Light deprivation produces distinct morphological orchestrations on RGCs and cortical cells in a depressive-like

Chanyi Lu1, Qi-Qin Li1, Yao-Yao Li1

  • 1School of Ophthalmology & Optometry, The Eye Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China; State Key Laboratory Cultivation Base and Key Laboratory of Vision Science, Ministry of Health P. R. China and Zhejiang Provincial Key Laboratory of Ophthalmology and Optometry, China.

Neuroscience Letters
|September 5, 2017
PubMed

Insights

Depression alters neuronal morphology, with light deprivation promoting dendritic growth in some retinal cells (RGA) while simplifying others in the visual cortex. This suggests cross-modal plasticity in the brain.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Psychiatry

Background:

  • Depression pathogenesis research has focused on neural and synaptic changes.
  • Neuronal morphological alterations in depression remain underexplored.

Purpose of the Study:

  • Investigate morphological changes in retinal ganglion cells (RGCs) and cortical layer 5 pyramidal cells (L5PCs) in a mouse model of depression.
  • Identify cell-type-specific responses to depressive states at the neuronal level.

Main Methods:

  • Utilized a light deprivation (LD) model to induce a depressive-like state in YFP-H transgenic mice.
  • Classified RGC subtypes (RGA, RGB, RGC) based on soma and dendritic field (DF) size.
  • Analyzed morphological changes in RGCs and L5PCs of the primary visual and auditory cortices.

Main Results:

  • Light deprivation (LD) induced cell-type-specific changes in RGCs, notably promoting dendritic growth in RGA cells.
  • LD suppressed the overall morphology of primary visual and auditory cortical L5PCs.
  • LD increased dendritic spine density in primary visual cortical L5PCs, indicating potential compensatory mechanisms.

Conclusions:

  • Neuronal morphological changes, including cross-modal plasticity, occur in RGCs and cortical L5PCs during a depressive-like state.
  • Findings offer insights into depression pathogenesis at the single neuronal morphological level.

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