Paolo Botta

ORCID: 0000-0003-0570-5774
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Memory and Neural Mechanisms
  • Neuroendocrine regulation and behavior
  • Ion channel regulation and function
  • Neuroscience of respiration and sleep
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Vestibular and auditory disorders
  • Biochemical Analysis and Sensing Techniques
  • Receptor Mechanisms and Signaling
  • Legal and Labor Studies
  • Genetic Neurodegenerative Diseases
  • Management, Economics, and Public Policy
  • Retinal Development and Disorders
  • Circadian rhythm and melatonin
  • Photoreceptor and optogenetics research
  • Nicotinic Acetylcholine Receptors Study
  • Neural dynamics and brain function
  • Italian Social Issues and Migration
  • Mitochondrial Function and Pathology
  • Neurotransmitter Receptor Influence on Behavior
  • Mosquito-borne diseases and control
  • Genetics and Neurodevelopmental Disorders
  • Renin-Angiotensin System Studies
  • Aging, Elder Care, and Social Issues
  • Hearing, Cochlea, Tinnitus, Genetics

Lundbeck (Denmark)
2022-2024

Friedrich Miescher Institute
2011-2021

Columbia University
2018-2021

Champalimaud Foundation
2016

Harvard University
2016

University of Basel
2016

University of New Mexico
2007-2014

Baylor University
2010

University of Memphis
2010

Nanyang Technological University
2010

SH3 and multiple ankyrin repeat domains 3 (SHANK3) haploinsufficiency is causative for the neurological features of Phelan-McDermid syndrome (PMDS), including a high risk autism spectrum disorder (ASD). We used unbiased, quantitative proteomics to identify changes in phosphoproteome Shank3-deficient neurons. Down-regulation protein kinase B (PKB/Akt)-mammalian target rapamycin complex 1 (mTORC1) signaling resulted from enhanced phosphorylation activation serine/threonine phosphatase 2A...

10.1126/science.aad5487 article EN Science 2016-02-05

Fear extinction is an adaptive process whereby defensive responses are attenuated following repeated experience of prior fear-related stimuli without harm. The formation memories involves interactions between various corticolimbic structures, resulting in reduced central amygdala (CEA) output. Recent studies show, however, the CEA not merely output relay fear but contains multiple neuronal subpopulations that interact to calibrate levels responding. Here, by integrating behavioural, vivo...

10.1038/s41467-021-24068-x article EN cc-by Nature Communications 2021-07-06

Acute alcohol consumption causes deficits in motor coordination and gait, suggesting an involvement of cerebellar circuits, which play a role the fine adjustment movements learning. It has previously been shown that ethanol modulates inhibitory transmission cerebellum affects synaptic plasticity at excitatory climbing fiber (CF) to Purkinje cell synapses. However, it not examined thus far how acute application long-term depression (LTD) potentiation (LTP) parallel (PF) synapses, are assumed...

10.1152/jn.90384.2008 article EN Journal of Neurophysiology 2008-10-15

Cerebellar Purkinje neurons (PNs) receive inhibitory GABAergic input from stellate and basket cells, which are located in the outer inner portions of molecular layer, respectively. Ethanol (EtOH) was recently shown to increase transmission at PNs via a mechanism that involves enhanced calcium release presynaptic internal stores (<i>J Pharmacol Exp Ther</i> 323:356–364, 2007). Here, we further characterized effect EtOH on GABA assessed its impact PN excitability. Using whole-cell patch-clamp...

10.1124/jpet.108.144865 article EN Journal of Pharmacology and Experimental Therapeutics 2008-08-28

Background: Adolescent rats are less sensitive to the motor‐impairing effects of ethanol than adults. However, cellular and molecular mechanisms underlying this age‐dependent effect have yet be fully elucidated. Method: Male various ages were used investigate ethanol‐induced ataxia its correlates. In addition, Purkinje neurons from adolescent adult recorded both in vivo vitro. Finally, protein kinase C (PKCγ) expression was determined 3 brain regions rats. Results: The present...

