scholarly journals Vagus nerve recordings: new opportunities to investigate autonomic function in humans

2020 ◽  
Vol 598 (17) ◽  
pp. 3543-3544
Author(s):  
Jeanie Park

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Karen-Anne McVey Neufeld ◽  
John Bienenstock ◽  
Aadil Bharwani ◽  
Kevin Champagne-Jorgensen ◽  
YuKang Mao ◽  
...  

Abstract The vagus nerve can transmit signals to the brain resulting in a reduction in depressive behavior as evidenced by the long-term beneficial effects of electrical stimulation of the vagus in patients with intractable depression. The vagus is the major neural connection between gut and brain, and we have previously shown that ingestion of beneficial bacteria modulates behaviour and brain neurochemistry via this pathway. Given the high levels of serotonin in the gut, we considered if gut-brain signaling, and specifically the vagal pathway, might contribute to the therapeutic effect of oral selective serotonin reuptake inhibitors (SSRI). Mesenteric nerve recordings were conducted in mice after treatment with SSRI to ascertain if this class of drugs resulted in increased vagal excitability. Patch clamp recordings of enteric neurons were carried out to measure activity of primary afferent neurons in the gut in response to SSRI and to assess the importance of gut epithelium in transducing signal. The tail suspension test (TST) was used following 14d feeding of SSRI in vagotomised and surgical sham mice to measure depressive-like behaviour. Brain mRNA expression was examined via PCR and the intestinal microbiome was assessed. Mesenteric nerve recordings in BALB/c mice demonstrated that oral treatment with SSRI leads to a significant increase in vagal activity. This effect was not observed in mice treated with a representative noradrenaline-dopamine reuptake inhibitor. It is known that signals from the gut can be transmitted to the vagus via the enteric nervous system. Exposure of the gut to SSRI increased the excitability of intrinsic primary afferent neurons in the myenteric plexus, through an intestinal epithelium dependent mechanism, and alpha-diversity of gut microbiota was altered. Critically, blocking vagal signaling from gut to brain, via subdiaphragmatic vagotomy, abolished the antidepressive effects of oral SSRI treatment as determined by the tail suspension test. This work suggests that vagus nerve dependent gut-brain signaling contributes to the effects of oral SSRI and further, highlights the potential for pharmacological approaches to treatment of mood disorders that focus on vagal stimulation and may not even require therapeutic agents to enter the circulation.



2020 ◽  
Vol 330 ◽  
pp. 108467 ◽  
Author(s):  
Todd J. Levy ◽  
Umair Ahmed ◽  
Tea Tsaava ◽  
Yao-Chuan Chang ◽  
Peter J. Lorraine ◽  
...  


Author(s):  
Bruce D. Nearing ◽  
Inderjit S. Anand ◽  
Imad Libbus ◽  
Lorenzo A. Dicarlo ◽  
Bruce H. Kenknight ◽  
...  


2019 ◽  
Author(s):  
Ahmad Jiman ◽  
Elissa Welle ◽  
Paras Patel ◽  
David Ratze ◽  
Elizabeth Bottorff ◽  
...  

The carbon fiber microelectrode array (CFMA) has demonstrated promising results in recording single-unti neural activity. This protocol is for obtaining CFMA recordings from the cervical vagus nerve of rats in response to the application of potassium chloride (KCl) on the vagus nerve.



2016 ◽  
Vol 13 (4) ◽  
pp. 041002 ◽  
Author(s):  
David Guiraud ◽  
David Andreu ◽  
Stéphane Bonnet ◽  
Guy Carrault ◽  
Pascal Couderc ◽  
...  


