698 research outputs found
Apomorphine as a neuroprotective drug: a study in MPTP-treated mice and potential relevance to ischemia
No available abstrac
Mapping neuronal activity of the basal ganglia in experimental models of Parkinson's disease: contributions of the [14C]2-deoxyglucose method
No abstract availabl
Sexual pheromone or conventional odors increase extracellular lactate without changing glucose utilization in specific brain areas of the rat
Brain extracellular lactate levels increase following physiological stimuli. Monitoring lactate levels might be a tool for detecting dynamic changes in brain activity. In this study we compared changes of extracellular lactate in selected brain areas with rates of glucose utilization as measured by the [14C]2-deoxyglucose method, following olfactory stimulation. Conventional (green pepper essence, heptanal, exanal, octanal) and, above all, non-conventional (sexual pheromone) odors increased lactate in the rhinencephalum, but not in the striatum. Glucose utilization did not change in any area. This discrepancy may result from the different temporal resolution of the two methods employed and/or from the clearance of lactate, whose tissue content increases transiently following neuronal activation as a reflection of the initial oxygen debt
mTOR-related cell-clearing systems in epileptic seizures, an update
Recent evidence suggests that autophagy impairment is implicated in the epileptogenic mechanisms downstream of mTOR hyperactivation. This holds true for a variety of genetic and acquired epileptic syndromes besides malformations of cortical development which are classically known as mTORopathies. Autophagy suppression is sufficient to induce epilepsy in experimental models, while rescuing autophagy prevents epileptogenesis, improves behavioral alterations, and provides neuroprotection in seizure-induced neuronal damage. The implication of autophagy in epileptogenesis and maturation phenomena related to seizure activity is supported by evidence indicating that autophagy is involved in the molecular mechanisms which are implicated in epilepsy. In general, mTOR-dependent autophagy regulates the proliferation and migration of inter-/neuronal cortical progenitors, synapse development, vesicular release, synaptic plasticity, and importantly, synaptic clustering of GABAA receptors and subsequent excitatory/inhibitory balance in the brain. Similar to autophagy, the ubiquitin–proteasome system is regulated downstream of mTOR, and it is implicated in epileptogenesis. Thus, mTOR-dependent cell-clearing systems are now taking center stage in the field of epilepsy. In the present review, we discuss such evidence in a variety of seizure-related disorders and models. This is expected to provide a deeper insight into the molecular mechanisms underlying seizure activit
MPTP Neurotoxicity: Actions, Mechanisms, and Animal Modeling of Parkinson’s Disease
The study of neurotoxicity induced by MPTP led to drastically change the
perspective on Parkinson’s disease. In fact, the selective neurotoxicity induced
by MPTP rejuvenated PD research and generated a number of studies aimed at
elucidating the mechanisms of action of MPTP. Remarkably, these molecular
mechanisms turned out to be critical also for the survival of DA neurons in
idiopathic PD. In this chapter, the main concepts developed over the last three
decades to understand key molecular steps which are pivotal in MPTP toxicity are
reported. This is the case of the role played by DAT and VMAT-2 in conditioning
the sensitivity to MPTP neurotoxicity. Similarly, the mitochondria as targets of
MPTP toxicity appear similarly affected by selective mutation of genes leading to
PD. Again, the fate of mitochondria and the ability to clear these organelles when
being dysfunctional are key in the modulation of MPTP toxicity. This also applies
for misfolded proteins such as alpha-synuclein. Again, multiple brain areas as
well as peripheral sites are increasingly recognized to be affected both during
MPTP toxicity and sporadic PD patients. Nowadays, it seems that MPTP per se
did not lead to the discovery of the environmental compound which causes PD;
nonetheless, the study of MPTP did disclose several molecular and cellular
pathways which are critical in the genesis of PD. This latter point fairly corresponds
to what enthusiastically is expected from MPTP when it was identified as
a causal agent of what it remains, a toxic form of environmental parkinsonism
Fornai e potere. I mestieri del pane a Bologna nel Duecento
Nella Bologna medievale la categoria dei fornai non ha diritto a riunirsi in associazione fino ai primi del XV secolo, al pari delle altre categorie del vettovagliamento urbano (mugnai, trasportatori di grano, brentatori). Essi dipendono dal Comune e il loro operato è rigidamente controllato dai funzionari dell'ufficio del Biado. Quest'ultimo deve garantire ai consumatori in città la qualità dei cereali smerciati all'ingrosso e al minuto sul mercato, nonché la qualità del pane venduto nelle piazze adibite a mercato alimentare. I fornai, pur essendo un gruppo professionale fondamentale nell'economia della città, non ricoprono importanti cariche politiche (come è invece il caso dei beccai), e neppure raggiungono alti livelli nel tenore di vita, tranne in qualche raro caso
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