Percepciones de justicia por mano propia y confianza en la policía

Este artículo describe una prueba empírica de la asunción común que confianza en la policía afecte percepciones de justicia por mano propia. Aparte de testear el papel de la confianza difusa (general) en la policía, también testeamos si la reacción de la policía en un nivel situacional afecte como el público ve un acto subsiguiente de justicia por mano propia. En un estudio experimental (N = 385), participantes recibieron una viñeta (un caso específico) sobre justicia por mano propia. Usando un diseño inter-sujeto, variamos la reacción policial al delito original (activa/pasiva) y la violencia del justiciero (alta/baja). Encontramos que con más confianza difusa en la policía hubo menos apoyo para el vigilantismo. Adicionalmente, los otros factores experimentales tuvieron un impacto importante. Los ciudadanos están sensitivos a la variación situacional cuando juzgan un delito. Además, nuestros resultados ponen énfasis en la importancia de la acción policial al nivel situacional en la formación de la opinión pública.Facultad de Humanidades y Ciencias de la Educació

Localization of pre- and postsynaptic cholinergic markers in rodent forebrain: A brief history and comparison of rat and mouse

Rat and mouse models are widely used for studies in cognition and pathophysiology, among others. Here, we sought to determine to what extent these two model species differ for cholinergic and cholinoceptive features. For this purpose, we focused on cholinergic innervation patterns based on choline acetyltransferase (ChAT) immunostaining, and the expression of muscarinic acetylcholine receptors (mAChRs) detected immunocytochemically. In this brief review we first place cholinergic and cholinoceptive markers in a historic perspective, and then provide an overview of recent publications on cholinergic studies and techniques to provide a literature survey of current research. Next, we compare mouse (C57Bl/J6) and rat (Wistar) cholinergic and cholinoceptive systems simultaneously stained, respectively, for ChAT (analyzed qualitatively) and mAChRs (analyzed qualitatively and quantitatively). In general, the topographic cholinergic innervation patterns of both rodent species are highly comparable, with only considerable (but region specific) differences innumberof detectable cholinergic interneurons, which are more numerous in rat. In contrast, immunolabeling for mAChRs, detected by the monoclonal antibody M35, differs markedly in the forebrain between the two species. In mouse brain, basal levels of activated and/or internalized mAChRs (as a consequence of cholinergic neurotransmission) are significantly higher. This suggests a higher cholinergic tone in mouse than rat, and hence the animal model of choice may have consequences for cholinergic drug testing experiments.

Chronic Excess of Corticosterone Increases Serotonergic Fibre Degeneration in Aged Rats

Evidence is presented for the potentiating role of corticosterone on axonal degeneration of serotonergic neurones during ageing. Aged rats, 24 months old, were implanted subcutaneously with 2 × 100 mg pellets of corticosterone. Serotonergic and cholinergic (ChAT- and NADPHd-positive) fibre degenerations in the anteroventral thalamic nucleus (AVT) were measured 2 months after corticosterone implantation. Numbers of immunoreactive serotonergic raphe and mesolimbic cholinergic neurones were also quantified. Basal plasma corticosterone and adrenocorticotropin (ACTH) concentrations were assayed at 2, 4, 6, and 8 weeks after implantation in the plasma and at 1, 2, 4 and 6 weeks in urine. The degree of serotonergic fibre aberrations in the AVT increased significantly after corticosterone exposure, while that of ChAT-positive and NADPHd-stained axon aberrations showed a modest but nonsignificant increase. A positive correlation between the magnitudes of serotonergic and cholinergic fibre aberrations appeared in the AVT, but only in the corticosterone-treated rats. The number of serotonin immunopositive neurones in the raphe nuclei after corticosterone decreased marginally, while that of mesopontine ChAT-positive neurones was not influenced. Measurements of basal plasma corticosterone and ACTH, as well as urine corticosterone, revealed that the steroid implantation increased the plasma corticosterone level for at least 4 weeks and decreased ACTH level for at least 6 weeks. By the week 8, the pituitary-adrenal function was apparently restored. However, at sacrifice, both the weight of adrenal glands and that of thymus remained reduced, indicating the long-lasting effects of corticosterone on target tissues. It is concluded that the raphe serotonergic neurones and their projecting fibres are sensitive to corticosterone excess in aged rats and become more vulnerable to degeneration processes than under normal ageing conditions. Cholinergic neurones of brainstem origin, which also express massive NADPHd activity, are more resistant against corticosterone, but their axon degeneration correlates to serotonergic fibre degeneration.

Cerebral Hypoperfusion Yields Capillary Damage in the Hippocampal CA1 Area that Correlates with Spatial Memory Impairment

The impact of chronic cerebral hypoperfusion on cognitive function and cerebral capillary morphology in the hippocampus was examined. Young adult Wistar rats were subjected to permanent ligation of both common carotid arteries (two-vessel occlusion). One month after vascular occlusion, a small but non-significant impairment in the acquisition of spatial information was registered compared with sham-operated controls. Two months after surgery, the occluded animals displayed an impaired performance throughout the training period. One year after surgery, the acquisition curves demonstrated a significant attenuation of the learning rate in the occluded rats group, whereas no significant differences in long-term retention were observed. Thus, chronic hypoperfusion induced by two-vessel occlusion gave rise to impairment of spatial memory. Following behavioural testing, the rats were killed at the age of 17 months, and capillaries in the CA1 and dentate gyrus were examined using transmission electron microscopy. Typical age-related capillary abnormalities such as degenerative pericytes and thickened basement membranes (with or without fibrosis) were detected in the hippocampus of sham animals. In occluded rats, the occurrence of capillaries displaying such abnormalities almost doubled in the CA1 region, but was similar in the dentate gyrus, compared with sham controls. A highly significant correlation was found between the last Morris maze performance and the percentage of capillaries with deposits in the basement membrane in the hippocampal CA1 area of occluded rats, which was not present in the sham animals. We conclude that a long-term hypoperfusion accelerated the development of age-related ultrastructural aberrations of capillaries in the hippocampal CA1 area, but not in the dentate gyrus. Thus, not only neurons, but also capillaries in the hippocampal CA1 area are sensitive to an impaired microcirculation. Moreover, the cognitive performance of hypoperfused rats correlated closely with the condition of the capillaries in the CA1 area, suggesting that capillary integrity is one of the important determinants of brain function in conditions that compromise cerebral microcirculation.

Interleukin-6 Upregulates Neuronal Adenosine A1 Receptors: Implications for Neuromodulation and Neuroprotection

The immunological response in the brain is crucial to overcome neuropathological events. Some inflammatory mediators, such as the immunoregulatory cytokine interleukin-6 (IL-6) affect neuromodulation and may also play protective roles against various noxious conditions. However, the fundamental mechanisms underlying the long-term effects of IL-6 in the brain remain unclear. We now report that IL-6 increases the expression and function of the neuronal adenosine A1 receptor, with relevant consequences to synaptic transmission and neuroprotection. IL-6-induced amplification of A1 receptor function enhances the responses to readily released adenosine during hypoxia, enables neuronal rescue from glutamate-induced death, and protects animals from chemically induced convulsing seizures. Taken together, these results suggest that IL-6 minimizes the consequences of excitotoxic episodes on brain function through the enhancement of endogenous adenosinergic signaling.