000			nab a22 7a 4500
999			_c17997 _d17997
003			PC17997
005			20250616132913.0
008			250616b xxu||||| |||| 00| 0 eng d
040			_cH12O
041			_aeng
100			_92616 _aLópez Muñoz, Francisco _eInstituto de Investigación i+12
245	0	0	_aMechanism of action of guanfacine: a postsynaptic differential approach to the treatment of attention deficit hyperactivity disorder (adhd). _h[revisión]
260			_bActas españolas de psiquiatría, _c2016
300			_a44(3):107-12.
500			_aFormato Vancouver: Alamo C, López Muñoz F, Sánchez García J. Mechanism of action of guanfacine: a postsynaptic differential approach to the treatment of attention deficit hyperactivity disorder (adhd). Actas Esp Psiquiatr. 2016 May;44(3):107-12.
501			_a PMID: 27254403
504			_aContiene 38 referencias
520			_aThe treatment of ADHD has focused on the use of psychostimulants drugs such as methylphenidate or amphetamine and derivatives, or not stimulants agents, such as atomoxetine. These agents act mainly on catecholaminergic presynaptic mechanisms. Recently the European Medicines Agency (EMA) has approved another not psychostimulant drug, guanfacine extended release (ER), as a new option to the treatment of ADHD, which acts at postsynaptic level. Guanfacine stimulates postsynaptic alfa-2A adrenergic receptors so it inhibits the production of cAMP and closes HCN channels enhancing the effectiveness of the signal of the pyramidal neurons of the prefrontal cortex (PFC), thus improving working memory and attention. In addition, stimulation of the alpha-2A receptors promotes growth and maturation of the dendritic spines of pyramidal neurons of the medial PFc, that are associated with brain function such as learning and memory. In contrast with psychostimulants or atomoxetine, guanfacine mimics noradrenaline stimulation of postsynaptic receptors alfa-2A on the PFC.
710			_9625 _aInstituto de Investigación imas12
856			_uhttp://pc-h12o-es.m-hdoct.a17.csinet.es/pdf/pc/1/pc17997.pdf _ySolicitar documento
942			_2ddc _cREV _n0