scholarly journals In vivo relationship between thalamic nicotinic acetylcholine receptor occupancy rates and antiallodynic effects in a rat model of neuropathic pain: Persistent agonist binding inhibits the expression of antiallodynic effects

Synapse ◽  
2010 ◽  
Vol 65 (1) ◽  
pp. 77-83 ◽  
Author(s):  
Masashi Ueda ◽  
Yasuhiko Iida ◽  
Tomoki Yoneyama ◽  
Tomoki Kawai ◽  
Mikako Ogawa ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Acetylcholine Receptor ◽  
Nicotinic Acetylcholine Receptor ◽  
Rat Model ◽  
Receptor Occupancy ◽  
Agonist Binding ◽  
Nicotinic Acetylcholine ◽  
Occupancy Rates

scholarly journals Influence of neuropathic pain on nicotinic acetylcholine receptor plasticity and behavioral responses to nicotine in rats

Pain ◽  
2018 ◽  
Vol 159 (11) ◽  
pp. 2179-2191 ◽  
Author(s):  
Gloria Brunori ◽  
Jennifer Schoch ◽  
Daniela Mercatelli ◽  
Akihiko Ozawa ◽  
Lawrence Toll ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Acetylcholine Receptor ◽  
Nicotinic Acetylcholine Receptor ◽  
Behavioral Responses ◽  
Nicotinic Acetylcholine ◽  
Receptor Plasticity

Light-Induced Calcium Influx Into Retinal Axons Is Regulated by Presynaptic Nicotinic Acetylcholine Receptor Activity In Vivo

1999 ◽  
Vol 81 (2) ◽  
pp. 895-907 ◽  
Author(s):  
James A. Edwards ◽  
Hollis T. Cline
Keyword(s):  
Acetylcholine Receptor ◽  
Nicotinic Acetylcholine Receptor ◽  
Visual Stimulus ◽  
Optic Tectum ◽  
Visual Stimulation ◽  
Calcium Influx ◽  
Nicotinic Acetylcholine ◽  
Retinal Axons ◽  
Retinotectal System

Light-induced calcium influx into retinal axons is regulated by presynaptic nicotinic acetylcholine receptor activity in vivo. Visual activity is thought to be a critical factor in controlling the development of central retinal projections. Neuronal activity increases cytosolic calcium, which was hypothesized to regulate process outgrowth in neurons. We performed an in vivo imaging study in the retinotectal system of albino Xenopus laevis tadpoles with the fluorescent calcium indicator calcium green 1 dextran (CaGD) to test the role of calcium in regulating axon arbor development. We find that visual stimulus to the retina increased CaGD fluorescence intensity in retinal ganglion cell (RGC) axon arbors within the optic tectum and that branch additions to retinotectal axon arbors correlated with a local rise in calcium in the parent branch. We find three types of responses to visual stimulus, which roughly correlate with theon, off, and sustained response types of RGC reported by physiological criteria. Imaging in bandscan mode indicated that patterns of calcium transients were nonuniform throughout the axons. We tested whether the increase in calcium in the retinotectal axons required synaptic activity in the retina; intraocular application of tetrodotoxin (10 μM) or nifedipine (1 and 10 μM) blocked the stimulus-induced increase in RGC axonal fluorescence. A second series of pharmacological investigations was designed to determine the mechanism of the calcium elevation in the axon terminals within the optic tectum. Injection of bis-( o-aminophenoxy)- N, N, N′, N′-tetraacetic acid-AM (BAPTA-AM) (20 mM) into the tectal ventricle reduced axonal calcium levels, supporting the idea that visual stimulation increases axonal calcium. Injection of BAPTA (20 mM) into the tectal ventricle to chelate extracellular calcium also attenuated the calcium response to visual stimulation, indicating that calcium enters the axon from the extracellular medium. Caffeine (10 mM) caused a large increase in axonal calcium, indicating that intracellular stores contribute to the calcium signal. Presynaptic nicotinic acetylcholine receptors (nAChRs) may play a role in axon arbor development and the formation of the topographic retinotectal projection. Injection of nicotine (10 μM) into the tectal ventricle significantly elevated RGC axonal calcium levels, whereas application of the nAChR antagonist αBTX (100 nM) reduced the stimulus-evoked rise in RGC calcium fluorescence. These data suggest that light stimulus to the retina increases calcium in the axon terminal arbors through a mechanism that includes influx through nAChRs and amplification by calcium-induced calcium release from intracellular calcium stores. Such a mechanism may contribute to developmental plasticity of the retinotectal system by influencing both axon arbor elaboration and the strength of synaptic transmission.

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