In past literature on animal models, invasive vagal nerve stimulation using high frequencies has shown to be effective at modulating the activity of the olfactory bulb (OB). Recent advances in invasive vagal nerve stimulation in humans, despite previous findings in animal models, used low frequency stimulation and found no effect on the olfactory functioning. The present article aimed to test potential effects of non-invasive, high and low frequency vagal nerve stimulation in humans, with supplementary exploration of the orbitofrontal cortex using near-infrared spectroscopy (NIRS). Healthy, male adult participants (n = 18) performed two olfactory tests [odor threshold test (OTT) and supra-threshold test (STT)] before and after receiving high-, low frequency vagal nerve stimulation and placebo (no stimulation). Participant's olfactory functioning was monitored using NIRS, and assessed with two behavioral olfactory tests. NIRS data of separate stimulation parameters were statistically analyzed using repeated-measures ANOVA across different stages. Data from olfactory tests were analyzed using paired parametric and non-parametric statistical tests. Only high frequency, non-invasive vagal nerve stimulation was able to positively modulate the performance of the healthy participants in the STT (p = 0.021, Wilcoxon sign-ranked test), with significant differences in NIRS (p = 0.014, post-hoc with Bonferroni correction) recordings of the right hemispheric, orbitofrontal cortex. The results from the current article implore further exploration of the neurocircuitry involved under vagal nerve stimulation and the effects of non-invasive, high frequency, vagal nerve stimulation toward olfactory dysfunction which showcase in Parkinson's and Alzheimer's Diseases. Despite the sufficient effect size (moderate effect, correlation coefficient (r): 0.39 for the STT) of the current study, future research should replicate the current findings with a larger cohort.
Median nerve stimulation (MNS) had been performed in the existing literature to alleviate symptoms of nausea and vomiting. The observed facilitative effects are thought to be mediated by the vagal pathways, particularly the vagus nerve (VN) brainstem nuclei of the dorsal motor nucleus of vagus and nucleus tractus solitarius (DMV-NTS). Sense of smell is one of the major sensory modalities for inducing vomiting and nausea as a primary defense against potentially harmful intake of material. This study aimed to test effects of non-invasive, high and low frequency MNS on human olfactory functioning, with supplementary exploration of the orbitofrontal cortex (OFC) using near-infrared spectroscopy (NIRS). Twenty healthy, male, adults performed supra-threshold odor intensity tests (labeled magnitude scale, LMS) for four food-related odorant samples (presented in three different concentrations) before and after receiving high-, low frequency MNS and placebo (no stimulation), while cortical activities in the OFC was monitored by the NIRS. Data of the NIRS and LMS test of separate stimulation parameters were statistically analyzed using mixed-model analysis of variance (ANOVA). Only the high frequency MNS showed effects for suppressing the intensity perception of the moderate concentration of Amyl Acetate (p:0.042) and strong concentration of Isovaleric Acid (p:0.004) and 1-Octen-3-ol (p:0.006). These behavioral changes were coupled with significant changes in the NIRS recordings of the left (p:0.000) and right (p:0.003) hemispheric orbitofrontal cortices. This is the first study that applied non-invasive, high frequency MNS to suppress the supra-threshold odor ratings of specific concentrations of odors. The vagal networks are potential relays of MNS to influence OFC. Results from the current article implore further research into non-invasive, high frequency MNS in the investigation of its modulatory effects on olfactory function, given its potential to be used for ameliorating nausea and malnutrition associated with various health conditions.
Maternal immune activation (MIA) during gestation is a significant risk factor for development of schizophrenia and other neurodevelopmental diseases. In animal models of this risk factor, MIA during pregnancy can produce offspring that recapitulate certain aspects of the behavioral and neurophysiological impairments seen in schizophrenia. Here, the authors tested the effect of polyinosinic-polycytidylic acid (poly I:C)-induced MIA in a task that explicitly assays the interaction between motivation and cognition. In our paradigm, discrimination accuracy during a sustained-attention task is differentially impacted by environmental cues that signal the probability of reward for accurate performance. Cognition-motivation interactions are implicated in producing functional impairments in patients. Therefore, to the extent that this MIA model recapitulates such impairments, the authors predicted impaired ability of reward-associated signals to modulate cognitive performance in MIA rat offpsring. Adult offspring of dams in which MIA was induced displayed impaired prepulse inhibition relative to controls, verifying a functional effect of poly I:C induction. Despite this deficit, there were no differences between MIA and control rats in any aspects of task learning or performance, including under extinction and reacquisition conditions. These results indicate that MIA spares functioning of some of the cognitive, motivational, and decision-making processes that are impacted in schizophrenia and suggest that MIA as an isolated manipulation does not model the full range and nuance of the cognitive and motivational impairments in the disease. The authors suggest that some aspects of the functional impairment in schizophrenia and other neurodevelopmental diseases may be better modeled using multiple "hit" models of disease risk. (PsycINFO Database Record
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