Regulatory Molecules of Synaptic Plasticity in Anxiety Disorder

Abstract

Synaptic plasticity is the capacity of synaptic transmission between neurons to be strengthened or weakened. There are many signal molecules accumulated in the presynaptic and postsynaptic membranes that can lead to the regulation of synaptic plasticity and involvement in numerous of neurological and psychiatric diseases, including anxiety disorder. However, the regulatory mechanisms of synaptic plasticity in the development of anxiety disorder have not been well summarized. This review mainly aims to discuss the biological functions and mechanisms of synaptic plasticity-related molecules in anxiety disorder, with a particular focus on the metabotropic glutamate receptors, brain-derived neurotrophic factor, hyperpolarization-activated cyclic nucleotide–gated channels, and postsynaptic density 95. The summarized functions and mechanisms of synaptic plasticity-related molecules in anxiety will provide insight into novel neuroplasticity modifications for targeted therapy for anxiety.

Keywords:

• synaptic plasticity
• anxiety
• mGluRs
• BDNF
• HCN
• PSD95

Abbreviations

mGluRs, metabotropic glutamate receptors; BDNF, brain-derived neurotrophic factor; HCN, hyperpolarization-activated cyclic nucleotide–gated; PSD95, postsynaptic density; LTP, long-term potentiation; LTD, long-term depression; NMDAR, N-methyl-D-aspartic acid receptor; BLA, basolateral amygdala; MCPG, α-methyl-4-carboxyphenylglycine; CeA, central amygdala; MeA, medial amygdala; CNBD, cyclic nucleotide–binding domain; ACC, anterior cingulate cortex; AMPAR, α-amino-3-hydroxy-5-methyl-4-isoxazole-propionicacid receptor.

Acknowledgments

This work was supported by Shanghai Sailing Program (grant 20YF1446100); Shanghai Municipal Health Commission (grant shslczdzk04901); and Future program (WL-QNRC-2022002K).

Disclosure

The authors report no conflicts of interest in this work.