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Receptors 5-HT1A

abubakar123
15.06.2018

Content:

  • Receptors 5-HT1A
  • 5-HT1A receptors in depression – getting to the hub of the matter
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  • The serotonin 1A receptor (or 5-HT1A receptor) is a subtype of serotonin receptor (5-HT receptor) that binds the neurotransmitter serotonin (5-hydroxytryptamine. 5-HT1A receptors in clinical psychopharmacology: neuropharmacology, their role in anxiety, depression and schizophrenia. List of approved partial agonists. In this review, we examine the function of 5-HT1A receptor sub-populations and re-interpret our understanding of their role in mental illness in.

    Receptors 5-HT1A

    The inhibitory effect of 8-OH-DPAT on the firing activity of dorsal raphe serotoninergic neurons in rats is attenuated by lesion of the frontal cortex. Control of dorsal raphe serotonergic neurons by the medial prefrontal cortex: Rationale and Current Status of Research. Monoamine dysfunction and the pathophysiology and treatment of depression. Brain 5-HT1 binding sites in depressed suicides.

    Psychopharmacology Berl ; Response, partial response, and nonresponse in primary care treatment of depression. Archives of internal medicine. Development and natural history of mood disorders. From synapse to nucleus: Epub Dec Cell-specific repressor or enhancer activities of Deaf-1 at a serotonin 1A receptor gene polymorphism. Increased serotonin-1A 5-HT1A autoreceptor expression and reduced raphe serotonin levels in deformed epidermal autoregulatory factor-1 Deaf-1 gene knock-out mice.

    F, a preferential post-synaptic 5-HT1A receptor agonist: Epub May Psychopharmacology Berl Sep; 1: Autoradiographic analysis of serotonin 5-HT1A receptor binding in the human brain postmortem: PET imaging of serotonin 1A receptor binding in depression. Serotonin type-1A receptor imaging in depression. Serotonin-1A receptor imaging in recurrent depression: The pharmacology of anxiety.

    Curr Top Behav Neurosci. Responsiveness of 5-HT 1A and 5-HT2 receptors in the rat orbitofrontal cortex after long-term serotonin reuptake inhibition. Comparative study of pre- and postsynaptic 5-HT1A receptor modulation of anxiety in two ethological animal tests. Electrophysiological, biochemical, neurohormonal and behavioural studies with WAY, a potent, selective and silent 5-HT1A receptor antagonist.

    A critical period for experience-dependent synaptic plasticity in rat barrel cortex. Pharmacotherapy of social anxiety disorder. Role of 5-HT1A autoreceptors in the mechanism of action of serotoninergic antidepressant drugs: Inhibition by the serotonin 5-HT1A receptor in development and stress. The serotonergic system and anxiety. Nat Rev Drug Discov. Serotonin1A receptor acts during development to establish normal anxiety-like behaviour in the adult.

    The developmental origins of anxiety. Cost of disorders of the brain in Europe Epub Sep Role of the medial prefrontal cortex in 5-HT1A receptor-induced inhibition of 5-HT neuronal activity in the rat.

    The central 5-HT1A receptors: Ann N Y Acad Sci. Elevated anxiety and antidepressant-like responses in serotonin 5-HT1A receptor mutant mice. Role of uptake inhibition and autoreceptor activation in the control of 5-HT release in the frontal cortex and dorsal hippocampus of the rat. Association study between the serotonin 1A receptor HTR1A gene and neuroticism, major depression, and anxiety disorders. Effect of 5-HT1A receptor agonists in two models of anxiety after dorsal raphe injection.

    Psychopharmacology Berl ; 2: Decreased brain serotonin 5-HT1A receptor availability in medication-naive patients with major depressive disorder: Further evidence for the importance of 5-HT1A autoreceptors in the action of selective serotonin reuptake inhibitors.

    Raphe 5-HT1A autoreceptors, but not postsynaptic 5-HT1A receptors or beta-adrenoceptors, restrain the citalopram-induced increase in extracellular 5-hydroxytryptamine in vivo. Response to fluoxetine and serotonin 1A receptor CG polymorphism in Taiwan Chinese major depressive disorder. Serotonergic vulnerability and depression: What do we know about serotonin? Serotonin uptake sites and serotonin receptors are altered in the limbic system of schizophrenics. Increased fear response to contextual cues in mice lacking the 5-HT1A receptor.

    Regional patterns of compensation following genetic deletion of either 5-hydroxytryptamine 1A or 5-hydroxytryptamine 1B receptor in the mouse.

