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Updated: Feb 2, 2026

Recording Gamma Band Oscillations in Pedunculopontine Nucleus Neurons
Published on: September 14, 2016
TrpV1 receptor activation rescues neuronal function and network gamma oscillations from Aβ-induced impairment in
Hugo Balleza-Tapia1, Sophie Crux1,2, Yuniesky Andrade-Talavera1
1Neuronal Oscillations Laboratory, Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Neurogeriatrics Division, Karolinska Institutet, Stockholm, Sweden.
Abstract:
Amyloid-β peptide (Aβ) forms plaques in Alzheimer's disease (AD) and is responsible for early cognitive deficits in AD patients. Advancing cognitive decline is accompanied by progressive impairment of cognition-relevant EEG patterns such as gamma oscillations. The endocannabinoid anandamide, a TrpV1-receptor agonist, reverses hippocampal damage and memory impairment in rodents and protects neurons from Aβ-induced cytotoxic effects. Here, we investigate a restorative role of TrpV1-receptor activation against Aβ-induced degradation of hippocampal neuron function and gamma oscillations. We found that the TrpV1-receptor agonist capsaicin rescues Aβ-induced degradation of hippocampal gamma oscillations by reversing both the desynchronization of AP firing in CA3 pyramidal cells and the shift in excitatory/inhibitory current balance. This rescue effect is TrpV1-receptor-dependent since it was absent in TrpV1 knockout mice or in the presence of the TrpV1-receptor antagonist capsazepine. Our findings provide novel insight into the network mechanisms underlying cognitive decline in AD and suggest TrpV1 activation as a novel therapeutic target.
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