The Effects of Peripheral Vagal Nerve Stimulation at a Memory-Modulating Intensity on Norepinephrine Output in the Basolateral Amygdala.

Abstract

Vagal nerve stimulation (VNS) is known to improve cognitive processing, presumably by affecting activity in central nervous system structures that process recently acquired information. It has long been assumed that these effects are related to stimulation-induced increases of norepinephrine (NE) release in limbic brain structures. The present study examined this hypothesis by administering VNS at an intensity and duration that improves memory and then measuring fluctuations in NE output in the basolateral amygdala (BLA) with in vivo microdialysis. In Experiment 1, VNS caused a 98% increase in NE output relative to baseline. In Experiment 2, methyl atropine was given 10 min before VNS to assess whether stimulation-induced increases in amygdala NE are mediated by afferent or efferent vagal branches. Methyl atropine did not alter NE release in the BLA in comparison with saline. The significance of these findings in understanding how peripheral neural activity modulates limbic structures to encode and store new information into memory is discussed.

The P3 Event-Related Potential is a Biomarker for the Efficacy of Vagus Nerve Stimulation in Patients with Epilepsy

“…In addition, the basal firing rate in the LC is significantly increased after long-term treatment with VNS [46]. In rats, VNS induces an increase of NE concentration in the hippocampus [47], the amygdala [48], and the cerebral cortex [47,49]. Moreover, lesions of the LC block the anticonvulsant effect of VNS [50].…”

Gutsy Moves: The Amygdala as a Critical Node in Microbiota to Brain Signaling

“…[61] Thus, visceral information collected by the vagus nerve may ultimately influence amygdala activity. Indeed, vagus nerve stimulation has been shown to stimulate the release of norepinephrine in the amygdala [63] and to modulate amygdala-prefrontal cortex connectivity while enhancing behavioral outcomes (i.e., reduced fear/depressive symptoms) in both preclinical models of fear extinction [64] and clinical investigations of major depressive disorder. [65] Conversely, disruption of vagal communication by subdiaphragmatic deafferentation of the vagus nerve has been shown to impair fear extinction but reduce anxiety-like behavior in rats.…”

Advances in the treatment of depression

“…However, the central projections of the vagus nerve via the nucleus tractus solitarius innervate multiple brain areas implicated in mood regulation, and functional brain imaging studies have confirmed that VNS alters activity of many of these cortical and subcortical regions. 133 VNS may affect function of the GABA, 134,135 dopamine 136 and especially norepinephrine [137][138][139][140] systems, although these data are not unequivocal. 136 Importantly, effects on these neurotransmitter systems, when present, have not consistently been associated with therapeutic response.…”