Nicotinic acetylcholine receptors (nAChRs) are expressed in Trpm5 positive taste receptor cells (TRCs)

  title={Nicotinic acetylcholine receptors (nAChRs) are expressed in Trpm5 positive taste receptor cells (TRCs)},
  author={Jie Qian and Shobha Mummalaneni and John R. Grider and Mohamad Imad Damaj and Vijay Lyall},
  journal={PLoS ONE},
Nicotine evokes chorda tympani (CT) taste nerve responses and an aversive behavior in Trpm5 knockout (KO) mice. The agonists and antagonists of nicotinic acetylcholine receptors (nAChRs) modulate neural and behavioral responses to nicotine in wildtype (WT) mice, Trpm5 KO mice and rats. This indicates that nicotine evokes bitter taste by activating a Trpm5-dependent pathway and a Trpm5-independent but nAChR-dependent pathway. Rat CT responses to ethanol are also partially inhibited by nAChR… 
Nicotinic acetylcholine receptor (CHRN) expression and function in cultured human adult fungiform (HBO) taste cells
It is demonstrated that a subset of HBO cells express CHRNs that also co-express TRPM5, T1R3 or T2R38, and it is concluded that CHRNs are expressed inTRPM5 positive HBO cells.
β4-Nicotinic Receptors Are Critically Involved in Reward-Related Behaviors and Self-Regulation of Nicotine Reinforcement
It is shown that the lack of functional β4*nAChRs result in deficits in reward sensitivity including increased ICSA at high doses of nicotine that is restored by re-expression of β4-nAchRs in the MHb-IPN pathway, which indicates that β4 is a critical modulator of reward-related behaviors.
Distribution of α7 Nicotinic Acetylcholine Receptor Subunit mRNA in the Developing Mouse
The results suggest that prenatal nicotine exposure could potentially affect the nervous system with limited effects in non-neural tissues.
Morphology and chemical characteristics of taste buds associated with P2X3‐immunoreactive afferent nerve endings in the rat incisive papilla
The results suggest that incisive taste buds are morphologically and cellularly homologous to lingual taste buds and are innervated by P2X3‐immunoreactive nerve endings derived from the GG.
Stimulation of brain nicotinic acetylcholine receptors activates adrenomedullary outflow via brain inducible NO synthase‐mediated S‐nitrosylation
Central mechanisms for the (±)‐epibatidine‐induced responses are examined, focusing on brain NOS and NO‐mediated mechanisms, soluble GC (sGC) and protein S‐nitrosylation (a posttranslational modification of protein cysteine thiol groups), in urethane‐anaesthetized male Wistar rats.
Interactions between Chemesthesis and Taste: Role of TRPA1 and TRPV1
The effect of some chemesthetic agonists of TRPA1 and TRPV1 and their influence on bitter, sour, and salt taste qualities are reviewed.
The Effect of Swimming Endurance Exercise on Cell Death and Nicotinic Acetylcholine Receptor Gene Expression in Brain of Rat: An Experimental Study of Alzheimer's Disease Model
Exercise is probably useful for prevention of cell death and reduced α7nAChR gene expression rate in Alzheimer’s rat and the percentage of Alzheimer's-induced cell death (p<0.05).


Nicotinic Acetylcholine Receptor (nAChR) Dependent Chorda Tympani Taste Nerve Responses to Nicotine, Ethanol and Acetylcholine
It is concluded that nAChRs expressed in a subset of taste cells serve as common receptors for the detection of the TRPM5-independent bitter taste of nicotine, acetylcholine and ethanol.
Nicotine-Induced Effects on Nicotinic Acetylcholine Receptors (nAChRs), Ca2+ and Brain-Derived Neurotrophic Factor (BDNF) in STC-1 Cells
It is concluded that STC-1 cells and intestinal enteroendocrine cells express nAChRs, which is modulated by exposure to nicotine in a dose- and time-dependent manner.
Nicotine activates TRPM5-dependent and independent taste pathways
Whether nicotine activates peripheral and central taste pathways via TRPM5-dependent mechanisms, which are essential for responses to other bitter tastants such as quinine, and/or via nicotinic acetylcholine receptors (nAChRs), is investigated to create a unique sensory representation that contributes to the sensory experience of tobacco products.
Mouse taste cells with G protein-coupled taste receptors lack voltage-gated calcium channels and SNAP-25
The taste receptor cells responsible for the transduction of bitter, sweet, and umami stimuli are unlikely to communicate with nerve fibers by using conventional chemicalSynaptic signaling mechanisms are expressed in separate populations of taste cells.
Partial Agonists of the α3β4* Neuronal Nicotinic Acetylcholine Receptor Reduce Ethanol Consumption and Seeking in Rats
It is shown that the functional potencies of CP-601932 and PF-4575180 at α3β4 nAChRs correlate with their unbound rat brain concentrations, suggesting that the effects on ethanol self-administration are mediated via interaction with α3 β4 n AChRs.
Differential effects of bitter compounds on the taste transduction channels TRPM5 and IP3 receptor type 3.
It is found that nicotine inhibits TRPM5 currents with an effective inhibitory concentration of ~1.3mM at -50 mV, implying the existence of a TR PM5-independent pathway for the detection of nicotine bitterness.
The Novel α7β2-Nicotinic Acetylcholine Receptor Subtype Is Expressed in Mouse and Human Basal Forebrain: Biochemical and Pharmacological Characterization
This study represents the first direct confirmation of α7β2-nAChR expression in human and mouse forebrain, supporting previous mouse studies that suggested relevance of β2 subunit–specific α7α7/α7 subunit interface sites in Alzheimer disease etiopathogenesis.
Nicotinic acetylcholine receptor expression in human airway correlates with lung function.
  • D. Lam, S. Luo, J. Minna
  • Biology, Medicine
    American journal of physiology. Lung cellular and molecular physiology
  • 2016
NAChR expression in bronchial epithelium was found to correlate with lung function and insight was given into the potential of targeting nAChRs for therapy in smoking-related inflammation in the airway.
Modulation of nicotinic receptor channels by adrenergic stimulation in rat pinealocytes.
Results suggest that NE released from sympathetic terminals at night attenuates nicotinic cholinergic signaling, and removal of ATP from the intracellular pipette solution blocked the reduction of nAChR currents, suggesting involvement of protein kinases.