Efectos neurobiológicos de la psicoterapia / Neurobiologic effects of psycotherapy / Efeitos neurobiologicos da psicoterapia

La psicoterapia permanece como una opción de tratamiento vigente en diversos tipos de trastornos psiquiátricos. Aunque su efectividad ha sido ampliamente demostrada desde hace mas de dos décadas, los mecanismo biológicos mediante los cuales ejerce un efecto sobre el funcionamiento cerebral del paciente y su comportamiento, continúan siendo desconocidos. En este artículo se revisan los posibles mecanismos que median su efecto sobre el funcionamiento cerebral, entre ellos las bases celulares y moleculares de la memoria, las modificaciones en los sistemas neurotransmisores y la plasticidad sináptica. La revisión de la evidencia acumulada permite sugerir que la psicoterapia ejerce un efecto neurofisiológico al mismo nivel de los fármacos con acción psicotrópica, no obstante, diferencias en especificidad regional y de sistema blanco pueden explicar las diferencias que se observan entre estas dos formas de tratamiento...

Psychotherapy remains an effective option in the treatment of diverse types of psychiatric disorders. Although its effectiveness has been widely demonstrated for more than two decades, the biological mechanisms by means of which it exerts an effect over the brain function and the patient's behavior, continues to be unknown. In this article we review the possible mechanisms that mediate its effect on the brain function, among them the cellular and molecular bases of memory, the modifications in the neurotransmitter systems and the synaptic plasticity. The review of the accumulated evidence allows us to suggest that psychotherapy exerts a neurophysiologic effect at the same level of psychotropic drugs; however, differences in regional specificity and of the white system may explain the differences that are observed between these two forms of treatment...

A psicoterapia permanece como uma opção vigente de tratamento em tipos diversos de transtornos psiquiátricos. Embora sua eficácia seja demonstrada extensamente por mais de duas décadas, o mecanismo biológico por meio de qual exerce um efeito na função cerebral do paciente e de seu comportamento, continua sendo desconhecido. Neste artigo são revistos os possíveis mecanismos que mediam seu efeito na função cerebral, entre eles as bases celulares e moleculares da memória, as modificações nos sistemas neurotransmissores e a plasticidade sináptica. A revisão da evidência acumulada permite sugerir que a psicoterapia exerce um efeito neurofisiológico ao mesmo nível que os fármacos com ação psicotrópica, entretanto, diferenças em especificidade regional e do sistema branco podem explicar as diferenças que são observadas entre estas dois formas do tratamento...

Synaptic physiology of central CRH system.

Corticotropin-Releasing Hormone (CRH) or Corticotropin-Releasing Factor (CRF) and its family of related naturally occurring endogenous peptides and receptors are becoming recognized for their actions within central (CNS) and peripheral (PNS) nervous systems. It should be recognized that the term 'CRH' has been displaced by 'CRF' [Guillemin, R., 2005. Hypothalamic hormones a.k.a. hypothalamic releasing factors. J. Endocrinol. 184, 11-28]. However, to maintain uniformity among contributions to this special issue we have used the original term, CRH. The term 'CRF' has been associated recently with CRH receptors and designated with subscripts by the IUPHAR nomenclature committee [Hauger, R.L., Grigoriadis, D.E., Dallman, M.F., Plotsky, P.M., Vale, W.W., Dautzenberg, F.M., 2003. International Union of Pharmacology. XXXVI. Corticotrophin-releasing factor and their ligands. Pharmacol. Rev. 55, 21-26] to denote the type and subtype of receptors activated or antagonized by CRH ligands. CRH, as a hormone, has long been identified as the regulator of basal and stress-induced ACTH release within the hypothalamo-pituitary-adrenal axis (HPA axis). But the concept, that CRH and its related endogenous peptides and receptor ligands have non-HPA axis actions to regulate CNS synaptic transmission outside the HPA axis, is just beginning to be recognized and identified [Orozco-Cabal, L., Pollandt, S., Liu, J., Shinnick-Gallagher, P., Gallagher, J.P., 2006a. Regulation of Synaptic Transmission by CRF Receptors. Rev. Neurosci. 17, 279-307; Orozco-Cabal, L., Pollandt, S., Liu, J., Vergara, L., Shinnick-Gallagher, P., Gallagher, J.P., 2006b. A novel rat medial prefrontal cortical slice preparation to investigate synaptic transmission from amygdala to layer V prelimbic pyramidal neurons. J. Neurosci. Methods 151, 148-158] is especially noteworthy since this synapse has become a prime focus for a variety of mental diseases, e.g. schizophrenia [Fischbach, G.D., 2007. NRG1 and synaptic function in the CNS. Neuron 54, 497-497], and neurological disorders, e.g., Alzheimer's disease [Bell, K.F., Cuello, C.A., 2006. Altered synaptic function in Alzheimer's disease. Eur. J. Pharmacol. 545, 11-21]. We suggest that "The Stressed Synapse" has been overlooked [c.f., Kim, J.J., Diamond, D.M. 2002. The stressed hippocampus, synaptic plasticity and lost memories. Nat. Rev., Neurosci. 3, 453-462; Radley, J.J., Morrison, J.H., 2005. Repeated stress and structural plasticity in the brain. Ageing Res. Rev. 4, 271-287] as a major contributor to many CNS disorders. We present data demonstrating CRH neuroregulatory and neuromodulatory actions at three limbic synapses, the basolateral amygdala to central amygdala synapse; the basolateral amygdala to medial prefrontal cortex synapse, and the lateral septum mediolateral nucleus synapse. A novel stress circuit is presented involving these three synapses. We suggest that CRH ligands and their receptors are significant etiological factors that need to be considered in the pharmacotherapy of mental diseases associated with CNS synaptic transmission.