Anticholinergic and Neuroleptic Drugs
Frank A. Barile in Clinical Toxicology, 2004
A variety of chemicals, drugs, and herbal derivatives possess anticholinergic properties defined by their ability to block the neurotransmitter acetylcholine (ACh). This effect is a result of a direct interference with either of two types of cholinergic receptors — peripheral muscarinic or nicotinic receptors. Anticholinergic effects are also a consequence of adverse drug reactions (ADR), as seen with the tricyclic and phenothiazine antidepressants. In addition, many anticholinergic compounds exert their action by occupying central cholinergic receptors, thus producing alterations upon the CNS.
J
Manuchair Ebadi in Desk Reference of Clinical Pharmacology, 2008
Atropine and its allied drugs (hyoscyamine, scopolamine, homatropine, etc.) are autonomic blocking agents that inhibit the action of the postganglionic cholinergic nerves and were, therefore, formerly designated as depressants of the parasympathetic system, or as antiparasympathomimetic agents. These drugs differ from nicotine and curare, which are also depressants of the parasympathetic system but which act as blocking agents on preganglionic cholinergic nerves. Atropine in therapeutic doses has no effect on the nicotinic actions of acetylcholine but specifically blocks all muscarinic responses of injected acetylcholine, whether excitatory as in the intestine, or inhibitory as in the heart. It fails, however, to block all cholinergic nerve stimulations and also exerts effects that are not explicable on the basis of its antagonism to acetylcholine. In addition to their action in blocking the muscarinic effects of acetylcholine, atropine and its allies exert important effects on the central nervous system (see also Figures 12 and 26).
Non-adrenergic Non-cholinergic Autonomic Transmission
Kenneth J. Broadley in Autonomic Pharmacology, 2017
This chapter considers the role of the non-adrenergic non-cholinergic transmitters of autonomic nerves. They are generally co-transmitters, which by definition are two or more transmitters released from the same neurone by the invading action potential and which influence the activity of an effector cell, being the target cell or the neurone itself. The main types of co-transmitters of the autonomic nerves are peptides, purines and nitric oxide, and the locations and pharmacology. Neuropeptides are synthesized only in the cell bodies of autonomic neurones, unlike the conventional transmitters or adenosine-triphosphate, which are synthesized at the nerve terminal in the cytoplasm and within the storage vesicle. The neuropeptides are initially synthesized in the Golgi apparatus, as large precursor molecules which may consist of 100 amino acid residues. Neuropeptide Y is a 36-residue peptide with a tyrosine at the N-terminus and a tyrosine amide at the C-terminus.
The cholinergic neurotransmitter system in human memory and dementia: A review
Published in The Quarterly Journal of Experimental Psychology Section A, 1986
The present paper reviews three types of evidence implicating the role of acetylcholine in human memory and dementia: (1) neuropathological evidence that the cholinergic transmitter system is depleted in Alzheimer-type dementia; (2) psychopharmacological studies that have employed “cholinergic blockade” as a model of cholinergic depletion; and (3) clinical studies of cholinergic “replacement” therapy in Alzheimer-type dementia. The evidence that the cholinergic system is depleted in Alzheimer-type dementia has been complemented by the finding that cholinergic blockade in healthy subjects causes a substantial learning (or “acquisition”) deficit in episodic memory. The overall results of studies of replacement therapy have generally been disappointing, but a few have reported benefits in recall and recognition tests. The role of the cholinergic system in many aspects of memory remains to be elucidated; but it seems unlikely that cholinergic depletion accounts for all aspects of the memory disorder in Alzheimer-type dementia, and possibly the depletions of other neurotransmitters also contribute to the memory impairment.
Distribution and Clinical Significance of the Autonomic Nervous System in the Human Nasal Mucosa
Published in Acta Oto-Laryngologica, 1972
Biopsied specimens from the human inferior concha were studied histochemically to elucidate the function of the cholinergic nerve fiber, adrenergic nerve fiber, and myoepithelial basket cell and capillary. There are rich cholinergic nerve fibers in the inferior concha. They terminate mainly in the nasal gland and the blood vessels. Lacking in adrenergic nerve fiber, the nasal gland is therefore cholinergic. When the cholinergic nerve is over-stimulated by triggers, such as allergic or other reactions, the nasal gland and vessel work as a functional unit and produce profuse nasal secretion. Studies on human specimens reveal that the greater superficial petrosal nerve, vidian nerve and sphenopalatine ganglion are cholinergic in nature. The anterior ethmoid nerve also contains abundant cholinergic fibers. The nerve fibers in the vidian nerve are mainly cholinergic. The rationale for vidian neurectomy for allergic rhinitis is discussed.
Lack of effects of thyroid hormones on muscarine cholinergic receptors in rat brain and heart
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 1984
The muscarinic cholinergic antagonist 3H-quinuclidinyl benzilate was used to study muscarinic cholinergic receptors in the brain and the heart from triiodothyronine, thyroxine and 6-propyl-2-thiouracil treated rats. Scatchard analysis of the saturation binding studies revealed for each rat in both brain and heart tissue a single group of muscarinic cholinergic receptor binding sites of high affinity. The density and the affinity of muscarinic cholinergic receptors in brain and heart homogenates from treated rats were not different from values obtained in control rats with the exception of triiodothyronine treated rats which showed a slightly but significantly increased equilibrium dissociation constant in the brain homogenates. Furthermore, we observed that the density of the muscarinic cholinergic receptors in the brain was significantly lower in the month of August as compared to March-April, which suggests a seasonal variation. No similar change was observed in heart homogenates. Our results suggest that cardiovascular and central nervous symptoms in patients with thyroid diseases cannot be ascribed to changes in muscarinic cholinergic receptors.
Related Knowledge Centers
- Choline
- Lecithin
- Neurotransmitter
- Inositol
- Acetylcholine