Neurotransmitters noradrenaline serotonin

Not really. Epinephrine itself is not psychoactive and there s no evidence that it s chemically addictive. However, there are people who seem to thrive on dangerous activities, but this may be less to do with the so-called adrenaline rush , and more to do with the release of endorphins (natural painkillers that act in similar way to morphine (see p347) and may also be addictive), and of other neurotransmitters (noradrenaline, serotonin and dopamine) which are linked to learning. The idea is that if the activity doesn t hurt or kill the creature, the levels of these molecules in the brain increase and the creature is rewarded with feelings of pleasure or satisfaction, and this positive feedback makes the creature... 

Some arousal-related neurotransmitters, including noradrenaline, serotonin, and acetylcholine, feed back to inhibit POA sleep-active neurons. This aspect of the system has been reviewed previously (McGinty Szymusiak, 2000 Saper et al., 2001). Therefore, once sleep-active neurons are activated, arousal-related neurons are inhibited, and inhibitory control of sleep-active neurons by arousal systems is reduced. In this way, sleep onset is facilitated. That is, the mutually inhibitory systems can switch more quickly from wake to sleep, and back. These mutually inhibitory interactions also promote stability of both waking and sleep. 

Neurochemical theories for the affective disorders propose that there is a link between dysfunctional monoaminergic synapses within the central nervous system (CNS) and mood problems. The original focus was the neurotransmitter noradrenaline, or NA (note noradrenaline is called norepinephrine, or NE, in American texts). Schildkraut (1965) suggested that depression was associated with an absolute or relative deficiency of NA, while mania was associated with a functional excess of NA. Subsequently, another monoamine neurotransmitter 5-hydroxytryptamine (5-HT), or serotonin, was put forward in a rival indoleamine theory (Chapter 2). However, it was soon recognised that both proposals could be reconciled with the available clinical biochemical and pharmacological evidence (Luchins, 1976 Green and Costain, 1979). 

Iproniazid, an MAOI no longer available because of its hepatotoxicity, was the first effective antidepressant to be discovered it was introduced shortly before the discovery of imipramine. All MAOIs are presumed to have a similar mode of action, namely to inhibit the intra- and interneuronal metabolism of the biogenic amine neurotransmitters (noradrenaline, dopamine and serotonin). These amines are primarily metabolized by MAO-A (noradrenaline and serotonin) or MAO-B (dopamine). The irreversible MAOIs are inhibitors of MAO-A while selegiline (deprenyl), used as an adjunctive treatment for Parkinson s disease, is a selective, irreversible inhibitor of MAO-B. 

Barbiturates, benzodiazepines, and GHB affect the activity of the neurotransmitter GABA, resulting in more chloride ions entering the neuron and making it more resistant to excitation. As a consequence, the output of excitatory neurotransmitters, including norepinephrine (noradrenaline), serotonin, and dopamine, is reduced. 

Neurotransmitters—Chemical messengers in the brain. Common neurotransmitters include serotonin, glutamate, dopamine, gamma aminobutyric acid (GABA), noradrenaline, and histamine. 

Despite the recent advances in molecular biology, the mechanisms of action and the physiological functions of the anandamide system remain obscure. It would appear that the cannabinoid receptors and the anandamides reside within the neurons. Thus unlike the classical neurotransmitters noradrenaline and serotonin, the anandamides are not released into the synaptic cleft and are not involved in intemeuronal communication. Instead the anandamides modulate the excitability and inhibitory responsiveness of neurons by acting on cannabinoid hetero-ceptors located on inhibitory and excitatory terminals. In this way, the... 

Tricyclic antidepressants, which inhibit or reduce the reabsorption (reuptake) of the main neurotransmitters (noradrenaline and serotonin) into nerve endings. 

Q4 The neurotransmitters GABA (gamma-aminobutyric acid) and serotonin (5-HT) are mainly associated with anxiety disorders. In addition the sympathetic component of responses observed in anxiety, which stimulates a dry mouth, tachycardia, sweating and so on, involves the neurotransmitter noradrenaline. 

The broad physiological effects of EA are based mostly on their interaction with the neurotransmitter receptors on the cells. The presence of hidden structures resembling some important neurohumoral mediators (e.g., noradrenaline, serotonin, dopamine) (Scheme 1) in the molecules of EA could explain their interactions (agonistic or antagonistic) with these receptors [2]. 

