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Methods for the Modulation and Analysis of NF-κB-dependent Adult Neurogenesis

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Published on: February 13, 2014

BDNF regulates neuronal sensitivity to endocannabinoids.

Patrick Maison¹, Deborah J Walker, Frank S Walsh

¹Wolfson Centre for Age-Related Diseases, King' College London, London Bridge, London SE1 1UL, United Kingdom.

Neuroscience Letters

|October 13, 2009

Summary

This summary is machine-generated.

Brain-derived neurotrophic factor (BDNF) enhances neuronal sensitivity to endocannabinoids (eCBs) by upregulating CB1 receptors and downregulating MAGL. This suggests a positive feedback loop for neuronal survival.

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Area of Science:

Neuroscience
Molecular Biology
Neurochemistry

Background:

Diacylglycerol lipases (DAGLalpha/beta) produce 2-arachidonylglycerol (2-AG), the primary endocannabinoid (eCB) in the brain.
2-AG modulates neuronal functions like axonal guidance, synaptic plasticity, neurogenesis, and neuroprotection.
Monoacylglycerol lipase (MAGL) typically terminates 2-AG signaling, but mechanisms regulating neuronal eCB sensitivity are poorly understood.

Purpose of the Study:

To investigate the role of brain-derived neurotrophic factor (BDNF) in modulating neuronal sensitivity to endocannabinoids (eCBs).
To elucidate the molecular mechanisms by which BDNF influences eCB signaling pathways in neurons.

Main Methods:

Utilized cultured cerebellar granule neurons (CGNs).
Assessed changes in CB1 receptor and monoacylglycerol lipase (MAGL) transcript expression following BDNF treatment.
Measured Akt phosphorylation as an indicator of neuronal sensitivity to 2-AG and noladin ether (NE).

Main Results:

BDNF treatment increased CB1 receptor transcripts and decreased MAGL transcripts in CGNs.
BDNF pre-treatment conferred a stable increase in neuronal sensitivity to eCBs, evidenced by enhanced Akt phosphorylation.
Akt phosphorylation occurred at lower NE concentrations in BDNF-treated neurons compared to controls.

Conclusions:

BDNF plays a critical role in determining neuronal sensitivity to endocannabinoids (eCBs).
BDNF upregulates CB1 receptors and downregulates MAGL, potentiating eCB signaling.
Findings suggest a BDNF-mediated positive feedback loop that may contribute to neuronal survival.