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D1 receptors regulate dendritic morphology in normal and stressed prelimbic cortex.
Grant L Lin1, Candace B Borders1, Leslie J Lundewall1
1Department of Psychological & Brain Sciences, Indiana University, Bloomington, IN 47405, USA.
Psychoneuroendocrinology
|October 12, 2014
Summary
Stress causes retraction of brain cell dendrites in the medial prefrontal cortex (mPFC). Blocking dopamine D1 receptors (D1R) during stress prevented this, but caused retraction in unstressed rats, highlighting dopamine
Area of Science:
- Neuroscience
- Stress Research
- Dopamine Signaling
Background:
- Stress and prefrontal cortex dysfunction are linked to psychological disorders.
- Medial prefrontal cortex (mPFC) structure and function are altered by stress.
- Chronic stress induces dendritic retraction in the prelimbic region (PL) of the mPFC.
Purpose of the Study:
- To investigate the role of dopamine D1 receptor (D1R) signaling in stress-induced dendritic remodeling in the PL of the mPFC.
- To determine if D1R blockade during stress prevents dendritic retraction and to assess the effect of D1R blockade in unstressed conditions.
Main Methods:
- Rats were subjected to daily restraint stress for 10 days.
- Dopamine D1 receptor antagonist SCH23390 or vehicle was infused into the PL region.
- Dendritic morphology of pyramidal neurons in the PL was analyzed using Golgi histology.
Main Results:
- Stressed rats receiving vehicle showed significant dendritic retraction in the PL compared to unstressed controls.
- D1R blockade in the PL prevented stress-induced dendritic retraction.
- D1R blockade in unstressed rats also led to dendritic retraction, indicating a role in maintaining normal morphology.
Conclusions:
- Dopaminergic transmission via D1R in the mPFC directly mediates stress-induced retraction of apical dendrites.
- Dopamine signaling is crucial for maintaining normal dendritic morphology in the absence of stress.
- These findings elucidate the specific mechanisms of stress-induced neural plasticity in the mPFC.
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