Optogenetic activation of mouse airway parasympathetic neurons to provoke bronchoconstriction

2019 ◽  
Author(s):  
Alexandra Pincus ◽  
Allison Fryer ◽  
David Jacoby
Keyword(s):  
Parasympathetic Neurons

Co-culture of Parasympathetic Neurons and Cardiomyocyte

2015 ◽  
Vol 135 (7) ◽  
pp. 813-818 ◽  
Author(s):  
Kosuke Oiwa ◽  
Kenta Shimba ◽  
Takashi Numata ◽  
Akimasa Takeuchi ◽  
Kiyoshi Kotani ◽  
...  
Keyword(s):  
Parasympathetic Neurons

TRPC1, TRPC3, and TRPC4 in Rat Orofacial Structures

2017 ◽  
Vol 204 (5-6) ◽  
pp. 293-303 ◽  
Author(s):  
Masatoshi Fujita ◽  
Tadasu Sato ◽  
Takehiro Yajima ◽  
Eiji Masaki ◽  
Hiroyuki Ichikawa
Keyword(s):  
Transient Receptor Potential ◽  
Sympathetic Neurons ◽  
Receptor Potential ◽  
Monovalent Cation ◽  
Calcitonin Gene ◽  
Cervical Ganglion ◽  
Parasympathetic Neurons ◽  
Transient Receptor ◽  
And Function ◽  
And Control

TRPC (transient receptor potential cation channel subfamily C) members are nonselective monovalent cation channels and control Ca2+ inflow. In this study, immunohistochemistry for TRPC1, TRPC3, and TRPC4 was performed on rat oral and craniofacial structures to elucidate their distribution and function in the peripheries. In the trigeminal ganglion (TG), 56.1, 84.1, and 68.3% of sensory neurons were immunoreactive (IR) for TRPC1, TRPC3, and TRPC4, respectively. A double immunofluorescence method revealed that small to medium-sized TG neurons co-expressed TRPCs and calcitonin gene-related peptide. In the superior cervical ganglion, all sympathetic neurons showed TRPC1 and TRPC3 immunoreactivity. Parasympathetic neurons in the submandibular ganglion, tongue, and parotid gland were TRPC1, TRPC3, and TRPC4 IR. Gustatory and olfactory cells were also IR for TRPC1, TRPC3, and/or TRPC4. In the musculature, motor endplates expressed TRPC1 and TRPC4 immunoreactivity. It is likely that TRPCs are associated with sensory, autonomic, and motor functions in oral and craniofacial structures.

Localization of sympathetic and parasympathetic neurons innervating pancreas and spleen in the cat

1996 ◽  
Vol 59 (1-2) ◽  
pp. 12-16 ◽  
Author(s):  
Xiao Hua Chen ◽  
Masahiro Itoh ◽  
Wei Sun ◽  
Takanori Miki ◽  
Yoshiki Takeuchi
Keyword(s):  
Parasympathetic Neurons

Endogenous Acetylcholine and Nicotine Activation Enhances GABAergic and Glycinergic Inputs to Cardiac Vagal Neurons

2003 ◽  
Vol 89 (5) ◽  
pp. 2473-2481 ◽  
Author(s):  
Jijiang Wang ◽  
Xin Wang ◽  
Mustapha Irnaten ◽  
Priya Venkatesan ◽  
Cory Evans ◽  
...  
Keyword(s):  
Nicotinic Receptors ◽  
Nucleus Ambiguus ◽  
Cholinergic Activity ◽  
Fluorescent Tracer ◽  
Sinus Arrhythmia ◽  
Synaptic Inputs ◽  
Cardiorespiratory Interaction ◽  
Parasympathetic Neurons ◽  
Glycinergic Neurotransmission

The heart slows during expiration and heart rate increases during inspiration. This cardiorespiratory interaction is thought to occur by increased inhibitory synaptic events to cardiac vagal neurons during inspiration. Since cholinergic receptors have been suggested to be involved in this cardiorespiratory interaction, we tested whether endogenous cholinergic activity modulates GABAergic and glycinergic neurotransmission to cardiac vagal neurons in the nucleus ambiguus, whether nicotine can mimic this facilitation, and we examined the nicotinic receptors involved. Cardiac vagal neurons in the rat were labeled with a retrograde fluorescent tracer and studied in an in vitro slice using patch-clamp techniques. Application of neostigmine (10 μM), an acetylcholinerase inhibitor, significantly increased the frequency of both GABAergic and glycinergic inhibitory postsynaptic currents (IPSCs) in cardiac vagal neurons. Exogenous application of nicotine increased the frequency and amplitude of both GABAergic and glycinergic IPSCs. The nicotinic facilitation of both GABAergic and glycinergic IPSCs were insensitive to 100 nM α-bungarotoxin but were abolished by dihydro-β-erythrodine (DHβE) at a concentration (3 μM) specific for α4β2 nicotinic receptors. In the presence of TTX, nicotine increased the frequency of GABAergic and glycinergic miniature synaptic events, which were also abolished by DHβE (3 μM). This work demonstrates that there is endogenous cholinergic facilitation of GABAergic and glycinergic synaptic inputs to cardiac vagal neurons, and activation of α4β2 nicotinic receptors at presynaptic terminals facilitates GABAergic and glycinergic neurotransmission to cardiac vagal neurons. Nicotinic facilitation of inhibitory neurotransmission to premotor cardiac parasympathetic neurons may be involved in generating respiratory sinus arrhythmia.

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