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25 results for “Nicotinic acetylcholine receptor”
Data from: Positive allosteric modulation of the α7 nicotinic acetylcholine receptor as a treatment for cognitive deficits after traumatic brain injury
<p><span>Cognitive impairments are a common consequence of traumatic brain injury (TBI). The hippocampus is a subcortical structure that plays a key role in the formation of declarative memories and is highly vulnerable to TBI. The α7 nicotinic acetylcholine receptor (nAChR) is highly expressed in the hippocampus and reduced expression and function of this receptor are linked with cognitive impairments in Alzheimer's disease and schizophrenia. Positive allosteric modulation of α7 nAChRs with AVL-3288 enhances receptor currents and improves cognitive functioning in naïve animals and healthy human subjects. Therefore, we hypothesized that targeting the α7 nAChR with the positive allosteric modulator AVL-3288 would enhance cognitive functioning in the chronic recovery period of TBI. To test this hypothesis, adult male Sprague Dawley rats received moderate parasagittal fluid-percussion brain injury or sham surgery. At 3 months after recovery, animals were treated with vehicle or AVL-3288 at 30 min prior to cue and contextual fear conditioning and the water maze task. Treatment of TBI animals with AVL-3288 rescued learning and memory deficits in water maze retention and working memory. AVL-3288 treatment also improved cue and contextual fear memory when tested at 24 hr and 1 month after training, when TBI animals were treated acutely just during fear conditioning at 3 months post-TBI. Hippocampal atrophy but not cortical atrophy was reduced with AVL-3288 treatment in the chronic recovery phase of TBI. AVL-3288 application to acute hippocampal slices from animals at 3 months after TBI rescued basal synaptic transmission deficits and long-term potentiation (LTP) in area CA1. Our results demonstrate that AVL-3288 improves hippocampal synaptic plasticity, and learning and memory performance after TBI in the chronic recovery period. Enhancing cholinergic transmission through positive allosteric modulation of the α7 nAChR may be a novel therapeutic to improve cognition after TBI.</span></p>
Data from: Positive allosteric modulation of the α7 nicotinic acetylcholine receptor as a treatment for cognitive deficits after traumatic brain injury
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Fig. 4 in An electrophysiological characterization of naturally occurring tobacco alkaloids and their action on human α4β2 and α7 nicotinic acetylcholine receptors
Fig. 4. Concentration–response curves were obtained by using the whole-cell mode of the patch-clamp technique at a holding potential of −70 mV from CHO cells stably expressing human α4β2 (continuous black lines) or human α7 (dotted grey lines) nAChRs. The lines represent the fits to the Hill equation for nicotine (1) (circles symbols), anabasine (12) (triangles symbols), nornicotine (7) (squared symbols), and S-anatabine (16) (diamonds symbols). The fit parameters are presented (Table 1). The averaged normalized current response is plotted as a function of the maximal current to ACh (ImaxACh). Two backgrounds highlight the concentration range of the tobacco alkaloids levels measured in human plasma (grey background with diagonal lines) and in human cerebrospinal fluid (grey background with horizontal lines). Data are presented as mean ± SD.
Fig. 3 in An electrophysiological characterization of naturally occurring tobacco alkaloids and their action on human α4β2 and α7 nicotinic acetylcholine receptors
Fig. 3. Sequential applications of brief ACh pulses are plotted as a function of time for three ACh concentrations. (a) EC20 = 0.4 μM (circles), EC50 = 1.2 μM (squares), EC90 = 11.1 μM (triangles) for human α4β2 receptors. (b) EC20 = 33.3 μM (circles), EC60 = 300 μM (squares), EC90 = 900 μM (triangles) for human α7 receptors. Experiments were performed by using the whole-cell mode of the patch-clamp technique at a holding potential of −70 mV in CHO cells stably expressing the human α4β2 and α7 nAChRs. EC, effective concentration. Data are presented as mean ± SD.
Fig. 2 in An electrophysiological characterization of naturally occurring tobacco alkaloids and their action on human α4β2 and α7 nicotinic acetylcholine receptors
Fig. 2. Representative traces of currents elicited by using the agonist mode (a and c) and PAM mode (b and d) in the whole-cell mode of the patch-clamp technique at a holding potential of −70 mV in CHO cells stably expressing human α4β2 (a and b) and human α7 (c and d) nAChRs. Agonist mode (a, c): 0.3% DMSO (left); 33.3 μM of the tobacco alkaloid anabasine (middle); 33.3 and 900 μM ACh for α4β2 and α7, respectively (right). PAM mode (b, d): 0.4 and 100 μM ACh for α4β2 and α7, respectively (left); co-application of 33.3 μM of the tobacco alkaloid trans-anatalline (middle); 0.4 or 100 μM ACh for α4β2 and α7, respectively (right). Thick dotted lines represent the pre-application period of the alkaloid (≥2 min). Thin dotted lines represent zero current.; PAM, positive allosteric modulator.
