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- Bone injury and repair trigger central and peripheral NPY Neuronal PathwaysPublication . Alves, Cecília J.; Alencastre, Inês S.; Neto, Estrela; Ribas, João; Ferreira, Sofia; Vasconcelos, Daniel M.; Sousa, Daniela M.; Summavielle, Teresa; Lamghari, MeriemBone repair is a specialized type of wound repair controlled by complex multi-factorial events. The nervous system is recognized as one of the key regulators of bone mass, thereby suggesting a role for neuronal pathways in bone homeostasis. However, in the context of bone injury and repair, little is known on the interplay between the nervous system and bone. Here, we addressed the neuropeptide Y (NPY) neuronal arm during the initial stages of bone repair encompassing the inflammatory response and ossification phases in femoral-defect mouse model. Spatial and temporal analysis of transcriptional and protein levels of NPY and its receptors, Y1R and Y2R, reported to be involved in bone homeostasis, was performed in bone, dorsal root ganglia (DRG) and hypothalamus after femoral injury. The results showed that NPY system activity is increased in a time- and space-dependent manner during bone repair. Y1R expression was trigged in both bone and DRG throughout the inflammatory phase, while a Y2R response was restricted to the hypothalamus and at a later stage, during the ossification step. Our results provide new insights into the involvement of NPY neuronal pathways in bone repair.
- Methamphetamine mimics the neurochemical profile of aging in rats and impairs recognition memoryPublication . Melo, Pedro; Magalhães, Ana; Alves, Cecília J.; Tavares, Maria Amélia; Sousa, Liliana de; Summavielle, Teresa; Moradas-Ferreira, PedroBrain neurochemistry and cognition performance are thought to decline with age. Accumulating data indicate that similar events occur after prolonged methamphetamine (MA) exposure. Using the rat as a model, the present study was designed to uncover common alteration patterns in brain neurochemistry and memory performance between aging and prolonged MA exposure. To this end, animals were treated with a chronic binge MA administration paradigm (20 mg/kg/day from postnatal day 91 to 100). Three-age control groups received isovolumetric saline treatment and were tested at the MA age-matched period, and at 12 and 20 months. We observed that both MA and aged animals presented a long, but not short, time impairment in novelty preference and an increased anxiety-like behavior. Neurochemical analysis indicated similar MA- and age-related impairments in dopamine, serotonin and metabolites in the striatum, prefrontal cortex and hippocampus. Thus, the present data illustrate that MA may be used to mimic age-related effects on neurotransmitter systems and advocate MA treatment as a feasible animal model to study neuronal processes associated with aging.