Involvement Of Cholinergic Pathways Research Articles

Regulation of antro-pyloro-duodenal and fundic motility by GLP-1(7-36)amide (GLP-1): Involvement of cholinergic pathways

Regulation of antro-pyloro-duodenal and fundic motility by GLP-1(7-36)amide (GLP-1): Involvement of cholinergic pathways

Regulation of antro-pyloro-duodenal and fundic motility by GLP-1(7-36)amide (GLP-1): Involvement of cholinergic pathways

Regulation of antro-pyloro-duodenal and fundic motility by GLP-1(7-36)amide (GLP-1): Involvement of cholinergic pathways

Tracking cholinergic pathways from psychological and chemical stressors to variable neurodeterioration paradigms.

Cholinergic hyperexcitation can be induced by both acute psychological stress and exposure to acetylcholinesterase inhibitors. Both factors are known risk factors for delayed neurodeterioration processes such as Alzheimer's disease and Parkinson's disease. Recent publications on the involvement of cholinergic pathways in these and other neurodeterioration syndromes are reviewed.

FS stress induces long-lasting memory facilitation: Involvement of cholinergic pathways

We tested in vivo the hypothesis that foot-shock (FS) stress-induced prolongation of latencies in the one-trial step-through passive avoidance learning task in mice occurred through a long-term facilitation process. Whereas behavioral responses in control mice lasted for 24 h, decreasing progressively in the subsequent days, FS-stress exposure for 15 min before training (pretraining), immediately after training (posttraining), or 15 min before the test (pretest) resulted in a profound and sustained enhancement of test latencies that lasted for at least 96 h. These facilitating effects disappeared when FS exposure was delivered with a 2- or 3-h difference with respect to the training trial. Scopolamine (Scop) (1 mg/kg, intraperitoneally) 30 min before the training session caused impairment of test latencies in control and pretest stressed animals, but failed to affect both pre- and posttraining FS stress-induced enhancement. Our working hypothesis is that FS stress may increase the levels of acetylcholine in the presynaptic terminal or the firing rate of cholinergic input. Animals pretreated with FS stress daily for 1 or 4 days followed by the acute schedule described above showed no enhancements of test latencies. Pretraining Scop impaired test latencies in pre- and posttraining and pretest stressed animals, suggesting that unpredictability is a critical factor in activating behavioral long-term facilitation.

Cognitive Dysfunction in Myasthenia Gravis

The performance of patients with myasthenia gravis (MG) on selective neuropsychological tests was examined to assess the diagnostic applicability of such examinations. Twenty-seven patients with MG and twenty-seven age, sex, and education-matched controls were given a battery of tests designed to assess cognitive functions. The MG group displayed significantly lower scores on Mini-mental state test and memory tests. The results indicated that MG patients had cognitive impairment. Results are also discussed with respect to the involvement of cholinergic pathways in the central nervous system.

Sedative effects of α-sympathomimetic drugs and their antagonism by adrenergic and cholinergic blocking drugs

The depressing action of a number of α-sympathomimetic agents on the central nervous system was studied in chickens and mice. Clonidine, 2-(2,6-dimethylphenylamino)-2- Δ 2-oxazolidine 1–3, tetryzoline, naphazoline, tramazoline xylazine and oxymetazoline induced a loss of the righting reflex in chickens and prolonged the sleeping time induced by chloral in mice. These effects were dose-dependent and much more potent for the two former drugs. The actions in chickens and mouse were antagonized by previous treatment with four α-adrenergic blocking drugs (tolazoline, phentolamine, piperoxane, dibenamine) but not phenoxybenzamine. In chickens, chlorpromazine and imipramine also antagonized the action, but haloperidol was an antagonist only for naphazoline and tetryzoline. In mice, but not in chickens, atropine and mecamylamine were strong antagonists. These results suggest that activation of α-adrenergic receptors in the brain induces sedation and the involvement of cholinergic pathways in mice for this effect.