Brain Serotonin (brain + serotonin)

Distribution by Scientific Domains
Life Sciences75%

Terms modified by Brain Serotonin

  • brain serotonin synthesis
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    Selected Abstracts

    Serotonin transporter, 5-HT1A receptor, and behavior in DBA/2J mice in comparison with four inbred mouse strains

    JOURNAL OF NEUROSCIENCE RESEARCH, Issue 16 2009
    Nina K. Popova
    Abstract Prepulse inhibition (PPI), the reduction in acoustic startle produced when it is preceded by a weak prepulse stimulus, is impaired in schizophrenic patients. The DBA/2J mouse strain displayed deficient PPI and is therefore suggested as an experimental animal model for the loss of sensorimotor gating in schizophrenia. Brain serotonin (5-HT) has been implicated in the pathophysiology of several psychiatric disorders, including major depressive disorder and schizophrenia. In the present study, behavior, 5-HT transporter (5-HTT) mRNA level, 5-HT1A receptor mRNA level, and 5-HT1A receptor density in the brain regions were studied in DBA/2J mice in comparison with four inbred mouse strains (CBA/Lac, C57BL/6, BALB/c, and ICR). A decrease in 5-HTT mRNA level in the midbrain and a reduced density of 5-HT1A receptors in the frontal cortex without significant changes in 5-HT1A receptor mRNA level in DBA/2J mice were found. It was shown that, along with decreased PPI, DBA/2J mice demonstrated considerably reduced immobility in the tail suspension test and in the forced swim test. No significant interstrain differences in intermale aggression, or in light-dark box and elevated plus-maze tests, were found. The results suggested the involvement of decreased 5-HTT gene expression and 5-HT1A receptor density in genetically defined PPI deficiency and showed a lack of any association between PPI deficiency and predisposition to aggressive, anxiety, and depressive-like behaviors. © 2009 Wiley-Liss, Inc. [source]

    Alcohol and violence and the possible role of serotonin

    CRIMINAL BEHAVIOUR AND MENTAL HEALTH, Issue 1 2003
    Abdulla A.-B.
    Background There is undisputed evidence linking alcohol consumption and violence and other forms of aggressive behaviour, and also linking aggression with dysfunction of the brain indolylamine serotonin (5-hydroxytryptamine or 5-HT). Alcohol consumption also causes major disturbances in the metabolism of brain serotonin. In particular, acute alcohol intake depletes brain serotonin levels in normal (non-alcohol-dependent) subjects. On the basis of the above statements, it is suggested that, at the biological level, alcohol may induce aggressive behaviour in susceptible individuals, at least in part, by inducing a strong depletion of brain serotonin levels. Aims In this article, evidence supporting these interrelationships and interactions will be summarized and discussed, the alcohol,serotonin,aggression hypothesis will be reiterated, and potential intervention strategies will be proposed. Copyright © 2003 Whurr Publishers Ltd. [source]

    Altered presynaptic function in monoaminergic neurons of monoamine oxidase-A knockout mice

    EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 9 2002
    Catarina Å. Owesson
    Abstract Monoamine oxidase-A knockout (MAO-A KO) mice have elevated brain serotonin (5-HT) and noradrenaline (NA) levels, and one would therefore anticipate increased monoamine release and compensatory changes in other aspects of presynaptic monoamine function. In this study we used voltammetry in brain slices from the locus coeruleus (LC), dorsal raphe (DRN) and striatum (CPu) in 7-week-old MAO-A KO and C3H control mice to measure stimulated monoamine efflux and its control by amine transporters and autoreceptors. In LC, peak NA efflux on stimulation (99 pulses, 100 Hz) was higher in MAO-A KO than C3H mice (938 ± 58 nm cf. 511 ± 42 nm; P < 0.001). The NA uptake half time (t½) was longer in MAO-A KO than in C3H mice (6.0 ± 0.9 s cf. 1.9 ± 0.3 s; P < 0.001) and the selective NA reuptake inhibitor desipramine (50 nm) had a smaller effect in MAO-A KO mice. NA transporter binding was significantly lower in the LC of MAO-A KO mice compared to C3H controls (P < 0.01) but not in the DRN. The ,2 agonist dexmedetomidine (10 nm) decreased stimulated NA efflux more in C3H than in MAO-A KO mice (73.3% cf. 29.6% inhibition, P < 0.001). In DRN, peak 5-HT efflux on stimulation (99 pulses, 100 Hz) was greater (P < 0.01) in MAO-A KO (262 ± 44 nm) than C3H mice (157 ± 16 nm). Moreover, 5-HT uptake t½ was longer (P < 0.05) in MAO-A KO than in C3H mice (8.8 ± 1.1 s cf. 4.9 ± 0.6 s, P < 0.05) and the effect of citalopram (75 nm) was attenuated in MAO-A KOs. Serotonin transporter binding was also lower in both the DRN and LC of MAO-A KO mice. The 5-HT1A agonist 8-OH-DPAT (1 µm) decreased 5-HT efflux more in C3H than in MAO-A KO mice (38.3% inhibition cf. 21.6%, P < 0.001). In contrast, there were no significant differences between MAO-A KO and C3H mice in CPu dopamine efflux and uptake and the effect of the D2/3 agonist quinpirole was similar in the two strains. In summary, MAO-A KO mice show major dysregulation of monoaminergic presynaptic mechanisms such as autoreceptor control and transporter kinetics. [source]

    Role of TPH-2 in brain function: News from behavioral and pharmacologic studies

    JOURNAL OF NEUROSCIENCE RESEARCH, Issue 14 2007
    Roberto W. Invernizzi
    Abstract The recent discovery of TPH-2, a new isoform of tryptophan hydroxylase, the enzyme that catalyses the transformation of tryptophan into 5-hydroxytryptophan and the rate-limiting step in brain serotonin (5-HT) biosynthesis, has boosted new interest in the many functions of 5-HT in the brain and non-nervous tissues. Recent studies on TPH-2 are reviewed with particular attention to the role of this enzyme in behavior and in response to drugs as assessed by comparing strains of mice carrying a functional polymorphism of TPH-2. Most studies concur to indicate that 5-HT synthesis through TPH-2 influence nervous tissues whereas TPH-1 is responsible for the synthesis and action of 5-HT in peripheral organs. Partial impairment of brain 5-HT synthesis caused by polymorphism of the gene encoding TPH-2 causes reduced release of the neurotransmitter, increased aggressiveness, and alters the response to drugs inhibiting the reuptake of 5-HT. Strain comparison might be a useful strategy to investigate the genotype-dependent alterations of TPH-2. © 2007 Wiley-Liss, Inc. [source]