Biology subjects

Conti, F.

Publications and source records attributed to Conti, F..

4 recordsLinked to original sources

bioRxiv2025

Native community resistance modulates the spread of non-native species along Mediterranean mountain roads under global change

AimClimate warming, human modification, and global connectivity are eroding the abiotic barriers (i.e. climatic filtering and low propagule pressure) that have traditionally limited the spread of non-native species in mountain ecosystems. Meanwhile, these global changes are reshaping native plant communities, potentially weakening their biotic resistance to invasion. Yet, the role of native community resistance in modulating the upslope spread of non-native species remains overlooked, potentially masking indirect effects of global change in mountain ecosystems. LocationCentral Apennines Mountain range, Italy MethodsFollowing the Mountain Invasion Research Network (MIREN) protocol, we surveyed vegetation close and far from roads at 60 sites along three mountain roads in the Central Apennines. Using current and historical climatic data and aerial images from the 1950s to today, we quantified climate and land-use changes. Dominant plant traits and functional diversity were used to capture the biotic resistance of native communities. We then applied structural equation modelling to investigate how native biotic resistance regulates the effect of global change drivers, i.e. road disturbance and changes in land-use and climate, on the occurrence and cover of non-native species. ResultsVariance partitioning suggests that, beside climatic filtering, the biotic resistance of native communities is among the strongest drivers of non-native species occurrence and abundance. Although climate and land-use changes have had little direct influence on non-natives, land-use changes occurred over the past 70 years indirectly influenced invasions by altering native community resistance. Agricultural abandonment at low- to middle elevations, favoured short-statured native communities, offering low resistance. In contrast, forest expansion strengthened resistance through dominance of conservative native species. Main conclusionNative community resistance, alongside climate and disturbance, is a key determinant of invasion patterns along elevational gradients in Mediterranean mountains. Despite global changes facilitate non-native plant upward shifts, native communities can modulate this spread and may still maintain a certain resistance to invasion.

ecology↗

bioRxiv2025

An unsuspected physiological role for mGluRIII glutamate receptors in hippocampal area CA1

Group III metabotropic glutamate receptors (mGluRIII) are expressed broadly throughout the neocortex and hippocampus but are thought to inhibit neurotransmitter release only at a subset of synapses and in a target cell- specific manner. Accordingly, previous slice physiology experiments in hippocampal area CA1 showed that mGluRIII receptors inhibit glutamate and GABA release only at excitatory and inhibitory synapses formed onto GABAergic interneurons, not onto pyramidal cells. Here, we show that the supposed target cell-specific modulation of GABA release only occurs when the extracellular calcium concentration in the recording solution is higher than its physiological concentration in the cerebrospinal fluid. Under more physiological conditions, mGluRIII receptors inhibit GABA release at synapses formed onto both interneurons and pyramidal cells but limit glutamate release only onto interneurons. This previously unrecognized form of mGluRIII-dependent, pre-synaptic modulation of inhibition onto pyramidal cells is accounted for by a reduction in the size of the readily releasable pool, mediated by protein kinase A and its vesicle-associated target proteins, synapsins. Using in vivo whole-cell recordings in behaving mice, we demonstrate that blocking mGluRIII activation in the intact CA1 network results in net effects consistent with decreased inhibition and significantly alters CA1 place cell activity. Together, these findings challenge our current understanding of the role of mGluRIII receptors in the control of synaptic transmission and encoding of spatial information in the hippocampus.

neuroscience↗

bioRxiv2021

A failure of β-amyloid physiological function due to genetic deletion of α7 nicotinic acetylcholine receptors induces an Alzheimer's disease-like pathology

The accumulation of amyloid-beta peptide (A{beta}) and the failure of cholinergic transmission are key players in Alzheimers disease (AD). However, in the healthy brain, A{beta} contributes to synaptic plasticity and memory acting through 7 subtype nicotinic acetylcholine receptors (7nAChRs). Here, we hypothesized that the 7nAChR deletion blocks A{beta} physiological function and promotes a compensatory increase in A{beta} levels that, in turn, triggers an AD-like pathology. To validate this hypothesis, we studied the age-dependent phenotype of 7 knock out mice. We found that 7nAChR deletion caused an impairment of hippocampal synaptic plasticity and memory at 12 months of age, paralleled by an increase of Amyloid Precursor Protein expression and A{beta} levels. This was accompanied by other classical AD features such as a hyperphosphorylation of tau at residues Ser 199, Ser 396, Thr 205, a decrease of GSK-3{beta} at Ser 9, the presence of paired helical filaments and neurofibrillary tangles, neuronal loss and astrocytosis. Our findings suggest that 7nAChR malfunction might precede A{beta} and tau pathology, offering a different perspective to interpret the failure of anti-A{beta} therapies against AD and to find novel therapeutical approaches aimed at restoring 7nAChRs-mediated A{beta} function at the synapse.

neuroscience↗

bioRxiv2020

Non-canonical glutamate signaling in a genetic model of migraine with aura

Migraine with aura is an extremely common but poorly understood sensory circuit disorder. Monogenic models allow an opportunity to understand its mechanisms, in particular because the migraine aura is associated with spreading depolarizations that can be measured physiologically. Using fluorescent glutamate imaging in awake mice carrying a familial hemiplegic migraine type 2 mutation, we recorded previously undescribed spontaneous plumes of glutamate signaling that anatomically overlapped with reduced density of GLT-1a positive astrocyte processes. These events could be mimicked in wild-type animals by inhibition of glutamate clearance, which we show to be slower during sensory processing in FHM2 carriers. Plumes depended on calcium mediated vesicular release from neurons, but not action potentials. Importantly, a rise in both basal glutamate and plume frequency predicted the onset of spreading depolarization in WT and FHM2 animals, providing a novel mechanism in migraine with aura and by extension the many other neurological disorders where spreading depolarizations occur.

neuroscience↗