5-Hydroxytryptamine behavioral effects

Hole, K., Fuxe, K., and Jonsson, G. (1976) Behavioral effects of 5,7-dihydroxytryptamine lesions of ascending 5-hydroxytryptamine pathways. Brain Res., 107 385-399. 

McMahon, L. R. and Cunningham, K. A. 2001. Antagonism of 5-hydroxytryptamine 2A receptors attenuates the behavioral effects of cocaine in rats. Journal of Pharmacology and Experimental Theraphy, 297 357-363. 

Mayorga AJ, Dalvi A, Page ME, Zimov-Levinson S, Hen R, Lucki I (2001) Antidepressant-like behavioral effects in 5-hydroxytryptamine(lA) and 5-hydroxytryptamine(lB) receptor mutant mice. J Pharmacol Exp Ther 298 1101-1107 Mcllvain VA, Robertson DR, Maimone MM, McCasland JS (2003) Abnormal thalamocortical pathfinding and terminal arbors lead to enlarged barrels in neonatal GAP-43 heterozygous mice. J Comp Neiuol 462 252-264... 

Marsden, C. A., 1980, Involvement of 5-hydroxytryptamine and dopamine neurons in the behavioral effects of a-methyl tryptamine. Neuropharmacology 19 691-698. 

Other studies indicate that sucrose does not cause hyperactivity. Carbohydrate ingestion increases levels of serotonin (5-hydroxytryptamine), a brain neurotransmitter that promotes relaxation and sleep. Dietary sucrose should theoretically have a calming effect and reduce activity, manifestations which have been observed in case studies (63). To date, clinical investigations have failed to show a significant connection between sucrose consumption and aggressive or dismptive behavior (66). 

Segal, M., and Weinstock, M. (1983) Differential effects of 5-hydroxytryptamine antagonists on behaviors resulting from activation of different pathways arising from the raphe nuclei. Psychopharmacology, 79 72-78. 

Dennis J. McKenna, X.-M. Guan, and A. T. Shulgin. "3,4-methyl-enedioxyamphetamine (MDA) analogues exhibit differential effects on synaptosomal release of 3H-dopamine and 3H-5-hydroxytryptamine." Pharmacology, Biochemistry, and Behavior 38 (1991) 505-12. 

In addition to behavior changes, exposure to the alarm odor also has physiological effects. For instance, in pearl dace, Semotilus margarita, the levels of plasma cortisol and glucose increase 15 minutes after the alarm and are back to normal after 5 hours. The brain concentrations of dopamine, norepinephrine, 5-hydroxytryptamine, or tryptophan did not change (Rehnberg et al., 1987). The fish recovered physiologically much sooner than the behavioral activation For example. Von Frisch (1941) observed that minnows avoided the site of their encounter with alarm substance for many hours, even days. 

Simansky KJ, Vaidya AH (1990) Behavioral mechanisms for the anorectic action of the serotonin (5-HT) uptake inhibitor sertaline in rats comparison with directly acting 5-HT agonists. Brain Res Bull 25 953-960 Simmons RD, Blosser JC, Rosamond JR (1994) FPL 14294 A novel CCK-8 agonist with potent intranasal anorectic activity in the rat. Pharmacol Biochem Behav 47 701-708 Stevens R, Edwards S (1996) Effect of a 5-HT3 antagonist on peripheral 5-hydroxytryptamine-induced anorexia. Psychobiology 24 67-70... 

After injecting lobsters with the neurotransmitter serotonin (5-hydroxytryptamine 5-HT), Kravitz et al. (1980) and Livingstone et al. (1980) observed that the animals assumed an apparent dominant posture, which included raised and spread claws. Injection of another neurotransmitter, octopamine, resulted in an opposite effect. Some conflicting observations have been made following 5-HT injection (Peeke et al. 2000 Tierney and Mangiamele 2001 Panksepp and Huber 2002). These postures and behaviors are undoubtedly under highly complex regulation and the dose and method of application of 5-HT likely affect the observed outcomes. 

Cesium exhibits marked effects on the nervous system, both peripherally and centrally. This may be the consequence of the purported interchangeability of cesium with other group I metals. Certainly cesium ions will increase the frequency of miniature end-plate potentials, thought to be due to the slow entry of cesium ions into the nerve terminal [32]. In the central nervous system, it seems that cesium can share the same receptor as glycine and exerts its effects by activating the same chloride channel as the inhibitory neurotransmitter, glycine [33]. Indeed, in consequence of this action, cesium has been implicated as a causative agent of some epileptiform seizures [34]. More recently, pretreatment of rats with cesium chloride, followed by administration of the monoamine oxidase inhibitor tranylcypramine, has been shown to enhance 5-hydroxytryptamine (5-HT) behavioral syndrome. This may be due to either an increased amount of 5-HT synthesis and/or release, or a direct enhancement of the postsynaptic action of 5-HT [34b]. 

Serotonin, also known as 5-hydroxytryptamine (5-HT) is biosynthesized from tryptophan and is a neurotransmitter. Serotonin plays an important role in many behaviors including sleep, appetite, memory, and mood [52]. People with depressive disorders exhibit low levels of serotonin in the synapses. Protonated serotonin binds to a serotonin reuptake transporter protein, sometimes referred to as the serotonin transporter (SERT) and is then moved to an inward position on the neuron and subsequently released into the cjdoplasm. Selective serotonin reuptake inhibitors (SSRI) bind with high affinity to the serotonin binding site of the transporter. This leads to antidepressant effects by increasing extracellular serotonin levels which in turn enhances serotonin neurotransmission [53]. The SSRI class of antidepressants has fewer side effects than the monoamine oxidase inhibitors. 

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