The monoamine hypothesis proposes that, in depression, there is deficiency of the neurotransmitters noradrenaline and serotonin in the brain which can be altered by antidepressants. Drugs that affect depression can modify amine storage, release, or uptake (Fig. 19.2). Thus the concentration of amines... 

Whereas acetylcholine is degraded by a membrane-anchored acetylcholine esterase (ACE) in the synaptic cleft (choline is afterwards taken up presynaptically), the biogenic amines adrenaline, noradrenaline, serotonin, and dopamine are taken up by the presynaptic membrane by transporters (Fig. 3) or by extraneuronal cells in which they are degraded by a catecholamine O-methyltransferase (COMT). These transporter have similar structure and contain 12 transmembrane regions. Once in the presynapse, the neurotransmitters are either degraded by monoamine oxidase (MAO) or taken up by synaptic vesicles. A proton pumping ATPase of the vesicle membrane (V-type ATPase as in plant vacuoles) causes an increase of hydrogen ion concentrations in the vesicles. Uptake of the neurotransmitter serotonin, adrenaline and noradrenaline could be partly achieved either via a diffusion of the free base into the vesicles where they become protonated and concentrated by an "ion trap" mechanism and via specific proton-coupled antiporters. The excitatory amino acids, acetylcholine and ATP cannot diffuse and enter the vesicles via specific transporters. 

These are extracellular chemicals that are released during the transmission of impulses from one nerve cell to another or from a nerve cell to a muscle cell or gland. They include acetylcholine, adrenaline, noradrenaline, serotonin (5-hydroxytryptamine) and y-aminobutyric acid (GABA). Neurotransmitters are rapidly removed or broken down as it is essential that the resting membrane potential should be restored so that further impulses may be transmitted. 

Depression is beyond any doubt the major psychiatric disorder that could affect every fifth individual at least once during their lifetime. There are several theories to explain development of depression including the role of noradrenaline, serotonine, acetylcholine, and dysregulation of neurotransmission. Therefore, antidepressants have many different and well-defined mechanisms of action such as enhancement of neurotransmitter synthesis, inhibition of neurotransmitter reuptake, monoamino oxidase (MAO) inhibition, antagonism of the activity of presynaptic inhibitory receptors, or increase in the activity of postsynaptic receptors. The reason for TDM in this class of drugs is that the metabolism and elimination show wide interindividual variability thus, when standard doses are applied the serum concentration is often out of the therapeutic range [27]. 

Ubiquitous mitochondrial monoamine oxidase [monoamine oxygen oxidoreductase (deaminating) (flavin-containing) EC 1.4.3.4 MAO] exists in two forms, namely type A and type B [ monoamine oxidase (MAO) A and B]. They are responsible for oxidative deamination of primary, secondary, and tertiary amines, including neurotransmitters, adrenaline, noradrenaline, dopamine (DA), and serotonin and vasoactive amines, such as tyramine and phenylethylamine. Their nonselec-tive and selective inhibitors ( selective MAO-A and -B inhibitors) are employed for the treatment of depressive illness and Parkinson s disease (PD). 

Acute treatment with nonselective MAO inhibitors (iproniazid, tranylcypromine, phenelzine), as a consequence of inhibiting both forms of the enzyme, increase, brain levels of all monoamines (phenylethylamine, tryptamine, methylhistamine aminergic neurotransmitters (dopamine, noradr enaline, adrenaline and serotonin). By contrast MAO-A inhibitors (clorgyline) increase serotonin and noradrenaline, while MAO-B inhibitors (selegiline, rasagiline) increase brain levels... 

Noradrenaline transporters (NAT) are localized in the presynaptic plasma membrane of adrenergic nerve terminals. They belong to a family of proteins with 12 putative transmembrane proteins which are responsible for recycling of released neurotransmitters (noradrena-line/adrenaline, dopamine, serotonin, amino acid transmitters) back into the presynaptic nerve ending. Noradrenaline transporters can be blocked by a number of different antidepressant drags, including tricyclic antidepressants (e.g. desipramine) and selective noradrenaline reuptake inhibitors (e.g. reboxetine). 

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