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beta erythroidine/hipersensitivitas
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Prenatal nicotine exposure induces HPA axis-hypersensitivity in offspring rats via the intrauterine programming of up-regulation of hippocampal GAD67.
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The intrauterine programming of hypothalamic-pituitary-adrenal (HPA) axis hypersensitivity is associated with chronic adult diseases. Our previous studies demonstrated the HPA-axis hypersensitivity in offspring rats induced by prenatal nicotine exposure. The goal of the present study is to further
Impact of chronic nicotine on the development and maintenance of neuropathic hypersensitivity in the rat.
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BACKGROUND
Clinical data support a correlation between smoking and the incidence and severity of some chronic pain conditions. However, the impact of nicotine on neuropathic pain has been largely ignored in the laboratory setting.
OBJECTIVE
The purpose of these studies was to determine if chronic
Cell autonomy, receptor autonomy, and thermodynamics in nicotine receptor up-regulation.
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Chronic nicotine exposure, in smokers or in experimental rodents administered nicotine, produces elevated levels of nicotinic acetylcholine receptors in several brain regions. However, there are few data on up-regulation of receptors in specific neuronal subtypes. We tested whether functional
Spinal muscarinic and nicotinic subtypes activated by clonidine in postincisional pain.
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BACKGROUND
A recent model of acute incisional pain has been characterized that strongly parallels the postoperative period in patients experiencing evoked pain. In that setting, abundant literature has revealed antihypersensitive effects produced by intrathecally administered alpha2-adrenergic
A role for α4(non-α6)* nicotinic acetylcholine receptors in motor behavior.
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Nicotinic acetylcholine receptors (nAChRs) containing either the α4 and/or α6 subunit are robustly expressed in dopaminergic nerve terminals in dorsal striatum where they are hypothesized to modulate dopamine (DA) release via acetylcholine (ACh) stimulation from cholinergic interneurons. However,
Novel agonist of α4β2* neuronal nicotinic receptor with antinociceptive efficacy in rodent models of acute and chronic pain.
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UNASSIGNED
To demonstrate the antinociceptive and antihypersensitivity mechanisms of Cris-104 (1-{2-[5-(4-fluorophenyl)-1H-pyrazol-4-yl]ethyl}piperidine), a novel selective α4β2* nicotinic acetylcholine receptor (nAChR) agonist, in rodent acute/inflammatory and chronic pain
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