Neuropéptidos en el encéfalo humano / Neuropeptides in the human brain

Resumen: los estudios en el encéfalo humano se han realizado con el fin de responder a varias preguntas de carácter científico relacionados con la neuroanatomía, neurofisiología, neurofarmacología,la neurología y la conducta. El encéfalo es el órgano en el que se encuentra la regulación de los reflejos y los mecanismos inconscientes como la transmisión del dolor, los cardiovasculares, los respiratorios, entre otros. Estos mecanismos están mediados por sustancias químicas tales como los neuropéptidos, que son cadenas cortas de aminoácidos que se han encontrado ampliamente distribuidos en el sistema nervioso central y periférico, además de ejercer acciones fisiológicas actuando como neurotransmisores, neuromoduladores (acciones paracrinas y autocrinas) y neurohormonas.En los últimos treinta años se ha incrementado el conocimiento sobre la distribución y función de los neuropéptidos en el sistema nervioso central de mamíferos (ratas, gatos, perros, alpacas, primates y humanos). Así, el objetivo de esta revisión se dirige a describir los datos más relevantes disponibles sobre los neuropéptidos en el encéfalo humano. Para ello se revisan aspectosimportantes de los neuropéptidos en el encéfalo humano como: a) La distribución, b) Las relaciones anatómicas, c) Las funciones fisiológicas, d) La coexistencia, y e) Las investigaciones futuras a realizar.

Abstract: the human brain has been used in laboratory as an experimental model in order to answer several scientific questions related to neuroanatomy, neurophysiology, neuropharmacology, neurology and behavior. The brain is the organ in which the regulation of reflexes and ®unconscious¼ mechanisms(transmission of pain, cardiovascular, respiratory, etc.) are carried out. These mechanisms are mediated by chemicals such as neuropeptides, which are shorter chains of amino acids that have been showed widely distributed in the central and peripheral nervous system and to exert physiologicalactions acting as neurotransmitters, neuromodulators (paracrine action and autocrine) and neurohormones.In the last thirty years, it has increased the knowledge on the distribution and function of neuropeptides in the central nervous system of mammals (rats, cats, dogs, alpaca, primates, and humans). Thus, the aim of this paper is to describe the most relevant information available about neuropeptides in the human brain. To do so will raise issues about neuropeptides in the human brain as: a) The distribution; b) The anatomical relationship; c) The physiological functions; d) The coexistence;and e) The related future research to make.

Inducible-NOS but not neuronal-NOS participate in the acute effect of TNF-alpha on hypothalamic insulin-dependent inhibition of food intake.

TNF-alpha acts on the hypothalamus modulating food intake and energy expenditure through mechanisms incompletely elucidated. Here, we explore the hypothesis that, to modulate insulin-induced anorexigenic signaling in hypothalamus, TNF-alpha requires the synthesis of NO. TNF-alpha activates signal transduction through JNK and p38 in hypothalamus, peaking at 10(-8) M. This is accompanied by the induction of expression of the inducible and neuronal forms of NOS, in both cases peaking at 10(-12) M. In addition, TNF-alpha stimulates NOS catalytic activity. Pre-treatment with TNF-alpha at a low dose (10(-12) M) inhibits insulin-dependent anorexigenic signaling, and this effect is abolished in iNOS but not in nNOS knockout mice.

Catalepsy induced by intra-striatal administration of nitric oxide synthase inhibitors in rats.

Systemic administration of nitric oxide synthase (NOS) inhibitors induces catalepsy in a dose-dependent manner in male Albino-Swiss mice. The objective of the present work was to investigate if similar effects occur in rats and if these effects are centrally mediated. The results showed that systemic administration of N(G)-nitro-L-arginine (L-NOARG, 40-160 mg/kg, i.p.), a non-selective NOS inhibitor, induced catalepsy in rats. Similar effects were found after intracerebroventricular (i.c.v.) injection of L-NOARG (50-200 nmol) or N(G)-nitro-L-arginine methylester (L-NAME, 100-200 nmol). The dose-response curve of the former compound, however, had an inverted U shape. The effect of L-NOARG (100 nmol, i.c.v.) was completely prevented by pre-treatment with L-arginine (300 nmol, i.c.v.) but not by D-arginine (300 nmol, i.c.v.). Intra-striatal injection of N(G)-monomethyl-L-arginine (L-NMMA, 100 nmol), 7-nitroindazole (7-NIO, 100 nmol), L-NOARG (25-100 nmol) or L-NAME (50-200 nmol) also induced catalepsy. Similar to i.c.v. administration, the latter two compounds produced bell-shaped dose-response curves. The cataleptic effect of intra-striatal administration of L-NAME (100 nmol) was reversed by local treatment with L-arginine (100 nmol). These results suggest that interference with the striatal formation of nitric oxide may induce significant motor effects in rats.