    Reduced anxiety-related behaviour in transgenic mice overexpressing serotonin 1A receptors. Brain Res Mol Brain Res. Curr Top Med Chem. Brain serotonin system in the coordination of food intake and body weight Pharmacol. Reduced serotonin-1A receptor binding in social anxiety disorder. Transcriptional regulation at a HTR1A polymorphism associated with mental illness.

    Impaired repression at a 5-hydroxytryptamine 1A receptor gene polymorphism associated with major depression and suicide.

    Anxiety as a developmental disorder. Focus on The 5-HT1A receptor: Altered depression-related behaviors and functional changes in the dorsal raphe nucleus of serotonin transporter-deficient mice. Stimulation of cAMP synthesis by Gi-coupled receptors upon ablation of distinct Galphai protein expression. Gi subtype specificity of the 5-HT1A receptor. Regulation of 5-HT receptors and the hypothalamic-pituitary-adrenal axis.

    Implications for the neurobiology of suicide. Behavioral studies of serotonin receptor agonists as antidepressant drugs. Functional consequences of 5-HT transporter gene disruption on 5-HT 1a receptor-mediated regulation of dorsal raphe and hippocampal cell activity. Region-dependent effects of flibanserin and buspirone on adenylyl cyclase activity in the human brain. Int J Neuro- psychopharmacol.

    Exposure to inescapable but not escapable shock increases extracellular levels of 5-HT in the dorsal raphe nucleus of the rat. Serotonergic measures in suicide brain: J Neural Transm Gen Sect. The antidepressant fluoxetine restores plasticity in the adult visual cortex.

    Serotonin triggers a transient epigenetic mechanism that reinstates adult visual cortex plasticity in rats. Antidepressant-like behavioral effects in 5-hydroxytryptamine 1A and 5-hydroxytryptamine 1B receptor mutant mice. EEG effects of buspirone and pindolol: Psychopharmacology Berl Mar; 3: Epub Feb Corticosteroid receptors in brain: Receptor reserve for 5-hydroxytryptamine1A-mediated inhibition of serotonin synthesis: Serotonin 1A receptor binding and treatment response in late-life depression.

    Polymorphic variation at the serotonin 1-A receptor gene is associated with comorbid depression and generalized anxiety. Diathesis-stress theories in the context of life stress research: Comparison of the maturation of the adrenergic and serotonergic neurotransmitter systems in the brain: Late developmental stage-specific role of tryptophan hydroxylase 1 in brain serotonin levels.

    Serotonin 5-HT1A receptor binding in people with panic disorder: Comorbidity of mood and anxiety disorders: Epub Mar Reduced serotonin type 1A receptor binding in panic disorder.

    Signal transduction and functional selectivity of F, a preferential post-synaptic 5-HT1A receptor agonist. Biased agonism at serotonin 5-HT1A receptors: Cortical GABA, striatal dopamine and midbrain serotonin as the key players in compulsive and anxiety disorders-results from in vivo imaging studies.

    Sustained neurobehavioral effects of exposure to SSRI antidepressants during development: A study in male and female 5-HT transporter knockout rats: Mental Health Disorders Management: Behavioral and neurochemical effects of 5- 4-[4- 5-Cyanoindolyl -butyl -butyl]piperazinyl -benzofurancarboxamide EMD Increased anxiety of mice lacking the serotonin1A receptor.

    Higher 5-HT1A receptor binding potential during a major depressive episode predicts poor treatment response: Higher serotonin 1A binding in a second major depression cohort: Epub Sep 1.

    Can we really accelerate and enhance the selective serotonin reuptake inhibitor antidepressant effect?. A randomized clinical trial and a meta-analysis of pindolol in nonresistant depression. Epub Oct The depressive-like behaviors are correlated with decreased phosphorylation of mitogen-activated protein kinases in rat brain following chronic forced swim stress. Fluoxetine increases the activity of the ERK-CREB signal system and alleviates the depressive-like behavior in rats exposed to chronic forced swim stress.

    A role for the extracellular signal-regulated kinase signal pathway in depressive-like behavior. Serotonin receptor 1A knockout: The pharmacologic treatment of anxiety disorders: Somatodendritic localization of 5-HT1A and preterminal axonal localization of 5-HT1B serotonin receptors in adult rat brain. Serotonin-1A autoreceptors are necessary and sufficient for the normal formation of circuits underlying innate anxiety.

    Combined administration of a 5-hydroxytryptamine 5-HT1D antagonist and a 5-HT reuptake inhibitor synergistically increases 5-HT release in guinea pig hypothalamus in vivo.

