Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P08908 (5-HT1A)
 5,574 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antisocial behaviour is both heterogeneous and the product of interacting genetic and environmental factors acting at different levels of causation. Heritability studies show that individual differences in predisposition to antisocial behaviour are transmitted vertically in families by genetic mechanisms. Owing to aetiological heterogeneity and complexity, study of a variety of other behavioural phenotypes may shed more light on the antecedents of antisocial behaviour than direct studies on antisocial behaviour. Identification of genetic vulnerability factors would clarify mechanisms of vulnerability and the role of the environment. Direct gene analysis and genetic linkage analysis have identified structural variants in genes involved in neurotransmitter function, and some progress has been made towards relating these genetic variants to antisocial personality and other behaviours. Thyroid hormone receptor variants can cause attention deficit/hyperactivity disorder, and a monoamine oxidase A variant leads to aggressive behaviour in one family. Direct gene analyses have revealed non-conservative amino acid substitutions and structural variants (generally rare) at DRD2, DRD3 and DRD4 dopamine receptors and 5-HT1A, 5-HT2A, 5-HT2C and 5-HT7 serotonin receptors. The stage is set to identify the phenotypic significance of these as well as genetic variants at other loci which may be relevant as candidate genes for antisocial behaviour and related behavioural differences.
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PMID:Direct analysis of candidate genes in impulsive behaviours. 886 74

Thyroid hormones, particularly triiodothyronine (T3), have long been used for the treatment of depression, most frequently to enhance the therapeutic activity of other antidepressants. The purpose of this study was to evaluate possible underlying mechanisms for the antidepressant activity of T3. The effects of T3 20 microg/kg/d S.C. and fluoxetine 5mg/kg/d I.P. given alone or in combination for 7 days on the transcription rates of inhibitory serotonergic receptors (5-HT1A and 5-HT1B) were studied in different brain areas of male Sabra rats using real-time PCR. Significant effects of fluoxetine were found on the expression of 5-HT1B receptors in the frontal cortex and of T3 on the expression of 5-HT1A receptors in the amygdala and hippocampus and 5-HT1B receptors in the frontal and entorhinal cortices, the expression being reduced in all cases. An effect of the combination of T3 plus fluoxetine to reduce transcription was observed for 5-HT1A receptors, in the amygdala and dentate gyrus and for 5-HT1B receptors in the entorhinal cortex and anterior raphe nucleus. In the second experiment, the novelty suppressed feeding test (NFST) was used to examine the effects of fluoxetine 5mg/kg/d I.P. and T3 20 or 50 microg/kg/d, alone or in combination for 12 days, on latency to feed. Only the combinations of T3 (20 or 50 microg/kg/d) and fluoxetine (5mg/kg/d) yielded significant behavioral effects in this test. The results of our studies suggest that the mechanism underlying the antidepressant effect of T3 may involve a reduction in 5-HT1A and 5-HT1B receptor transcription rates.
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PMID:Effect of triiodothyronine on 5-HT1A and 5-HT1B receptor expression in rat forebrain and on latency to feed in the novelty suppressed feeding test. 2020 58