Transmitter, cholinergic

Cholinergic Transmission is the process of synaptic transmission which uses mainly acetylcholine as a transmitter. Cholinergic transmission is found widely in the peripheral and central nervous system, where acetylcholine acts on nicotinic and muscarinic receptors. 

Because of its motor, i.e., activating effect on vascular smooth muscle and its inhibitory effect on intestinal smooth muscle, the sympathetic nervous system has been cast into the role of the component of the nervous system that executes control of visceral function in times of physical emergency for the organism. The phrase fight or flight has been often used to describe the circumstances in which the adrenergic transmitters of the sympathetic system are dominant over the cholinergic parasympathetic system. This concept is perhaps oversimplified but it has the utility of a first approximation of how the two components of the ANS interact in the periphery. Sensory inputs which lead to increased blood pressure, for example, activate the sympathetic pathways. 

Complicated processes govern wakefulness, sleep, and the transitions leading to sleep initiation and maintenance. Although the neurophysiology of sleep is complex, certain neurotransmitters promote sleep and wakefulness in different areas of the central nervous system (CNS). Serotonin is thought to control non-REM sleep, whereas cholinergic and adrenergic transmitters mediate REM sleep. Dopamine, norepinephrine, hypocretin, substance P, and histamine all play a role in wakefulness. Perturbations of various neurotransmitters are responsible for some sleep disorders and explain why various treatment modalities are beneficial. 

Acetylcholine-mediated parasympathetic activity leads to production of the non-adrenergic-non-cholinergic transmitter nitric oxide. By enhancing the activity of guanylate cyclase, nitric... 

ACh regulates the cortical arousal characteristic of both REM sleep and wakefulness (Semba, 1991, 2000 Sarter Bruno, 1997, 2000). Medial regions of the pontine reticular formation (Figs. 5.2 and 5.7) contribute to regulating both the state of REM sleep and the trait of EEG activation. Within the medial pontine reticular formation, presynaptic cholinergic terminals (Fig. 5.1) that release ACh also are endowed with muscarinic cholinergic receptors (Roth et al, 1996). Autoreceptors are defined as presynaptic receptors that bind the neurotransmitter that is released from the presynaptic terminal (Kalsner, 1990). Autoreceptors provide feedback modulation of transmitter release. Autoreceptor activation... 

The basal forebrain is an important way station in the activation of the cerebral cortex from the reticular activating system. AMPA and NMDA injections into the basal forebrain increase wakefulness and reduce sleep (Cape Jones, 2000 Manfridi et al, 1999), effects that are blocked by AMPA and NMDA receptor antagonists (Manfridi et al, 1999). The excitatory cortical projections of the basal forebrain have long been considered purely cholinergic, but many basal forebrain neurons that project to the cortex are now known to contain Glu, which may function as a co-transmitter or even as the primary excitatory neurotransmitter (Manns et al, 2001). The basal forebrain also affects vigilance via synapses to HCT cells in the lateral hypothalamus some of these synapses are glutamatergic (Henny Jones, 2006). 

Neurotoxin that produces a massive release of transmitters from cholinergic and adrenergic nerve endings resulting in continuous stimulation of muscles. It also induces formation of an ion channel allowing the inward flow of calcium ions into the nerve cell. It is a white powder obtained from the venom of the black widow spider. 

Acetylcholine. Most of the acetylcholine in the basal ganglia is found in the striatum, as the neurotransmitter of the large spiny interneurons, which account for about 3% of all striatal neurons. Both muscarinic and nicotinic cholinergic receptors are found in the striatum. Postsynaptic muscarinic receptors may inhibit transmitter release from... 

Nicotinic cholinergic receptors are located on cells that release a wide variety of transmitters (see chapter by Barik and Wonnacott, in this volume), so that nicotine interacts with multiple neurochemical pathways. The roles of cholinergic, dopaminergic, and endogenous opioid systems in physical dependence and withdrawal have been most thoroughly studied and documented. Research on the role of other transmitters and neurochemical mechanisms is rather scattered. Overall, however, research with rodent models of physical dependence has provided a wealth of potential targets for experimental treatments to aid smoking cessation. 

Acetylcholine has been implicated in learning and memory in all mammals, and the gross deficits in memory found in patients suffering from Alzheimer s disease have been ascribed to a defect in central cholinergic transmission. This transmitter has also been implicated in the altered mood states found in mania and depression, while many different classes of psychotropic drugs are known to have potent anticholinergic properties which undoubtedly have adverse consequences for brain function. 

Each neuron usually releases only one type of neurotransmitter. Neurons that release dopamine are referred to as dopaminergic, for example, while those that release acetylcholine are cholinergic, etc. The transmitters that are released diffuse through the synaptic cleft and bind on the other side to receptors on the postsynaptic membrane. These receptors are integral membrane proteins that have binding sites for neurotransmitters on their exterior (see p. 224). 

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