Impact of Transcutaneous Auricular Vagus Nerve Stimulation on Spatial Learning and Memory in Acrolein-Induced Alzheimer's Disease-Like Hippocampal Neuronal Damage in Wistar Rats.

BACKGROUND

Data about the utility of vagus nerve stimulation (VNS) as a potential therapy for neurodegenerative disorders are still inconclusive. We used a rat model of acrolein-induced hippocampal neurodegeneration to investigate the effect of VNS on spatial learning and memory.

METHODS

A total of 24 Wistar rats were randomly allocated to one of the four groups: no acrolein exposure (n = 6), control (n = 6), sham (n = 6), and experimental (n = 6). The control, sham, and experimental groups were exposed to acrolein 2.5 mg/kg/day by gastric gavage for eight weeks. After acrolein exposure, the experimental and sham groups received transcutaneous auricular VNS and greater auricular nerve stimulation, respectively, under 2% isoflurane anesthesia for four weeks. Then, all animal groups were assessed for spatial learning and memory in a Morris water maze before being euthanized for hippocampus histological examination.

RESULTS

The mean time to find the hidden platform varied significantly between the no acrolein exposure group and each of the acrolein-exposed groups. The results of one-way ANOVA indicated a significant difference in the average swimming time between the four study groups (F = 14.64, p < 0.001). Results from the post-hoc analysis indicated that the mean difference was statistically significant between the "no acrolein exposure" and "control" groups (p < 0.001), the "no acrolein exposure" and "experimental" groups (p = 0.001), and between the "control" and "sham" groups (p< 0.001). There was no statistically significant difference in swimming time to find the hidden escape platform between the sham and experimental groups (p = 0.060).

CONCLUSION

Transcutaneous auricular VNS has no significant effect on spatial learning or memory in Wistar rats with acrolein-induced hippocampus neuronal damage, indicating the need to review the long-standing notion that hippocampal neuronal loss causes spatial navigation deficits.