    Mood is indirectly related to serotonin, norepinephrine and dopamine levels in humans: The use of placebos in unipolar major depression: Requirement of hippocampal neurogenesis for the behavioral effects of antidepressants. The C G polymorphism of the 5-HT1A gene promoter and antidepressant response in mood disorders: Influence of escitalopram treatment on 5-HT 1A receptor binding in limbic regions in patients with anxiety disorders.

    Curr Opin Investig Drugs. A Systematic Review of the Published Literature". Archived from the original on 20 June Drug Metabol Drug Interact. Methods Find Exp Clin Pharmacol. Effects on sleep REM latency and body temperature". Curr Top Med Chem. Implications for the development of novel antidepressants with a short onset of action".

    Archived from the original on Pharmacology Biochemistry and Behavior. Lesch KP, Gutknecht L Kalipatnapu S, Chattopadhyay A Regulation of cyclic AMP levels and T cell proliferation by 5-hydroxytryptamine".

    Parks CL, Shenk T Retrieved 11 April Cell surface Intracellular Co-receptor. Signal transducing adaptor protein Scaffold protein. Intracrine action Neurocrine signaling Synaptic transmission Chemical synapse Neuroendocrine signaling Exocrine signalling Pheromones Mechanotransduction Phototransduction Ion channel gating Gap junction.

    GPR 1 3 4 6 12 15 17 18 19 20 21 22 23 25 26 27 31 32 33 34 35 37 39 42 44 45 50 52 55 61 62 63 65 68 75 77 78 81 82 83 84 85 87 88 92 A B B GPR 56 64 97 98 AR-A Beta blockers e. Agomelatine Atypical antipsychotics e.

    With this aim, the effect of either a selective 5-HT 1A receptor antagonist WAY; N [4- 2-methoxyphenylpiperazinyl]ethyl]- N pyridinylcyclohexane carboxamide or a selective 5-HT 1A receptor agonist 8-OH-DPAT; 8-hydroxy di- n -propylamine tetralin hydrobromide was investigated in mice in combination with venlafaxine by means of the forced swimming test, a paradigm aimed at screening potential antidepressants, and the hot-plate test, a phasic pain model.

    Surprisingly, the results showed that WAY produced a large decrease in the antidepressant-like effect of venlafaxine, while 8-OH-DPAT rendered effective a non-effective dose of this antidepressant.

    These findings show that 5-HT 1A receptors play differing roles in modulating the antidepressant-like and antinociceptive effects of venlafaxine in the models investigated. The results imply that blockade of the 5-HT 1A receptors in the forebrain will counteract the favourable antidepressant-like effect at raphe nuclei level, and consequently, the overall effect evidenced is an antagonism.

    This suggests a predominant role of 5-HT 1A receptors located in the forebrain area for the antidepressant-like effect.

    In contrast, the antinociceptive effect of venlafaxine is probably potentiated due to the blockade of somatodendritic 5-HT 1A receptors in the same raphe nuclei, facilitating the descending monoaminergic pain control system. Pain is one of the most prevalent physical symptoms in depression, which makes the treatment and the prognosis of the illness difficult Greden, Antidepressants are the first-line drugs for the treatment of depression, but they are also among the first choices for the treatment of some painful conditions.

    Specifically, evidence exists that dual antidepressants [serotonin 5-HT and noradrenaline NA reuptake inhibitors] have greater efficacy than selective ones for pain relief, with the older tricyclics still being the first choice Eschalier et al. Recently, a number of controlled trials with the new dual class of antidepressants venlafaxine, duloxetine and milnacipran suggest that these compounds could have a therapeutic analgesic potential Briley, ; Saarto and Wiffen, ; Urquhart et al. In the case of venlafaxine, it has been shown to be effective in relieving pain of several aetiologies such as diabetic neuropathy, migraine and fibromyalgia Ozyalcin et al.

    In spite of these favourable clinical perspectives its analgesic mechanism of action remains elusive. Based on reports of the known comorbidity between chronic pain and depressive illness, it is possible that these disease states are linked, i. In particular, it has been suggested that 5-HT 1A receptors play a role in the regulation of cognitive, emotional, and pain states due to their elevated presence in specific brain areas, such as the raphe nuclei, cerebral cortex, limbic system, hypothalamus and spinal cord.

    In the raphe nuclei they function as somatodendritic autoreceptors, controlling 5-HT release and can be activated with an acute injection of an inhibitor of 5-HT reuptake, such as venlafaxine, limiting the increase in extracellular 5-HT in projection areas such as the forebrain Bortolozzi et al. Consequently, antidepressants' greater or lesser degree of clinical effectiveness has been related to the blockade of 5-HT 1A receptor activity in the raphe nuclei Adell et al.

