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Phenotyping CCL2 Containing Central Amygdala Neurons Controlling Alcohol Withdrawal-Induced Anxiety.
Kathryn M Harper1,2, Darin J Knapp1,2, Caroline A Todd1
1Department of Psychiatry, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, United States.
Frontiers in Cellular Neuroscience
|November 16, 2020
Summary
Neurons release chemokine (C-C motif) ligand 2 (CCL2), impacting anxiety-like behaviors. This study investigated CCL2
Area of Science:
- Neuroscience
- Behavioral Science
- Molecular Biology
Background:
- Chemokines, such as CCL2, influence behaviors including anxiety.
- The role of neuronal CCL2 in behavior and its mechanisms remain unclear.
- Alcohol withdrawal can induce anxiety-like behaviors.
Purpose of the Study:
- To investigate the role of neuronal CCL2 in anxiety-like behavior during alcohol withdrawal.
- To explore the mechanisms by which neuronal CCL2 affects behavior.
- To examine the interplay between CCL2 and CX3CL1 in anxiety.
Main Methods:
- CCL2 mRNA knockdown in rat central nucleus of the amygdala (CeA) neurons using HSV vectors.
- Measurement of fractalkine (CX3CL1) levels.
- Retrograde tracing and axonal transport blockade (colchicine) to study CCL2 transport.
- Confocal and electron microscopy to localize CCL2 at synapses.
Main Results:
- CCL2 knockdown in CeA neurons induced anxiety-like behavior during alcohol withdrawal.
- Both alcohol withdrawal and CCL2 knockdown increased CX3CL1 levels.
- CCL2 was found in CeA projection neurons to the BNST and VPAG.
- Evidence suggests CCL2 is transported via axons and released at nerve terminals.
Conclusions:
- Neurons are a significant source of CCL2 influencing anxiety-like behavior.
- CCL2 may be released from CeA neuronal terminals into regions like the BNST and VPAG.
- The balance of CCL2 and CX3CL1 may be crucial for regulating anxiety.
