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The infestation due to the olive fruit fly, Bactrocera oleae (Rossi), the key pest in most of world olive groves, has been monitored in six years, from 2004 to 2008 and in 2014, in eight coastal Sicilian olive groves consisting of ‘Cerasuola’ and ‘Nocellara del Belice’ cultivars. Infestation was recorded following the classical sampling method based on olive collection and dissection, in order to count live olive fruit fly instars (eggs, larvae and pupae) and exit holes. Four different infestation indexes, all of them calculated using data recorded at harvest, have been used to assess their relationship with the main three quality parameters of the olive oil obtained from the same olive samples processed within 24 hours by quality oil mills: free acidity (% oleic acid), peroxides (mEq O2 /kg of oil) and total phenols (mg·kg−1 oil). Each year and in each olive grove up to five plots were differently treated with different products allowed in organic agriculture, stopping sprays at least one month before harvest, obtaining different infestation levels. In this study a total of 43 theses were tested, 10 of them involving ‘Cerasuola’ and 33 ‘Nocellara del Belice’. The two indexes based on the exit holes produced by mature larvae in olives resulted strictly and positively correlated to the lowering of oil quality. Moreover, among the two infestation indexes based on the occurrence of exit holes at harvest, percentage of olives with exit holes and No. of exit holes per 100 olives, the latter is more sensitive in presence of high infestation levels. No significant relation between infestation indexes and total phenols resulted in our analyses. Nevertheless, when olives are harvested since the end of October to mid-November, and processed by quality oil mills, olives bearing up to 45 % of exit holes produced high quality extra virgin olive oil. Furthermore, all olives bearing up to 62 % of exit holes still produced extra virgin olive oil. Our results, in spite of the widespread prejudices involving an overestimation of damages due to low olive fly infestation, are very close to recent studies on correlation between olive fly attacks and olive oil quality. Late harvesting can lead to worse results at the same olive fly exit holes levels, confirming that timing and quality procedures of harvesting and oil extraction are important almost as much as olive fly control.

The appearance of motor manifestations in Parkinson's disease (PD) is invariably linked to degeneration of nigral dopaminergic neurons of the substantia nigra pars compacta. Traditional views on PD neuropathology have been grounded in the assumption that the prime event of neurodegeneration involves neuronal cell bodies with the accumulation of metabolic products. However, this view has recently been challenged by both clinical and experimental evidence. Neuropathological studies in human brain samples and both in vivo and in vitro models support the hypothesis that nigrostriatal synapses may indeed be affected at the earliest stages of the neurodegenerative process. The mechanisms leading to either structural or functional synaptic dysfunction are starting to be elucidated and include dysregulation of axonal transport, impairment of the exocytosis and endocytosis machinery, altered intracellular trafficking, and loss of corticostriatal synaptic plasticity. The aim of this review is to try to integrate different lines of evidence from both pathogenic and genetic animal models that, to different extents, suggest that early synaptic impairment may represent the key event in PD pathogenesis. Understanding the molecular and cellular events underlying such synaptopathy is a fundamental step toward developing specific biomarkers of early dopaminergic dysfunction and, more importantly, designing novel therapies targeting the synaptic apparatus of selective, vulnerable synapses. © 2016 International Parkinson and Movement Disorder Society.

Broad-spectrum muscarinic receptor antagonists have represented the first available treatment for different movement disorders such as dystonia. However, the specificity of these drugs and their mechanism of action is not entirely clear. We performed a systematic analysis of the effects of anticholinergic drugs on short- and long-term plasticity recorded from striatal medium spiny neurons from DYT1 dystonia knock-in (Tor1a(+/Δgag) ) mice heterozygous for ΔE-torsinA and their controls (Tor1a(+/+) mice). Antagonists were chosen that had previously been proposed to be selective for muscarinic receptor subtypes and included pirenzepine, trihexyphenydil, biperiden, orphenadrine, and a novel selective M1 antagonist, VU0255035. Tor1a(+/Δgag) mice exhibited a significant impairment of corticostriatal synaptic plasticity. Anticholinergics had no significant effects on intrinsic membrane properties and on short-term plasticity of striatal neurons. However, they exhibited a differential ability to restore the corticostriatal plasticity deficits. A complete rescue of both long-term depression (LTD) and synaptic depotentiation (SD) was obtained by applying the M1 -preferring antagonists pirenzepine and trihexyphenidyl as well as VU0255035. Conversely, the nonselective antagonist orphenadrine produced only a partial rescue of synaptic plasticity, whereas biperiden and ethopropazine failed to restore plasticity. The selectivity for M1 receptors was further demonstrated by their ability to counteract the M1 -dependent potentiation of N-methyl-d-aspartate (NMDA) current recorded from striatal neurons. Our study demonstrates that selective M1 muscarinic receptor antagonism offsets synaptic plasticity deficits in the striatum of mice with the DYT1 dystonia mutation, providing a potential mechanistic rationale for the development of improved antimuscarinic therapies for this movement disorder.