ABSTRACT
La esquizofrenia es una enfermedad neuropsiquiátrica que cursa con múltiples síntomas y signos del área del pensamiento, percepción, emoción, movimientos y conducta. Su etiología está aún en discusión, existiendo hipótesis genéticas, neuroanatómicas, neuroquímicas e inmunológicas. En este trabajo estudiamos la interacción del sistema nervioso autónomo colinérgico y del sistema inmune como base biológica de algunos de los síntomas negativos de esta enfermedad. Tres ítems merecen subrayarse:a)la presencia de anticuerpos en el suero de los pacientes capaces de interactuar con la membrana de corteza frontal; b) dichos anticuerpos son capaces, además, de interactuar con los receptores muscarínicos (mACH) del subtipo M1; c) posible correlación entre los eventos biológicos y el déficit cognitivo de estos pacientes. Concluímos que la presencia de anticuerpos dirigidos contra los receptores mACh del subtipo M1 de la corteza frontal en los pacientes esquizofrénicos, podría ser un marcador biológico del déficit atencional de esta enfermedad
Subject(s)
Antibodies , Cognition Disorders , Muscarinic Antagonists , Schizophrenia/etiology , Case-Control StudiesABSTRACT
En un modelo animal de depresión reactiva se estudiaron los mecanismos neurobiológicos implicados, relacionados con la actividad muscarínica colinérgica a nivel cerebral y de células inmuno competentes. Comprobamos una hipersensibilidad colinérgica a nivel central, tal como fuera descripta en la depresión genética. A nivel linfocitario las células B presentaron una expresión atípica de receptores colinérgicos. En los linfocitos T, en cambio, encontramos un aumento de receptores. La hiperactividad de células B fue acompañada por la aparición tardía de anticuerpos séricos anti-M1. El papel fisiopatológico de dichos anticuerpos queda por dilucidar
Subject(s)
Adjustment Disorders , Immunocompetence , Receptors, CholinergicABSTRACT
Here we demonstrate that T. cruzi antigen molecule SAPA (shed acute phase antigen) with neuraminidase-trans sialidase activity triggers down-regulation of T lymphocyte proliferation by interacting with T lymphocyte muscarinic acetylcholine receptors (mAChR). SAPA attachment to mAChR from Lyt 2.2+ T cells resulted in synthesis of cyclic GMP (cGMP) and secretion of PGE2, an immunoregulator effector substance. These T suppressor cell signals were blunted by atropine and by indomethacin. Cell sorter analysis showed that the interaction of SAPA with purified T cells, affected the ratio of L3T4+/Lyt 2.2+ T cells increasing the percentage of Lyt 2.2+ T cells, effect that was inhibited by the mAChR antagonist, atropine. The interaction between SAPA and mAChR from Lyt 2.2+ T cells may result, therefore, in the down-regulation of the host immune response as consequence of T suppressor/cytotoxic cells activation and PGE2 release as they were observed. These results support the theory of an immunosuppressive state that contribute to the chronic course of Chagas'disease.
Subject(s)
Animals , Mice , Antigens, Protozoan/drug effects , Atropine/pharmacology , Cyclooxygenase Inhibitors/pharmacology , Dinoprostone/metabolism , Down-Regulation/drug effects , Indomethacin/pharmacology , Muscarinic Antagonists/pharmacology , Receptors, Muscarinic/immunology , T-Lymphocytes/drug effects , Trypanosoma cruzi/immunology , Cell Division , Chagas Disease/immunology , Chronic Disease , Concanavalin A , Cyclic GMP/immunology , Dinoprostone/immunology , Flow Cytometry , Mice, Inbred BALB C , T-Lymphocytes/cytology , T-Lymphocytes/immunologyABSTRACT
En el presente trabajo se muestran las ventajas de la utilización de un patrón de 129I para comprobar diariamente que la respuesta del equipo de detección es constante para el 125I y poder determinar además la eficiencia para dicho nucleido. Una alternativa para conocer ese valor consiste en la aplicación de un método de coincidencia. La comparación de los resultados logrados con uno y otro método, demuestra que ambos valores de eficiencia son iguales. Por otra parte se analizan algunas cuestiones relacionadas con las ecuaciones teóricas utilizadas
Subject(s)
Humans , Spectrometry, Gamma/methods , Iodine Radioisotopes/analysisABSTRACT
As severall side effects of neuroleptics would be related to their interactions with several neurotransmitter receptors (R) haloperidol action on muscarinic cholinergic (mACh) R on frontal cerebral cortex preparations was analyzed. Here we shown that haloperidol was able to inhibit in a concentration dependent manner the binding of specific mAChR radiollabeled antagonist on cerebral cortex membranes. This effect would be related to its interaction on mAChR of the M1 subtype as haloperidol blocked the stimulation of phosphoiinositides (Pis) turnover induced by low concentrations of carbachol similarly as the M1 antagonist pirenzepine. However at high carbachol concentrations haloperidol triggered a potentiating stimulation of Pis hydrolysis that was only blocked by the alpha1 adrenergic antagonist prazosin indicating and alpha1 agonistic action of haloperidol on these Rs. These multireceptor actions of haloperidol found "in vitro"would strengthen its assocation with "in vivo"neuroleptic-induced side effects.
Subject(s)
Animals , Rats , Antipsychotic Agents/pharmacology , Cerebral Cortex/drug effects , Haloperidol/pharmacology , In Vitro Techniques , Muscarinic Antagonists , Receptors, Muscarinic/drug effects , Binding Sites , Carbachol , Inositol Phosphates , Muscarinic Agonists , Quinuclidinyl BenzilateABSTRACT
We previously reported that aqueous extract of Larrea divaricata Cav had an antiproliferative activity upon tumoral lymphoid cells (BW 5147), without affecting normal immunity. To determine the probable mechanism of the inhibitory action of the extract upon cell growth, the participation of intracellular signals involved in the inhibition of cell proliferation, namely the activation of adenylate cyclase system was studied. The production of cyclic 3', 5 adenosine monophosphate (cAMP) in presence and absence of extract was analized. The extract increased the cAMP levels, but neither the cAMP production nor the inhibitory effect of the extract on proliferation were blocked by a beta adrenergic receptor antagonist (propranolol) or by histaminergic receptor antagonistis (cimetidine and mepyramine). So, we concluted that the antiproliferative activity of the extract of BW 5147 cells would be mediated by an increase in cAMP intracellular levels no related to the activation of the membrane receptors here studied. In parallel, the extract was administered to a pregnant rat with a spontaneous mammarian carcinoma and "in vivo"antitumoral activity was found.