10.1111/j.1530-0277.2010.01303.x article EN Alcoholism Clinical and Experimental Research 2010-09-22

Cerebellar granule neurons (CGNs) extrasynaptically express GABA(A) receptors containing alpha(6)beta(x)delta subunits, which mediate tonic inhibitory currents. Although it has been shown that the function of these is potently and directly enhanced by ethanol, this finding not reproducible across different laboratories. In outbred Sprague-Dawley rats, a naturally occurring arginine (R) to glutamine (Q) mutation in position 100 alpha(6) subunit was reported increase ethanol sensitivity...

10.1124/jpet.107.127894 article EN Journal of Pharmacology and Experimental Therapeutics 2007-08-17

The organization of fear memory involves the participation multiple brain regions. However, it is largely unknown how formed, which circuit pathways are used for "printing" engrams across regions, and role identified circuits in retrieval. With advanced genetic methods, we combinatorially blocked presynaptic output manipulated N-methyl-D-aspartate receptor (NMDAR) basolateral amygdala (BLA) medial prefrontal cortex (mPFC) before after cued conditioning. Further, tagged fear-activated neurons...

10.1016/j.isci.2023.108050 article EN cc-by-nc-nd iScience 2023-09-26

Studies with rodents suggest that acute ethanol exposure impairs information flow through the cerebellar cortex, in part, by increasing GABAergic input to granule cells. Experiments an increase excitability of specialized interneurons regulate cell activity (i.e., Golgi cells [GoCs]) contributes this effect. In GoCs, increases spontaneous action potential firing frequency, decreases afterhyperpolarization amplitude, and depolarizes membrane potential. these effects could be mediated...

10.1111/j.1530-0277.2011.01658.x article EN Alcoholism Clinical and Experimental Research 2011-10-17

Golgi cells (GoCs) are specialized interneurons that provide inhibitory input to granule in the cerebellar cortex. GoCs pacemaker neurons spontaneously fire action potentials, triggering spontaneous postsynaptic currents and also contributing generation tonic GABAA receptor-mediated cells. In turn, cell axons feedback glutamatergic GoCs. It has been shown high frequency stimulation of induces a transient pause GoC firing type 2-metabotropic glutamate receptor (mGluR2)-dependent manner. Here,...

10.3389/fnint.2014.00010 article EN cc-by Frontiers in Integrative Neuroscience 2014-01-01

Background: Tauopathies such as Alzheimer’s disease (AD) and frontotemporal dementia (FTD) are characterized by formation of neurofibrillary tangles consisting hyperphosphorylated tau protein. Early pathophysiological functional changes related to considered occur prior extensive neurodegeneration. Hyperphosphorylated has been detected in postmortem retinas AD FTD patients, the visual pathway is an easily accessible system a clinical setting. Hence, assessment function may offer potential...

10.3233/jad-220964 article EN Journal of Alzheimer s Disease 2023-03-31

Summary Exploration of novel environments ensures survival and evolutionary fitness. This behavior is expressed through exploratory bouts arrests, which change dynamically based on experience. Neural circuits mediating should therefore integrate experience use it to select the proper behavioral output. Using a spatial exploration assay, we uncovered an experience-dependent increase momentary arrests in visited locations where animals previously arrested. Quantitative analyses neuronal...

10.1101/797001 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2019-10-08

Tau protein pathology is a hallmark of many neurodegenerative diseases, including Alzheimer's Disease or frontotemporal dementia. Synaptic dysfunction and abnormal visual evoked potentials have been reported in murine models tauopathy, but little known about the state network activity on single neuronal level prior to brain atrophy. In present study, oscillatory rhythms single-cell calcium primary cortex pyramidal neuron population were investigated basal light states rTg4510 tauopathy mouse...

10.1016/j.nbd.2023.106012 article EN cc-by-nc-nd Neurobiology of Disease 2023-01-23
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