Neuronal receptors

Receptors mediating neuronal apoptosis may be grouped in tw o types—dependence receptors and non-dependence receptors. 

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In addition, adenosine is implicated in sleep regulation. During periods of extended wakefulness, extracellular adenosine levels rise as a result of metabolic activity in the brain, and this increase promotes sleepiness. During sleep, adenosine levels fall. Caffeine promotes wakefulness by blocking the interaction of extracellular adenosine with its neuronal receptors. ... 

Ibogaine protects the N-methyl-D-aspartate neuron receptors against excessive release of excitatory amino acids and represents, therefore, a potential therapeutic agent for the treatment of Alzheimer s disease, Huntington s chorea, and other... 

Santuccione, A., Sytnyk, V., Leshchyns ka, I., and Schachner, M. (2005) Prion protein recruits its neuronal receptor NCAM to lipid rafts to activate p59fyn and to enhance neurite outgrowth. J. Cell Biol. 169, 341-354. 

Mixture of neurotoxins that block the acetylcholine receptors. The /3-bungarotoxin is a pre-synaptic neural toxin, a-bungarotoxin is a postsynaptic neural toxin, and K-bungarotoxin is specific to the neuronal receptors in ganglions. They are obtained from the venom of the banded krait (Bungarus multicinctus). 

The molecular nature of the neuronal receptors is now becoming understood with the advent of molecular biological techniques. The molecular structure of the mechanosensitive channels has been established only recently. In principle mechanosensitive channels must be opened by mechanical deformation of the neural membrane in which they are em-... 

Nicotinic receptors are of the ionotropic type which, on stimulation by acetylcholine, nicotine or related agonists, open to allow the passage of sodium ions into the neuron. There are structural differences between the peripheral and neuronal receptors, the former being pentamers composed of two alpha and one beta, gamma and delta sub-units while the latter consist of single alpha and beta sub-units. It is now known that there are at least four variants of the alpha and two of the beta sub-units in the brain. In Alzheimer s disease it would appear that there is a selective reduction in the nicotinic receptors which contain the alpha 3 and 4 sub-units (Figure 2.9). 

Unlike the muscarinic receptors, repeated exposure of the neuronal receptors to nicotine, both in vivo and in vitro, results in an increase in the number of receptors similar changes are reported to occur after physostigmine is administered directly into the cerebral ventricles of rats. These changes in the density of the nicotinic receptors are accompanied by an increased release of acetylcholine. Following the chronic administration of physostigmine, however, a desensitization of the receptors occurs. Functionally nicotinic receptors appear to be involved in memory formation in clinical studies it has been shown that nicotine can reverse the effects of scopolamine on short-term working memory and both... 

MecfianismofAction An antidepressant that inhibits the MAO enzyme system at central nervous system (CNS) storage sites. The reduced MAO activity causes an increased concentration in epinephrine, norepinephrine, serotonin, and dopamine at neuron receptor sites. Therapeutic Effect Produces antidepressant effect. 

Mechanism of Action A tetracyclic compound that blocks reuptake norepi nephri ne by CNS presynaptic neuronal membranes, increasing availability at postsynaptic neuronal receptor sites, and enhances synaptic activity. Therapeutic Effect Produces antidepressant effect, with prominent sedative effects and low anticholinergic activity. Pharmacokinetics Slowly and completely absorbed after PO administration. Protein binding 88%. Metabolized in liver by hydroxylation and oxidative modification. Excreted in urine. Unknown if removed by hemodialysis. Half-life 27-58 hr. 

Mechanism of Action An MAOI that inhibits the activity of the enzyme monoamine oxidase at CNS storage sites, leading to increased levels of the neurotransmitters epinephrine, norepinephrine, serotonin, and dopamine at neuronal receptor sites. Therapeutic Effect Relieves depression. 

A therapeutic decrement may be inherent in the repeated application of antidepressant treatments. In this context, patients who are repeatedly treated with antidepressants appear to become increasingly more resistant to subsequent treatment strategies, including ECT [Amsterdam et al. 1994b]. A number of clinical and biochemical factors, including progressive virulence of recurrent depressive episodes, reduced plasticity of neuronal receptor regulatory mechanisms, and the development of secondary (and even tertiary de-... 

Bunce K, Tyers M, Beranek P Clinical evaluation of S-HTj receptor antagonists as anti-emetics. Trends Pharmacol Sci 12 46-48, 1991 Bunney WE Neuronal receptor function in psychiatry strategy and theory, in Neuroreceptors Basic and Clinical Aspects. Edited by Usdin E, Bunney WE Jr, Davis JM. New York, Wiley, 1981... 

Figure 3.9 The blood-brain barrier (BBB) is a major impediment to the delivery of drugs to the brain. In the brain, in order for a drug molecule to leave a capillary and snccessfnlly jonmey to a neuronal receptor, it must traverse multiple barriers. The walls of capillaries in the brain are different from those in non-brain tissnes. Tight junctions prevent the drugs from readily crossing the capillary. Next, in the brain, another type of cell, called an astrocyte, forms an additional barrier that must be traversed. Astrocytes are not present outside of the brain.

Drugs that alter sleep produce their effects on the brain by altering the actions of neurotransmitters and consequently how neurons communicate with each other. However, different drugs can alter the actions of neurotransmitters in different ways. Stimulants such as amphetamine cause neurons to release excess amounts of neurotransmitters like dopamine and serotonin. Other drugs, such as the prescription sleeping pills Halcion or Ambien or antihistamines, can interact directly with the neurons receptors to either enhance or block the effects of the neurotransmitters. In later chapters, we will discuss how drugs that help you sleep or stay awake alter the chemistry of the brain. 

Nevertheless and despite the widely illegal recreational use of cannabis the effects of cannabinoids on the brain still are under active investigation. The discovery of neuronal receptor proteins for cannabinoids and the existence of endogenous cannabinoid substances (Sullivan, 2000) are the most important milestones to date. 

FIGURE 1 — 3. The synapse is enlarged conceptually here showing its specialized structures that enable chemical neurotransmission to occur. Specifically, a presynaptic neuron sends its axon terminal to form a synapse with a postsynaptic neuron. Energy for this process is provided by mitochondria in the presynaptic neuron. Chemical neurotransmitter is stored in small vesicles ready for release on firing of the presynaptic neuron. The synaptic cleft is the connection between the presynaptic neuron and the postsynaptic neuron. Receptors are present on both sides of this cleft and are key elements of chemical neurotransmission. 

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