly changes Schaffer Collateral input into hippocampal CA1 pyramidal cells (PC), by modulating both functional and structural aspects of these synapses. Host exposure to acute stress, in vivo CRF injection, and ex vivo CRF application all result in fast de novo formation and remodeling of existing dendritic spines. Functionally, CRF leads to a rapid increase in synaptic strength of Schaffer collateral input into CA1 neurons, e.g. increase in spontaneous neurotransmitter release, paired-pulse facilitation and repetitive excitability and improves long-term synaptic plasticity: LTP and LTD. In line with the changes in synaptic function, CRF increases the number of presynaptic vesicles, induces redistribution of vesicles towards the active zone increases active zone size, and improves the alignment of the pre- and post-synaptic compartments. Together, CRF rapidly enhances synaptic communication in the hippocampus, potentially playing a crucial role in the enhanced memory consolidation in acute stress.

Multiple Memory Subsystems: Reconsidering Memory in the Mind and Brain

“…However, our framework raises the possibility that the other subsystem (MSP) may not be affected in the same way. Indeed, rodent CA1 (MSP) is largely spared from negative effects of stress (Yamada et al, 2003) and may even be enhanced by stress (Karst & Joëls, 2005;Vandael et al, 2021). In humans, stress promotes "gist"-like memories with less specificity (e.g., Qin et al, 2012) and integration across related episodes (Bierbrauer et al, 2021) as well as detection of probability-based regularities associated with statistical learning (Tóth-Fáber et al, 2021).…”

Toward Antifragility: Social Defeat Stress Enhances Learning and Memory in Young Mice Via Hippocampal Synaptosome Associated Protein 25

“…There is ample evidence to support the notion that acute stress can facilitate memory by enhancing synaptic plasticity (Shields et al, 2017;Yuen et al, 2011). Acute stress-induced corticotropin-releasing factor rapidly increased synaptic strength of Schaffer collateral input into hippocampal CA1 neurons and enhanced memory consolidation (Vandael et al, 2021). Acute stress also promoted the acquisition and consolidation of hippocampusdependent memory through rapid release of norepinephrine and glucocorticoids (Osborne et al, 2015).…”