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Serotonin neuron-dependent and -independent reduction of dyskinesia by 5-HT1A and 5-HT1B receptor agonists in the rat Parkinson model.
Exp Neurol. 2009 Sep; 219(1):298-307.EN

Abstract

5-HT1 receptor agonists have been shown to reduce abnormal involuntary movements (AIMs) in the rat and monkey models of L-DOPA-induced dyskinesia. Different mechanisms have been proposed to underlie this effect. Activation of pre-synaptic 5-HT1 receptors has been suggested to inhibit dysregulated release of dopamine from the serotonin terminals, and thus, abnormal activation of striatal dopamine receptors. Activation of post-synaptic 5-HT1 receptors expressed in non-serotonergic neurons in different brain areas, by contrast, has been shown to result in decreased glutamate and GABA release, which may also contribute to the antidyskinetic effect. To unveil the relative contribution of these mechanisms, we have investigated the effect of increasing doses of 5-HT1A and 5-HT1B receptor agonists on AIMs induced by either L-DOPA or apomorphine. In contrast to L-DOPA-induced AIMs, which were dampened already at low doses of 5-HT1 agonists, reduction of apomorphine-induced AIMs required higher doses. Removal of the serotonin innervation suppressed L-DOPA-induced AIMs, but neither affected apomorphine-induced AIMs nor the inhibiting effect of 5-HT1 agonists on AIMs induced by the direct dopamine agonist, suggesting that such effect is independent on activation of pre-synaptic 5-HT1 receptors.

Authors+Show Affiliations

Neurobiology Unit, Wallenberg Neuroscience Center, Department of Experimental Medical Science, Lund University, Lund, Sweden.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19500572

Citation

Muñoz, Ana, et al. "Serotonin Neuron-dependent and -independent Reduction of Dyskinesia By 5-HT1A and 5-HT1B Receptor Agonists in the Rat Parkinson Model." Experimental Neurology, vol. 219, no. 1, 2009, pp. 298-307.
Muñoz A, Carlsson T, Tronci E, et al. Serotonin neuron-dependent and -independent reduction of dyskinesia by 5-HT1A and 5-HT1B receptor agonists in the rat Parkinson model. Exp Neurol. 2009;219(1):298-307.
Muñoz, A., Carlsson, T., Tronci, E., Kirik, D., Björklund, A., & Carta, M. (2009). Serotonin neuron-dependent and -independent reduction of dyskinesia by 5-HT1A and 5-HT1B receptor agonists in the rat Parkinson model. Experimental Neurology, 219(1), 298-307. https://doi.org/10.1016/j.expneurol.2009.05.033
Muñoz A, et al. Serotonin Neuron-dependent and -independent Reduction of Dyskinesia By 5-HT1A and 5-HT1B Receptor Agonists in the Rat Parkinson Model. Exp Neurol. 2009;219(1):298-307. PubMed PMID: 19500572.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Serotonin neuron-dependent and -independent reduction of dyskinesia by 5-HT1A and 5-HT1B receptor agonists in the rat Parkinson model. AU - Muñoz,Ana, AU - Carlsson,Thomas, AU - Tronci,Elisabetta, AU - Kirik,Deniz, AU - Björklund,Anders, AU - Carta,Manolo, Y1 - 2009/06/03/ PY - 2009/03/12/received PY - 2009/05/20/revised PY - 2009/05/22/accepted PY - 2009/6/9/entrez PY - 2009/6/9/pubmed PY - 2009/9/26/medline SP - 298 EP - 307 JF - Experimental neurology JO - Exp Neurol VL - 219 IS - 1 N2 - 5-HT1 receptor agonists have been shown to reduce abnormal involuntary movements (AIMs) in the rat and monkey models of L-DOPA-induced dyskinesia. Different mechanisms have been proposed to underlie this effect. Activation of pre-synaptic 5-HT1 receptors has been suggested to inhibit dysregulated release of dopamine from the serotonin terminals, and thus, abnormal activation of striatal dopamine receptors. Activation of post-synaptic 5-HT1 receptors expressed in non-serotonergic neurons in different brain areas, by contrast, has been shown to result in decreased glutamate and GABA release, which may also contribute to the antidyskinetic effect. To unveil the relative contribution of these mechanisms, we have investigated the effect of increasing doses of 5-HT1A and 5-HT1B receptor agonists on AIMs induced by either L-DOPA or apomorphine. In contrast to L-DOPA-induced AIMs, which were dampened already at low doses of 5-HT1 agonists, reduction of apomorphine-induced AIMs required higher doses. Removal of the serotonin innervation suppressed L-DOPA-induced AIMs, but neither affected apomorphine-induced AIMs nor the inhibiting effect of 5-HT1 agonists on AIMs induced by the direct dopamine agonist, suggesting that such effect is independent on activation of pre-synaptic 5-HT1 receptors. SN - 1090-2430 UR - https://www.unboundmedicine.com/medline/citation/19500572/Serotonin_neuron_dependent_and__independent_reduction_of_dyskinesia_by_5_HT1A_and_5_HT1B_receptor_agonists_in_the_rat_Parkinson_model_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4886(09)00226-X DB - PRIME DP - Unbound Medicine ER -