Abstract
BackgroundElectrical vagal nerve stimulation (VNS) has been used for years to treat patients with drug-resistant epilepsy. This technique also remains under investigation as a specific treatment of patients with Alzheimer’s disease. Recently we discovered that VNS induced hippocampal formation (HPC) type II theta rhythm, which is involved in memory consolidation. In the present study, we have extended our previous observation and addressed the neuronal substrate and pharmacological profile of HPC type II theta rhythm induced by VNS in anesthetized rats.MethodsMale Wistar rats were implanted with a VNS cuff electrode around the left vagus nerve, a tungsten microelectrode for recording the HPC field activity, and a medial septal (MS) cannula for the injection of a local anesthetic, procaine, and muscarinic agents. A direct, brief effect of VNS on the HPC field potential was evaluated before and after medial-septal drug injection.ResultsMedial septal injection of local anesthetic, procaine, reversibly abolished VNS-induced HPC theta rhythm. With the use of cholinergic muscarinic agonist and antagonists, we demonstrated that medial septal M1 receptors are involved in the mediation of the VNS effect on HPC theta field potential.ConclusionThe MS cholinergic M1 receptor mechanism integrates not only central inputs from the brainstem synchronizing pathway, which underlies the production of HPC type II theta rhythm, but also the input from the vagal afferents in the brain stem.
Highlights
Electrical vagal nerve stimulation (VNS) has been used for years to treat patients with drugresistant epilepsy [1,2,3,4,5]
With the use of cholinergic muscarinic agonist and antagonists, we demonstrated that medial septal M1 receptors are involved in the mediation of the VNS effect on hippocampal formation (HPC) theta field potential
The medial septal (MS) cholinergic M1 receptor mechanism integrates central inputs from the brainstem synchronizing pathway, which underlies the production of HPC type II theta rhythm, and the input from the vagal afferents in the brain stem
Summary
Electrical vagal nerve stimulation (VNS) has been used for years to treat patients with drugresistant epilepsy [1,2,3,4,5]. The latter findings suggest that VNS may affect memory by enhancing neural plasticity in brain structures associated with memory storage, such as the HPC This memory processing is related to an increase in the excitation of the hippocampal neuronal network and the presence of a local theta rhythm [24,25,26,27,28,29]. In agreement with this suggestion, Broncel et al [30], using several experimental protocols, have recently demonstrated that VNS induced the HPC theta rhythm in anesthetized rats. We have extended our previous observation and addressed the neuronal substrate and pharmacological profile of HPC type II theta rhythm induced by VNS in anesthetized rats
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