    A similar mechanism, which involves the raphe spinal pathway descending monoaminergic pain control system , has been suggested for 5-HT 1A autoreceptors in analgesia Mico et al. In forebrain areas, the activation of post-synaptic 5-HT 1A receptors has been related to the antidepressant effect of tricyclic antidepressants, selective serotonin reuptake inhibitors SSRIs , venlafaxine and electroconvulsive shock treatment Beique et al.

    Moreover, in the spinal cord, the activation of 5-HT 1A receptors has been related to both pro- and antinociceptive effects Millan, Considering these findings, different pharmacological consequences may be triggered by either the activation or antagonism of different 5-HT 1A receptor populations, this being of particular interest in the coexistence and treatment of pain and depression.

    From a preclinical point of view, conflicting data exist with respect to the effect of the modulation of 5-HT 1A receptors on the action of antidepressants. For instance, in the forced swimming test FST , one of the most used tests to detect antidepressant-like activity, the blockade of 5-HT 1A receptors enhanced the antidepressant-like activity of the selective and dual reuptake inhibitors Millan et al.

    These differing effects have also been reported in patients with clinical depression. In this sense, it has been demonstrated recently that pindolol a partial 5-HT 1A receptor antagonist accelerates the antidepressant response but does not increase the effectiveness of SSRIs in unresponsive patients for review see Artigas et al.

    In rats, different dosage ranges or experimental procedures might account for these differences. Regarding pain models, we and others have demonstrated an augmentation of the antinociceptive effect of different compounds with antidepressant-like effects when they are combined with 5-HT 1A antagonists Ardid et al.

    Unfortunately, at the present time no clinical data have been reported regarding this approach in humans with chronic pain. Taking into account that depression and pain are two entities which are sometimes interrelated and that venlafaxine has antidepressant and analgesic effects, and in view of the importance of 5-HT 1A receptors in modulating both states, the aim of the present study has been to investigate the role these receptors play in the modulation of these functions in the effect of venlafaxine.

    Experiments were performed using male albino CD1 mice 25—30 g. Animals were maintained under standard conditions: Animals were housed in groups of 10, and a 7-d acclimatization period was allowed before the experiments began. All mice were experimentally naive and used only once and 9—10 subjects were used per group. The experiments were performed during the light phase between The following drugs were used in the study: All drugs were freshly prepared immediately prior to use.

    They were dissolved in physiological saline 0. Control animals received saline only. The treatments were administered under blind conditions. The FST was used to determine the role of 5-HT 1A receptors in the antidepressant-like effect of venlafaxine, following the classic method described by Porsolt et al. Tests were video-recorded and subsequently a highly trained observer, who was unaware of the treatment, evaluated the duration of immobility during the last 4 min of the 6-min testing period.

    A mouse was judged to be immobile when it remained floating in the water making only the movements necessary to keep its head above the water. Reduction of immobility in this test was considered to indicate antidepressant activity. The hot-plate test was used as a phasic pain model in order to evaluate the role of 5-HT 1A receptors in the antinociceptive effect of venlafaxine.

    Animals were treated under the same conditions as for antidepressant testing. Latency was considered as the time in seconds between when the animal was placed on the hot-plate surface and when it either licked or shook its hind paw or jumped. These responses are considered to be supraspinally integrated Le Bars et al. Basal latency was determined as the mean of two trials with a delay of 30 min between each one in order to randomize animal groups.

    After this, test latency was determined after drug injection. A cut-off time was established at 60 s in order to avoid tissue damage to the animal. The activity was monitored for 10 min. First, dose—response relationships were established for venlafaxine in the FST 2. Second, the role of blockade of 5-HT 1A receptors on both the antidepressant-like and antinociceptive effects was studied. Fourth, locomotor activity was assessed in order to explore the possible role of motor activity in the results obtained in the FST and hot-plate test.

    In the FST, the antidepressant-like effect was evaluated and expressed as immobility time in seconds. Locomotor activity was expressed as the mean activity counted arbitrary units. In the hot-plate test, the level of analgesia was expressed as latency time in seconds. The effects of venlafaxine compared to the saline group were established by a one-way analysis of variance ANOVA followed by Dunnett's test.

    The factors of variation were venlafaxine treatment and 5-HT 1A receptor antagonist or agonist treatment.

    5-HT1A receptors in depression – getting to the hub of the matter

    One target that might help antidepressant drugs work faster is one of the many receptors for serotonin, the 5-HT1A receptor. Receptors are. The 5-HT1A receptor is an inhibitory G-protein-coupled receptor found in the region of origin of 5-HT projections in the CNS, the raphe nuclei of the brainstem. The Serotonin 5HT1A receptor is more important than you think. Even if you don't have your genetic data from 23andme, you should still read.

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