“Juan Lerma Gómez”的意思、由来-开放百科全书

Juan Lerma Gómez (born June 8, 1955) is a Spanish neuroscientist and research professor at the Instituto de Neurociencias in Alicante.^[1] Currently he is editor-in-chief of Neuroscience, the official journal of the International Brain Research Organization, and scientific director of the programme "Severo Ochoa Center of Excellence" (2014-2022).

Biography

Lerma studied biology at the Complutense University of Madrid, and in 1979 started research at the Hospital Ramón y Cajal, under the mentorship of Elio Garcia-Austt, obtaining his PhD in sciences at the Autonomous University of Madrid in 1983. After six years as a faculty member at the hospital's Department of Research, he became a tenured staff researcher in the Instituto Cajal supported by the Consejo Superior de Investigaciones Científicas. In 1987, he moved to the Albert Einstein College of Medicine as a Fogarty Fellow, working with Mike V. L. Bennett and R. Suzanne Zukin. In 1990, he returned to Spain at the Instituto Cajal where he established his own lab. In 2000, he was promoted to full professor. In 2004, he moved to the Instituto de Neurociencias (Neurosciences Institute) in Alicante. He became vice-director (2005-2007) and director (2007-2016).^[1]

Research

Lerma has focused his research on the molecular basis of neuronal communication, specifically on elucidating the properties and signaling mechanisms of glutamate receptors.

He described the existence of functional kainate receptors (KARs) in central neurons and applied single-cell RT-PCR to study neurotransmitter receptors.^[2]^[3]^[4] He described the KAR's fundamental role in controlling neuronal tissue excitability and epileptogenesis, demonstrating that KARs have a dual mechanism of signaling.^[5]^[6]^[7] He studied the role played by KARs at particular synapses and in the pathophysiology of brain diseases, in particular those related to mood disorders.^[8]^[9]

Publications

Professional service

Honors and awards

References

1. ^¹{{Cite web |url=http://in.umh-csic.es/grupos-detalle.aspx?grupo=29 |title=Research Group webpage |website=in.umh-csic.es |access-date=2018-07-25}}
2. ^{{Cite journal |last1=Paternain |first1=A. V |last2=Morales |first2=M |last3=Lerma |first3=J |year=1995 |title=Selective antagonism of AMPA receptors unmasks kainate receptor-mediated responses in hippocampal neurons |journal=Neuron |volume=14 |issue=1 |pages=185–189 |doi=10.1016/0896-6273(95)90253-8 |pmid=7826635}}
3. ^{{Cite journal |last=Lerma |first=J |last2=V Paternain |first2=A |last3=Naranjo |first3=J R |last4=Mellström |first4=B |year=1993 |title=Functional kainate-selective glutamate receptors in cultured hippocampal neurons |journal=PNAS |volume=90 |issue=24 |pages=11688–11692 |doi=10.1073/pnas.90.24.11688 |bibcode=1993PNAS...9011688L }}
4. ^{{Cite journal |last1=Rodríguez-Moreno |first1=A |last2=Herreras |first2=O |last3=Lerma |first3=J |year=1997 |title=Kainate receptors presynaptically downregulate GABAergic inhibition in the rat hippocampus |journal=Neuron |volume=19 |issue=4 |pages=893–901 |doi=10.1016/S0896-6273(00)80970-8 |pmid=9354335}}
5. ^{{Cite journal |title=Kainate receptor modulation of GABA release involves a metabotropic function |journal=Neuron |volume=20 |issue=6 |pages=1211–1218 |pmid=9655508 |year=1998 |last1=Rodríguez-Moreno |first1=A |last2=Lerma |first2=J |doi=10.1016/S0896-6273(00)80501-2}}
6. ^{{Cite journal |last=Rozas |first=José Luis |last2=Paternain |first2=Ana V. |last3=Lerma |first3=Juan |date=2003-07-31 |title=Noncanonical signaling by ionotropic kainate receptors |journal=Neuron |volume=39 |issue=3 |pages=543–553 |pmid=12895426 |doi=10.1016/S0896-6273(03)00436-7 }}
7. ^{{Cite journal |last=Valbuena |first=Sergio |last2=Lerma |first2=Juan |date=2016-10-19 |title=Non-canonical signaling, the hidden life of ligand-gated ion channels |journal=Neuron |volume=92 |issue=2 |pages=316–329 |doi=10.1016/j.neuron.2016.10.016 |pmid=27764665}}
8. ^{{Cite journal |title=Increased dosage of high-affinity kainate receptor gene grik4 alters synaptic transmission and reproduces autism spectrum disorders features |journal=Journal of Neuroscience |volume=35 |issue=40 |pages=13619–13628 |doi=10.1523/JNEUROSCI.2217-15.2015 |pmid=26446216 |year=2015 |last1=Aller |first1=M. Isabel |last2=Pecoraro |first2=Valeria |last3=Paternain |first3=Ana V. |last4=Canals |first4=Santiago |last5=Lerma |first5=Juan}}
9. ^{{Cite journal |title=Increased Grik4 gene dosage causes imbalanced circuit output and human disease-related behaviors |journal=Cell Reports |volume=23 |issue=13 |pages=3827–3838 |doi=10.1016/j.celrep.2018.05.086 |pmid=29949767 |year=2018 |last1=Arora |first1=Vineet |last2=Pecoraro |first2=Valeria |last3=Aller |first3=M. Isabel |last4=Román |first4=Celia |last5=Paternain |first5=Ana V. |last6=Lerma |first6=Juan}}
10. ^{{Cite web |url=https://scholar.google.com/citations?user=rjisMp8AAAAJ&hl=es |title=Juan Lerma |website=Google Scholar}}