Mauro Fa

Electrophysiological and pharmacological characteristics of nigral dopaminergic neurons in the conscious, head-restrained rat.

Prenatal exposure to a cannabinoid agonist produces memory deficits linked to dysfunction in hippocampal long-term potentiation and glutamate release.

Activation of D1, but not D2 receptors potentiates dizocilpine-mediated disruption of prepulse inhibition of the startle.

Stimulation of the locus coeruleus elicits noradrenaline and dopamine release in the medial prefrontal and parietal cortex.

Co-release of noradrenaline and dopamine in the cerebral cortex elicited by single train and repeated train stimulation of the locus coeruleus.

Kappa opioid receptor activation disrupts prepulse inhibition of the acoustic startle in rats.

Synaptic fatigue is more pronounced in the APP/PS1 transgenic mouse model of Alzheimer's disease.

Incorporation and metabolism of c9,t11 and t10,c12 conjugated linoleic acid (CLA) isomers in rat brain.

Prenatal exposure to a cannabinoid receptor agonist does not affect sensorimotor gating in rats.

Beta and gamma range EEG power-spectrum correlation with spiking discharges in DBA/2J mice absence model: role of GABA receptors.

Effects of topiramate on the prepulse inhibition of the acoustic startle in rats.

Predictors for rectal and intestinal acute toxicities during prostate cancer high-dose 3D-CRT: results of a prospective multicenter study.

Activation of GABA(B) receptors reverses spontaneous gating deficits in juvenile DBA/2J mice.

Alpha-synuclein involvement in hippocampal synaptic plasticity: role of NO, cGMP, cGK and CaMKII.

Levetiracetam attenuates spontaneous spike-and-wave discharges in DBA/2J mice.

Development of a set of nomograms to predict acute lower gastrointestinal toxicity for prostate cancer 3D-CRT.

Inhibition of calpains improves memory and synaptic transmission in a mouse model of Alzheimer disease.

Picomolar amyloid-beta positively modulates synaptic plasticity and memory in hippocampus.

Dysregulation of histone acetylation in the APP/PS1 mouse model of Alzheimer's disease.

GABAB receptor activation exacerbates spontaneous spike-and-wave discharges in DBA/2J mice.

Danish dementia mice suggest that loss of function and not the amyloid cascade causes synaptic plasticity and memory deficits.

Endogenous amyloid-β is necessary for hippocampal synaptic plasticity and memory.

Is It Time to Tailor the Prediction of Radio-Induced Toxicity in Prostate Cancer Patients? Building the First Set of Nomograms for Late Rectal Syndrome.