Abstract
BackgroundThe afferent projections from the auricular branch of the vagus nerve (ABVN) to the nucleus tractus solitaries (NTS) have been proposed as the anatomical basis for the increased parasympathetic tone seen in auriculo-vagal reflexes. As the afferent center of the vagus nerve, the NTS has been considered to play roles in the anticonvulsant effect of cervical vagus nerve stimulation (VNS). Here we proposed an “auriculo-vagal afferent pathway” (AVAP), by which transcutaneous auricular vagus nerve stimulation (ta-VNS) suppresses pentylenetetrazol (PTZ)-induced epileptic seizures by activating the NTS neurons in rats.ResultsThe afferent projections from the ABVN to the NTS were firstly observed in rats. ta-VNS increased the first grand mal latency of the epileptic seizure and decreased the seizure scores in awake rats. Furthermore, when the firing rates of the NTS neurons decreased, epileptiform activity manifested as electroencephalogram (EEG) synchronization increased with 0.37±0.12 s delay in anaesthetized rats. The change of instantaneous frequency, mean frequency of the NTS neurons was negative correlated with the amplitude of the epileptic activity in EEG traces. ta-VNS significantly suppressed epileptiform activity in EEG traces via increasing the firing rates of the neurons of the NTS. In comparison with tan-VNS, the anticonvulsant durations of VNS and ta-VNS were significantly longer (P<0.01). There was no significant difference between the anticonvulsant durations of VNS and ta-VNS (P>0.05). The anticonvulsant effect of ta-VNS was weakened by reversible cold block of the NTS.ConclusionsThere existed an anatomical relationship between the ABVN and the NTS, which strongly supports the concept that ta-VNS has the potential for suppressing epileptiform activity via the AVAP in rats. ta-VNS will provide alternative treatments for neurological disorders, which can avoid the disadvantage of VNS.
Highlights
The afferent projections from the auricular branch of the vagus nerve (ABVN) to the nucleus tractus solitaries (NTS) have been proposed as the anatomical basis for the increased parasympathetic tone seen in auriculo-vagal reflexes
Five different animal experiments were performed in the present study, including (1) afferent projections of the ABVN in rats by using cholera toxin subunit B (CTB) tracing technique, (2) transcutaneous auricular vagus nerve stimulation (ta-VNS) on t seizures in awake rats, (3) ta-VNS on electroencephalography (EEG) and the firing of the NTS neurons in anaesthetized rats, (4) ta-VNS on the field potentials (FPs) of the primary somatosensory in anaesthetized rats, and (5) the effect of reversible cooling the NTS neurons on epileptiform activity in EEG traces in anaesthetized rats. ta-VNS, transcutaneous auricular non-vagus nerve stimulation, or vagus nerve stimulation (VNS) were performed in experiment (2) – (5) as needed to observe the anticonvulsant efficacy of the ta-VNS
Afferent projections from the auricular concha to the NTS were demonstrated in the rats Under the fluorescent microscope, CTB-labeled terminals appeared in green fluorescent granules and were located ipsilaterally on the injection side
Summary
The afferent projections from the auricular branch of the vagus nerve (ABVN) to the nucleus tractus solitaries (NTS) have been proposed as the anatomical basis for the increased parasympathetic tone seen in auriculo-vagal reflexes. As the afferent center of the vagus nerve, the NTS has been considered to play roles in the anticonvulsant effect of cervical vagus nerve stimulation (VNS). The NTS plays important roles in autonomic regulations, and receives extensive projections from other brain structures. Both the autonomic system and Epilepsy is a disorder of the brain characterized by an enduring predisposition to generate epileptic seizures and by the neurobiologic, cognitive, psychological, and social consequences of this condition. The antiseizure effect of VNS is considered to be mediated via vagal afferent projections to the NTS, via pathways from the NTS to other brain structures which correlate with the pathogenesis of epilepsy, with a result to electroencephalogram (EEG) desynchronization [10]
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