Opioid peptides and gastrointestinal symptoms in autism spectrum disorders

Autism spectrum disorders (ASDs) are characterized by deficits in the individual’s ability to socialize, communicate, and use the imagination, in addition to stereotyped behaviors. These disorders have a heterogenous phenotype, both in relation to symptoms and regarding severity. Organic problems related to the gastrointestinal tract are often associated with ASD, including dysbiosis, inflammatory bowel disease, exocrine pancreatic insufficiency, celiac disease, indigestion, malabsorption, food intolerance, and food allergies, leading to vitamin deficiencies and malnutrition. In an attempt to explain the pathophysiology involved in autism, a theory founded on opioid excess has been the focus of various investigations, since it partially explains the symptomatology of the disorder. Another hypothesis has been put forward whereby the probable triggers of ASDs would be related to the presence of bacteria in the bowel, oxidative stress, and intestinal permeability. The present update reviews these hypotheses.

Immunohistochemical demonstration of opioids and tachykinins in human pineal gland.

The human pineal gland secretes melatonin in a circadian rhythm manner. The rhythm of melatonin synthesis is primarily controlled by the noradrenergic sympathetic system originating from the superior cervical ganglion. Several neurotransmitters/neuropeptides have been reported to influence the production of melatonin in the pineal glands of many mammalian species. Both opioid peptide, a pain suppressing peptide and substance P, a pain inducing peptide were also reported to be present in the pineal gland of several kinds of mammals. However, few studies have been demonstrated in humans. Therefore, in the present study, the immunohistochemical investigation was performed in the human pineal gland by using antisera raised against leu-enkephalin, met-enkephalin and beta-endorphin to demonstrate an opioidergic system; and antisera raised against substance P, neurokinin A, and neurokinin B to study a tachykinin system. A high amount of leu- and met-enkephalin immunoreactivities were observed in intrapineal neuronal-like cells while very few were presented in nerve fibers. This result suggests a local regulatory function or paracrine opioidergic control in human pineal. Substance P- and neurokinin A-immunoreactivities, but not neurokinin B were observed in the human pineal gland. They are located mostly in nerve fibers but a few in neuronal-like cells. The tachykininergic control of human pineal is mainly from the nerve fibers which have their perikaryal origin outside the gland. Some of the nerve fibers might originate from neurons in the brain and/or from a peripheral ganglion.

Endogenous opiate analgesia induced by tonic immobility in guinea pigs

A function of the endogenous analgesic system is to prevent recuperative behaviors generated by tissue damage, thus preventing the emission of species-specific defensive behaviors. Activation of intrinsic nociception is fundamental for the maintenance of the behavioral strategy adopted. Tonic immobility (TI) is an inborn defensive behavior characterized by a temporary state of profound and reversible motor inhibition elicited by some forms of physical restraint. We studied the effect of TI behavior on nociception produced by the formalin and hot-plate tests in guinea pigs. The induction of TI produced a significant decrease in the number of flinches (18 + or - 6 and 2 + or - 1 in phases 1 and 2) and lickings (6 + or - 2 and 1 + or - 1 in phases 1 and 2) in the formalin test when compared with control (75 + or - 13 and 22 + or - 6 flinches in phases 1 and 2; 28 + or - 7 and 17 + or - 7 lickings in phases 1 and 2). In the hot-plate test our results also showed antinociceptive effects of TI, with an increase in the index of analgesia 30 and 45 min after the induction of TI (0.67 0.1 and 0.53 + or - 0.13, respectively) when compared with control (-0.10 + or - 0.08 at 30 min and -0.09 0.09 at 45 min). These effects were reversed by pretreatment with naloxone (1 mg/kg, ip), suggesting that the hypoalgesia observed after induction of TI behavior, as evaluated by the algesimetric formalin and hot-plate tests, is due to activation of endogenous analgesic mechanisms involving opioid synapses

Obesidade, esse grande "iceberg" / Obesity, this large iceberg

Os autores fazem uma introdução sobre o diagnóstico da obesidade, sua abordagem e atualização, exercícios e sobre o sistema opióide-peptidérgico no desenvolvimento e manutenção da obesidade. Fazem ainda referência, com atualização, a substâncias tais como deidroepiandrosterona, orlistat e leptina

Clonidine-induced diuresis and its relation to endogenous opioid peptides

Para estudar a diurese induzida por clonidina, esta substância foi administrada, por via intraperitoneal, em ratos. Intenso efeito diurético foi observado com doses entre 0,025 e 1,25 mg/kg, além de excreçäo aumentada de íons sódio e potássio. Esse efeito diurético foi intensamente inibido pela administraçäo prévia de ioimbina (bloqueador de receptores alfa-dois adrenérgicos) ou N-metil-nalorfina (bloqueador de receptores) opióides que penetra mal o sistema nervoso central). Por outro lado, seu efeito diurético foi aumentado, pela administraçäo prévia de naloxona, um bloqueador de receptores opióides mi. É provável que a ativaçäo de receptores alfa-dois adrenérgicos pela clonidina possa induzir a liberaçäo de substâncias endógenas opióides que causem diurese através da ativaçäo de receptores periféricos com baixa afinidade por naloxona