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Updated: Jun 18, 2025

Inducing Long-Term Plasticity of Intrinsic Neuronal Excitability in Neurons of the Dorsal Lateral Geniculate Nucleus
Published on: September 20, 2024
Axo-axonic synaptic input drives homeostatic plasticity by tuning the axon initial segment structurally and
Rui Zhao1, Baihui Ren2, Yujie Xiao3
1Institutes of Brain Science, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Department of Neurobiology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Homeostatic plasticity in the axon initial segment (AIS) of principal neurons is tuned by chandelier cell inputs, impacting neuronal excitability and social behavior.
Area of Science:
- Neuroscience
- Cellular Neuroscience
- Systems Neuroscience
Background:
- Homeostatic plasticity stabilizes brain networks by adjusting neuronal firing properties.
- The axon initial segment (AIS) is a key site for regulating neuronal excitability.
- The role of direct synaptic input to the AIS in this plasticity remains unclear.
Purpose of the Study:
- To investigate whether synaptic inputs to the AIS drive homeostatic plasticity.
- To determine the specific contribution of different GABAergic inputs to AIS tuning.
- To link AIS plasticity to neuronal excitability and animal behavior.
Main Methods:
- Studied homeostatic plasticity in principal neurons (PNs) within the prelimbic (PL) region.
- Examined the effects of GABAergic synaptic input from chandelier cells (ChCs) and parvalbumin-positive basket cells on the AIS.
- Assessed changes in AIS morphology, sodium channel expression, and PN excitability.
- Monitored social behavior in relation to PL PN activity and AIS plasticity.
Main Results:
- GABAergic synaptic input from ChCs, but not basket cells, drives homeostatic tuning of the AIS in PNs.
- This tuning affects AIS morphology, sodium channel expression, and PN excitability.
- Altered AIS plasticity and PN excitability correlate with time-dependent changes in social behavior.
Conclusions:
- Homeostatic plasticity at the AIS, modulated by ChC input, plays a crucial role in maintaining neuronal function.
- AIS plasticity in PNs can compensate for imbalanced ChC input at both cellular and behavioral levels.
- This mechanism may be vital for counteracting neurological deficits related to network instability.
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