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5-HT2 Receptor

The Experts below are selected from a list of 273 Experts worldwide ranked by ideXlab platform

Frank J Nash – 1st expert on this subject based on the ideXlab platform

  • potentiation of 3 4 methylenedioxymethamphetamine induced dopamine release and serotonin neurotoxicity by 5 ht2 Receptor agonists
    European Journal of Pharmacology, 1994
    Co-Authors: Gary A Gudelsky, Bryan K Yamamoto, Frank J Nash


    Abstract The effects of the 5-HT2 Receptor agonists 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) and 5-methoxy-N,N-dimethyltryptamine (5-MeODMT) on 3,4-methylenedioxymethamphetamine (MDMA)-induced dopamine release and 5-HT depletion in the striatum were studied. The MDMA-induced increase in the extracellular concentration of dopamine in the striatum was enhanced significantly in rats treated with either DOI (2 mg/kg, ip.) or 5-MeODMt (15 mg/kg, ip.), as assessed using in vivo microdialysis. Neither DOI nor 5-MeODMT alone altered the extracellular concentration of dopamine in the striatum. The striatal concentration of 5-HT was decreased, but not significantly, 7 days following a single administration of MDMA (10 mg/kg, sc.). However, 7 days following the concomitant treatment with DOI and MDMA the striatal concentration of 5-HT was significantly less than that in rats treated with MDMA alone or the vehicle-treated controls. It is concluded that activation of 5-HT2 Receptors is an important determinant of the acute increase in extracellular dopamine and, consequently, the long-term depletion of brain 5-HT produced by MDMA.

Efrain C Azmitia – 2nd expert on this subject based on the ideXlab platform

  • activation of glycogen phosphorylase by serotonin and 3 4 methylenedioxymethamphetamine in astroglial rich primary cultures involvement of the 5 ht2a Receptor
    Brain Research, 1995
    Co-Authors: Jose C Poblete, Efrain C Azmitia


    Neurotransmitters, neuropeptides, and ions regulate glycogen levels in the brain by modulating the activity of glycogen synthase (GSase) and glycogen phosphorylase (GPase). GPase is co-localized with glial fibrillary acidic protein (GFAP), an astroglia-specific marker, suggesting that glycogen is localized in astroglial cells. Additionally, functional serotonin (5-HT) Receptors are found in both neurons and glia, and 5-HT is known to stimulate glycogenolysis. It is reported that 3,4-methylenedioxymethamphetamine (MDMA), a drug of abuse, stimulates the release and inhibits the reuptake of 5-HT, and selectively inhibits the activity of MAO-A. These biochemical consequences of MDMA lead to increased extra-cellular 5-HT levels. This study investigates the effects of MDMA(+) and serotonin (5-HT) on glycogen metabolism in the rat brain. A histochemical method was designed to visualize active glycogen phosphorylase (GPase) in an astroglial-rich primary culture.

    Serotonin activated GPase in a concentration-dependent manner (100 nM−100 μM). Maximal activation by 5-HT was achieved by 50 μM and resulted in a 167% increase in the number of reactive sites (P < 0.001). MDMA(+) (500 nM−50 μM) directly stimulated GPase activity with maximal activation induced by 5 μM, which caused a 70% increase in the number of reactive sites (P < 0.001). The 5-HT2 Receptor agonist, 1-(2,5-dimethoxy-4-bromophenyl)-2-aminopropane (DOB), also displayed a concentration-dependent increase in the number of GPase reactive sites. Maximal stimulation by DOB occurred at 100 nM which increased the number of reactive sites by 166% (P < 0.001). These effects of 5-HT and MDMA(+) were significantly attenuated by mianserin (200 nM), a 5-HT2 Receptor antagonist.

    An astrocyte-neuron metabolic link may be vital for synaptic homeostasis. By increasing 5-HT levels in the synapse, MDMA(+) may increase GPase activity and promote glycogenolysis via activation of the 5-HT2 Receptor. Prolonged GPase activity may lead to depletion of synaptic energy stores, thereby compromising the energy state of the synapse. The resulting deficiency in synaptic energy may contribute to terminal degeneration induced by substituted amphetamines.

AG Ramage – 3rd expert on this subject based on the ideXlab platform

  • Investigation of the role of 5-HT2 Receptor subtypes in the control of the bladder and the urethra in the anaesthetized female rat
    Co-Authors: AG Ramage


    Background and purpose: Micturition is controlled by central 5-HT-containing pathways. 5-HT2 Receptors have been implicated in this system especially in control of the urethra, which is a drug target for treating urinary incontinence. This study investigates the role of each of the three subtypes of this Receptor with emphasis on sphincter regulation.Experimental approach: Recordings of urethral and bladder pressure, external urethral sphincter (EUS) EMG, as well as the micturition reflex induced by bladder distension along with blood pressure and heart rate were made in anaesthetized rats. The effects of agonists and antagonists for 5-HT2 Receptor subtypes were studied on these variables.Key results: The 5-HT2C agonists Ro 60-0175, WAY 161503 and mCPP, i.v., activated the EUS, increased urethral pressure and inhibited the micturition reflex. The effects of Ro 60-0175 on the EUS were blocked by the 5-HT2C antagonist SB 242084 and the 5-HT2A antagonists, ketanserin and MDL 100907. SB 242084 also blocked the inhibitory action on the reflex, while the 5-HT2B antagonist RS 127445 only blocked the increase in urethral pressure. The 5-HT2A Receptor agonist DOI given i. v. or i.t. but not i. c. v. activated the EUS.Conclusions and implications: 5-HT2A/2C Receptors located in the sacral spinal cord activate the EUS, while central 5-HT2C Receptors inhibit the micturition reflex and 5-HT2B Receptors, probably at the level of the urethra, increase urethral smooth muscle tone. Furthermore, 5-HT2B and 5-HT2C Receptors do not seem to play an important role in the physiological regulation of micturition.

  • Chronic treatment, with mianserin prevents, DOCA-salt hypertension in rats – evidence for the involvement of central 5-HT2 Receptors
    Co-Authors: AG Ramage


    Central 5-HT2A Receptors have been implicated in central volume control by activating a central angiotensinergic pathway to cause the release of vasopressin. Interestingly, to induce DOCA-salt hypertension in rats vasopressin release is required. Thus the present experiments were carried out to determine whether continuous blockade of these Receptors over 20 days, with the non-selective 5-HT2 Receptor antagonist mianserin would prevent the development of deoxycorticosterone acetate (DOCA)-salt hypertension. Mianserin, given i.c.v. 90 or 60 mu g twice daily for 20 days prevented the development of hypertension in conscious rats receiving DOCA-salt but did not affect blood pressure in rats on salt alone. Further, the dose of 30 mu g given i.c.v. twice daily had no effect nor did the vehicle, polyethylene glycol (PEG), on the development of the hypertension. Mianserin 90 mu g twice daily i.c.v. was also shown to prevent the increase in fluid intake, urinary flow and sodium excretion caused by DOCA-salt treatment. These data indicate that this action of mianserin is not due to an intrinsic hypotensive action but an action which involves interference with the mechanism by which DOCA-salt treatment causes hypertension. Thus the data overall support the view that to induce hypertension with DOCA-salt a central 5-HT-containing pathway needs to be activated, which then activates 5-HT2 Receptors to cause the release of vasopressin which has previously been shown to be responsible for the initiation of DOCA-salt treatment hypertension. (c) 2005 Published by Elsevier B.V.