Fig. 1 in An electrophysiological characterization of naturally occurring tobacco alkaloids and their action on human α4β2 and α7 nicotinic acetylcholine receptors
Fig. 1. Representative traces of currents elicited in response to increasing concentrations of ACh. Currents were measured in agonist mode by using the whole-cell mode of the patch-clamp technique at a holding potential of −70 mV in CHO cells stably expressing human α4β2 (a) and human α7 (b) nAChRs. The half-maximal effective concentrations determined by using the Hill equation were 1.02 ± 1.0 μM (a) and 142 ± 16 μM (b) (n = 5–11 cells). Bars indicate (in μM): 0.1 (1), 0.4 (2), 1.2 (3), 3.7 (4), 11.1 (5), 33.3 (6), 100 (7), 300 (8), 900 (9), and 2700 (10). Dotted lines represent zero current.
PET Imaging of Nicotinic Acetylcholine Receptors
ClinicalTrials.gov study NCT01046513. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Data from: Evolution of vertebrate nicotinic acetylcholine receptors
Background: Many physiological processes are influenced by nicotinic acetylcholine receptors (nAChR), ranging from neuromuscular and parasympathetic signaling to modulation of the reward system and long-term memory. Due to the complexity of the nAChR family and variable evolutionary rates among its members, their evolution in vertebrates has been difficult to resolve. In order to understand how and when the nAChR genes arose, we have used a broad approach of analyses combining sequence-based phylogeny, chromosomal synteny and intron positions. Results: Our analyses suggest that there were ten subunit genes present in the vertebrate predecessor. The two basal vertebrate tetraploidizations (1R and 2R) then expanded this set to 19 genes. Three of these have been lost in mammals, resulting in 16 members today. None of the ten ancestral genes have kept all four copies after 2R. Following 2R, two of the ancestral genes became triplicates, five of them became pairs, and three seem to have remained single genes. One triplet consists of CHRNA7, CHRNA8 and the previously undescribed CHRNA11, of which the two latter have been lost in mammals but are still present in lizards and ray-finned fishes. The other triplet consists of CHRNB2, CHRNB4 and CHRNB5, the latter of which has also been lost in mammals. In ray-finned fish the neuromuscular subunit gene CHRNB1 underwent a local gene duplication generating CHRNB1.2. The third tetraploidization in the predecessor of teleosts (3R) expanded the repertoire to a total of 31 genes, of which 27 remain in zebrafish. These evolutionary relationships are supported by the exon-intron organization of the genes. Conclusions: The tetraploidizations explain all gene duplication events in vertebrates except two. This indicates that the genome doublings have had a substantial impact on the complexity of this gene family leading to a very large number of members that have existed for hundreds of millions of years.
Acetylcholine, Tobacco Smoking, Genes and Nicotinic Receptors
ClinicalTrials.gov study NCT02008292. IPD Sharing: NO. Countries: 1. Publications: 0.
Data from: Evolution of vertebrate nicotinic acetylcholine receptors
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Positive allosteric modulation of the α7 nicotinic acetylcholine receptor as a treatment for cognitive deficits after traumatic brain injury
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RNA sequencing data describing transcriptional changes in aorta of ApoE-/- mice after alpha 7 nicotinic acetylcholine receptor (α7nAChR) stimulation.
GEO Series GSE131162. Mus musculus. 12 samples. Type: Expression profiling by high throughput sequencing.
Alpha7 Nicotinic Acetylcholine Receptor Mediates Chronic Nicotine Inhalation-Induced Cardiopulmonary Dysfunction
GEO Series GSE196184. Mus musculus. 12 samples. Type: Expression profiling by high throughput sequencing.
α7 nicotinic acetylcholine receptor signaling modulates the inflammatory phenotype of fetal brain microglia: first evidence of interference by iron homeostasis.
GEO Series GSE101857. Ovis aries. 7 samples. Type: Expression profiling by high throughput sequencing.
α7 nicotinic acetylcholine receptor signaling modulates fetal sheep brain astrocytes transcriptome in response to endotoxin stress: comparison to microglial transcriptome and implications for autism s
GEO Series GSE123713. Ovis aries. 15 samples. Type: Expression profiling by high throughput sequencing.
PET Imaging of Extrathalamic α4β2-nicotinic Acetylcholine Receptors in Health and Disease With [18F]XTRA
ClinicalTrials.gov study NCT01894646. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Understanding Factors That Influence Electronic Cigarette Nicotine Delivery Through PET Imaging of Beta-2 Nicotinic Acetylcholine Receptors
ClinicalTrials.gov study NCT04258852. IPD Sharing: NO. Countries: 1. Publications: 0.
Short-term depletion of nicotinic acetylcholine receptor subunits in Drosophila enterocytes
GEO Series GSE236069. Drosophila melanogaster. 12 samples. Type: Expression profiling by high throughput sequencing.
whole brains from nicotinic acetylcholine receptor subunit mutant mice and littermate controls
GEO Series GSE5320. Mus musculus. 11 samples. Type: Expression profiling by array.
Nicotinic acetylcholine receptors and EGF induce c-Kit ligand/Stem Cell Factor (SCF) in a β-arrestin-1 and E2F1 dependent manner in NSCLC
GEO Series GSE44617. Homo sapiens. 4 samples. Type: Expression profiling by array.
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Allen Brain Atlas
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Annotated Behaviour and Observability Dataset (ABODe)
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DANDI Archive for NWB datasets
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