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Mansa Musa was the ruler of the Mali Empire in West Africa. Details recorded here should be sourced; unknown information is left blank.
MORE →Reflects the personal views, recollections, and perspective of the author, Mike Davis.
This is a personal recollection on the Move fire on May 13, 1985
The Muscarinic Acetylcholine receptor M1, also known as the Cholinergic receptor, Muscarinic 1, is a muscarinic receptor that in humans is encoded by the CHRM1 gene.[5] It is localized to 11q13.[5]
The locations of M1 receptor includes but not limited to various 'Secretory glands[6]
This receptor is found mediating slow EPSP at the ganglion in the postganglionic nerve,[7] and is common in exocrine glands and in the CNS.[8][9]
It is predominantly found bound to G proteins of class Gq[10][11] that use upregulation of phospholipase C and, therefore, inositol trisphosphate and intracellular calcium as a signalling pathway. A receptor so bound would not be susceptible to CTX or PTX. However, Gi (causing a downstream decrease in cAMP) and Gs (causing an increase in cAMP) have also been shown to be involved in interactions in certain tissues, and so would be susceptible to PTX and CTX respectively.
A structural but not sequential homolog of the human M1 receptor has been described in Acanthamoeba castellanii and Naegleria fowleri by a group of researchers working at Aga Khan University.[16][17]
Drugs with significant antimuscarinic side effects such as chlorpromazine appear to show inhibitory effects on cultured Naegleria fowleri cells.[18]
It couples to Gq, and, to a small extent, Gi and Gs. This results in slow EPSP and decreased K+ conductance.[14][19] It is preassembled to the Gq heterotrimer through a polybasic c-terminal domain.[10]
Delirium is only associated with the antagonism of post‐synaptic M1 receptors and to date other receptor subtypes have not been implicated
This article incorporates text from the United States National Library of Medicine, which is in the public domain.
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Source: Wikipedia. Article content is retrieved live through the MediaWiki API.
The Muscarinic Acetylcholine receptor M1, also known as the Cholinergic receptor, Muscarinic 1, is a muscarinic receptor that in humans is encoded by the CHRM1 gene. It is localized to 11q13. The locations of M1 receptor includes but not limited to various 'Secretory glands This receptor is found mediating slow EPSP at the ganglion in the postganglionic nerve, and is common in exocrine glands and in the CNS. It is predominantly found bound to G proteins of class Gq that use upregulation of phospholipase C and, therefore, inositol trisphosphate and intracellular calcium as a signalling pathway. A receptor so bound would not be susceptible to CTX or PTX. However, Gi (causing a downstream decrease in cAMP) and Gs (causing an increase in cAMP) have also been shown to be involved in interactions in certain tissues, and so would be susceptible to PTX and CTX respectively.
Acetylcholine (ACh) is an organic compound that functions in the brain and body of many types of animals (including humans) as a neurotransmitter. Its name is derived from its chemical structure: it is an ester of acetic acid and choline. Parts in the body that use or are affected by acetylcholine are referred to as cholinergic. Acetylcholine is the neurotransmitter used at the neuromuscular junction. In other words, it is the chemical that motor neurons of the nervous system release in order to activate muscles. This property means that drugs that affect cholinergic systems can have very dangerous effects ranging from paralysis to convulsions. Acetylcholine is also a neurotransmitter in the autonomic nervous system, both as an internal transmitter for both the sympathetic and the parasympathetic nervous system, and as the final product released by the parasympathetic nervous system. Acetylcholine is the primary neurotransmitter of the parasympathetic nervous system. In the brain, acetylcholine functions as a neurotransmitter and as a neuromodulator. The brain contains a number of cholinergic areas, each with distinct functions; such as playing an important role in arousal, attention, memory and motivation. Acetylcholine has also been found in cells of non-neural origins as well as microbes. Recently, enzymes related to its synthesis, degradation and cellular uptake have been traced back to early origins of unicellular eukaryotes. The protist pathogens Acanthamoeba spp. have shown evidence of the presence of ACh, which provides growth and proliferative signals via a membrane-located M1-muscarinic receptor homolog. Partly because of acetylcholine's muscle-activating function, but also because of its functions in the autonomic nervous system and brain, many important drugs exert their effects by altering cholinergic transmission. Numerous venoms and toxins produced by plants, animals, and bacteria, as well as chemical nerve agents such as sarin, cause harm by inactivating or hyperactivating muscles through their influences on the neuromuscular junction. Drugs that act on muscarinic acetylcholine receptors, such as atropine, can be poisonous in large quantities, but in smaller doses they are commonly used to treat certain heart conditions and eye problems. Scopolamine, or diphenhydramine, which also act mainly on muscarinic receptors in an inhibitory fashion in the brain (especially the M1 receptor) can cause delirium, hallucinations, and amnesia through receptor antagonism at these sites. So far as of 2016, only the M1 receptor subtype has been implicated in anticholinergic delirium. The addictive qualities of nicotine are derived from its effects on nicotinic acetylcholine receptors in the brain.
Pirenzepine (Gastrozepin), an M1 selective antagonist, is used in the treatment of peptic ulcers, as it reduces gastric acid secretion and reduces muscle spasm. It is in a class of drugs known as muscarinic receptor antagonists; acetylcholine is the neurotransmitter of the parasympathetic nervous system which initiates the rest-and-digest state (as opposed to fight-or-flight), resulting in an increase in gastric motility and digestion; whereas pirenzepine would inhibit these actions and cause decreased gastric motility leading to delayed gastric emptying and constipation. It has no effects on the brain and spinal cord as it cannot diffuse through the blood–brain barrier. Pirenzepine has been investigated for use in myopia control. It promotes the homodimerization or oligomerisation of M1 receptors.
N-Desmethylclozapine (NDMC), or norclozapine, is a major active metabolite of the atypical antipsychotic drug clozapine. Unlike clozapine, it possesses intrinsic activity at the D2/D3 receptors, and acts as a weak partial agonist at these sites similarly to aripiprazole and bifeprunox. Notably, NDMC has also been shown to act as a potent and efficacious agonist at the muscarinic acetylcholine M1 receptor and the δ-opioid receptor, unlike clozapine as well. It is a moderate-efficacy partial agonist of the muscarinic acetylcholine M1 and M2 receptors, a very weak partial agonist or antagonist of the M3 receptor, and a silent antagonist of the M4 receptor. It also binds with high affinity to the M5 receptor, but its intrinsic activity was not reported for this receptor. It was hypothesized that on account of its unique actions, NDMC might underlie the clinical superiority of clozapine over other antipsychotics. However, clinical trials found NMDC itself ineffective in the treatment of schizophrenia. This may be because it possesses relatively low D2/D3 occupancy compared to the 5-HT2 receptor (
Before the 1921 destruction of Tulsa’s Greenwood District, Black residents had created a remarkable center of business and community life. The district included stores, professional offices, entertainment venues and homes owned by Black citizens. Understanding Greenwood means learning what was built—not only what was burned.
MORE →Brown v. Board of Education in 1954.
