Acetylcholine neurones

Nestby, P., Vanderschuren, L.J., De Vries, T.J. et al. Ethanol, like psychostimulants and morphine, causes long-lasting hyperreactivity of dopamine and acetylcholine neurons of rat nucleus accumbens possible role in behavioural sensitization. Psychopharmacology (Berlin). 133 69, 1997. 

D2-receptor blocker removes inhibition of acetylcholine neurons in enteric nervous system... 

A CASE IN POINT ALZHEIMER S DISEASE Sometimes we can learn much about the role of a particular neurotransmitter system by investigating what happens when it is injured or diseased. In the brains of people with Alzheimer s disease, for example, acetylcholine neurons that project into the hippocampus and cortex very slowly die. The effects of this neuronal death have been the subject of research in my laboratory for more than 25 years. The loss of normal acetylcholine function in the cortex may be why patients with Alzheimer s... 

Experiments in my laboratory and in others have demonstrated that the appearance of this wave of electrical activity requires the normal function of acetylcholine within your frontal cortex. If the acetylcholine neurons that project into your frontal cortex are destroyed, then this wave cannot fully form and you will have great difficulty paying attention to important things, such as the impending appearance of a masked gunman. An example of such a wave is labeled post in the figure. In this case, the absence of acetylcholine does not allow the wave to fully develop. This research has demonstrated that acetylcholine s job is to instruct the neurons in your frontal cortex to pay attention to important information and be vigilant to... 

Sometimes, the severity of the cognitive symptoms in Alzheimer s disease can be reduced, at least to some degree, by drugs and dietary nutrients that enhance the function of acetylcholine neurons in the brain. To understand how this is possible, we need to look at how acetylcholine is produced in the brain in the first place. 

The mushrooms also cause sleepiness and then delirium, so at the very least, they probably interfere with the function of acetylcholine neurons within the cortex. Upon waking, people claim to feel very excited and aggressive for three to 4 hours and to be able to perform extraordinary physical feats. These symptoms... 

Many people drink coffee to reduce drowsiness. How does caffeine achieve this effect in the brain The answer begins with a consideration of the function of the acetylcholine neurons that control your ability to pay attention. Adenosine negatively controls the activity of these neurons, meaning that when adenosine binds to its receptor on acetylcholine neurons, their activity slows. The production and release of adenosine in your brain is linked to metabolic activity while you are awake. Therefore, the concentration of adenosine in the neighborhood of acetylcholine neurons increases constantly while your brain is active during the day. As the levels of adenosine increase, they steadily inhibit your acetylcholine neurons, your brain s activity gradually slows, and you begin to feel drowsy and ultimately fall asleep. Caffeine comes to the rescue because it, like theophylline... 

Adenosine is ubiquitous in the brain. Every cell can release it and does so rather continually while you are awake. It builds in concentration and slowly inhibits the activity of nearby neurons. Of particular concern is the inhibition of the attentioncontrolling acetylcholine neurons that project to the cortex. We need and want those neurons to be active so we consume drinks containing caffeine, a drug that quickly enters the brain and blocks the action of adenosine and releases acetylcholine neurons from the tyranny of inactivation once again, coffee comes to the rescue. 

The Internet is bursting with claims that pills and drinks containing extracts of the Ginkgo biloba plant may neutralize free radicals, dilate the blood vessels in your brain, make you smarter, and slow the aging process. How The claim is that Gingko biloba increases the function of acetylcholine neurons and thereby enhances memory and arouses and improves attentional ability. 

FIGURE 5.2 (See color insert following page 46.) Presynaptic and postsynaptic regions of the acetylcholine neuron, emphasizing the synthesis and degradation of acetylcholine and the cholinergic receptor suhtypes (Panel [A]) summary of the peripheral nervous system that utilizes acetylcholine as the transmitter (Panel [ B]). 

The concept of discrete neurotransmitter recognition sites or receptors on nerve cells was based on work on systems physiology and dmg action (1). It was not until 1921 however, that it was shown that information could be transferred between neurons via a chemical, in this instance acetylcholine [51-84-3] (ACh), C H gN02 (1). 

Acetylcholine is a neurotransmitter at the neuromuscular junction in autonomic ganglia and at postgangHonic parasympathetic nerve endings (see Neuroregulators). In the CNS, the motor-neuron collaterals to the Renshaw cells are cholinergic (43). In the rat brain, acetylcholine occurs in high concentrations in the interpeduncular and caudate nuclei (44). The LD q (subcutaneous) of the chloride in rats is 250 mg/kg. 

N-Heterocycles as neuronal acetylcholine receptors in drug discovery 97JMC4169. 

Cholinergic. An agent that mimics acetylcholine. Also refers to neurons that utilize acetylcholine as a neurotransmitter. 

Acetylcholine serves as a neurotransmitter. Removal of acetylcholine within the time limits of the synaptic transmission is accomplished by acetylcholinesterase (AChE). The time required for hydrolysis of acetylcholine at the neuromuscular junction is less than a millisecond (turnover time is 150 ps) such that one molecule of AChE can hydrolyze 6 105 acetylcholine molecules per minute. The Km of AChE for acetylcholine is approximately 50-100 pM. AChE is one of the most efficient enzymes known. It works at a rate close to catalytic perfection where substrate diffusion becomes rate limiting. AChE is expressed in cholinergic neurons and muscle cells where it is found attached to the outer surface of the cell membrane. 

The M-channels (M for muscarine) are expressed in the peripheral sympathetic neurons and CNS. In the absence of acetylcholine, the M-channel opens at resting membrane potential and dampens neuronal responsiveness to synaptic inputs. Acetylcholine inhibits M-channel activity by activation of Ml receptor. 

Nicotinic receptors (nicotinic acetylcholine receptors, nACHR) exist not only in the membrane of vertebrate skeletal muscle at the synapse between nerve and muscle (muscle-type nAChR) but also at various synapses throughout the brain, mainly at presynaptic positions (neuronal-type nAChR). Whereas the muscle-type nAChR is precisely composed of two a 1-subunits, one (3 -subunit, one y -subunit and one y -subunit (adult)... 

Dajas-Bailador F, Wonnacott S (2004) Nicotinic acetylcholine receptors and the regulation of neuronal signalling. Trends Pharmacol Sci 25 317-324... 

Jensen AA, Frolund B, Liljefors T et al (2005) Neuronal nicotinic acetylcholine receptors structural revelations, target identifications, and therapeutic inspirations. J Med Chem 48 4705—4745... 

Nicotine is the main psychoactive ingredient of tobacco and is responsible for the stimulant effects and abuse/ addiction that may result form tobacco use. Cigarette smoking rapidly (in about 3 sec ) delivers pulses of nicotine into the bloodstream. Its initial effects are caused by its activation of nicotinic acetylcholine (nACh) receptors. nACh receptors are ligand-gated ion-channels and pre- and postsynaptically located. Reinforcement depends on an intact mesolimbic dopamine system (VTA). nACh receptors on VTA dopamine neurons are normally activated by cholinergic innervation from the laterodorsal tegmental nucleus or the pedunculopontine nucleus. 

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