2020 ◽  
Vol 3 (Supplement_1) ◽  
pp. 141-142
Author(s):  
C West ◽  
A Stanisz ◽  
J Bienenstock ◽  
W A Kunze

Abstract Background Two thirds of vagal afferents supplying the small intestine terminate on intrinsic primary afferent neurons (IPANs) of the enteric nervous system via intraganglionic laminar endings (IGLEs) rather than the luminal epithelium (FASEB J, 28, 3064–3074, 2014). The IPAN to IGLE connection forms a functional intramural sensory synapse within the myenteric plexus. We have recently shown (Sci Rep, 9, 14290, 2019) that the antidepressant behavioural effects of selective serotonin reuptake inhibitors (SSRIs) are dependent on the vagus nerve and that intraluminal application of the SSRIs fluoxetine and sertraline increase vagal afferent firing rate in vitro. Aims We hypothesize that the vagal afferent response to intraluminal sertraline is mediated by IPAN to IGLE sensory signaling. Methods Mesenteric nerve recordings were performed using 2–3 cm jejunal segments and attached mesentery from 6–8 weeks old male Balb/c mice. Jejunal tissue was pinned out and dissected in a petri dish of Krebs to remove excess mesentery to isolate the mesenteric nerve bundle. Multi-unit electrical activity was recorded by patch-clamp electrode using an amplifier and signal converter by sucking onto the mesenteric nerve bundle with a glass micropipette. Baseline firing was recorded for 30 mins during luminal Krebs perfusion. The vagal afferent firing response to sertraline (10 µM) was measured in the absence or presence of 5 µM of the intermediate conductance calcium-dependent (IKCa) channel opener 5,6-dichloro-1-ethyl-1,3-dihydro-2H-benzimidazole-2-one (DCEBIO) to the serosa to selectively silence IPANs. Dataview software (J Neuroscience Methods, 185, 151, 2009) was used to isolate single unit firing post-hoc. Vagal fibre action potentials were identified by response to CCK. Results Intraluminal sertraline decreased the mean vagal interspike interval (increased vagal firing frequency) by 29% (p = 0.008) compared to Krebs control (N = 15 fibres). In contrast, addition of luminal sertraline in the presence of DCEBIO increased mean vagal interspike interval by 48% (p = 0.0103) compared to Krebs control (N = 12 fibres). Serosal addition of the N-type Ca2+ channel blocker w-Conotoxin GVIA simultaneously with luminal sertraline increased the mean vagal interspike interval by 12% (p = 0.0282) compared to Krebs control (N = 7 fibres). Conclusions Silencing of myenteric IPANs to vagus neurotransmission blocked excitatory response of vagal afferent fibres to intraluminal sertraline. Blocking myenteric neurotransmission reduced the vagus excitatory response to sertraline by more than 50%. These results suggest that the therapeutically necessary vagus nerve stimulation by sertraline involves activation of the myenteric intramural sensory synapse. Funding Agencies NSERC, OGS



Author(s):  
Yao-Chuan Chang ◽  
Umair Ahmed ◽  
Jacquelyn N. Tomaio ◽  
Loren Rieth ◽  
Timir Datta-Chaudhuri ◽  
...  


2019 ◽  
Vol 10 (1) ◽  
pp. 223-232 ◽  
Author(s):  
Victor Constantinescu ◽  
Daniela Matei ◽  
Irina Constantinescu ◽  
Dan Iulian Cuciureanu

Abstract Background Vagus nerve stimulation (VNS) exerts a cortical modulating effect through its diffuse projections, especially involving cerebral structures related to autonomic regulation. The influence of VNS on cardiovascular autonomic function in drug-resistant epilepsy patients is still debated. We aimed to evaluate the impact of VNS on cardiovascular autonomic function in drug-resistant epilepsy patients, after three months of neurostimulation, using the heart rate variability (HRV) analysis. Methodology Multiple Trigonometric Regressive Spectral analysis enables a precise assessment of the autonomic control on the heart rate. We evaluated time and frequency-domain HRV parameters in resting condition and during sympathetic and parasympathetic activation tests in five epilepsy patients who underwent VNS procedure. Results We found appropriate cardiac autonomic responses to sympathetic and parasympathetic activation tests, described by RMSSD, pNN50, HF and LF/HF dynamics after three months of VNS. ON period of the neurostimulation may generate a transient vagal activation reflected on heart rate and RMSSD values, as observed in one of our cases. Conclusion VNS therapy in epilepsy patients seems not to disrupt the cardiac autonomic function. HRV represents a useful tool in evaluating autonomic activity. More extensive studies are needed to further explore cardiac autonomic response after neurostimulation.



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