M
Marco Martina
Researcher at Northwestern University
Publications - 74
Citations - 4754
Marco Martina is an academic researcher from Northwestern University. The author has contributed to research in topics: Neuropathic pain & Patch clamp. The author has an hindex of 34, co-authored 73 publications receiving 4253 citations. Previous affiliations of Marco Martina include University of Freiburg & University of Trieste.
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Journal ArticleDOI
Functional and molecular differences between voltage-gated K^+ channels of fast-spiking interneurons and pyramidal neurons of rat hippocampus
TL;DR: The results indicate that the differential expression of Kv3 and Kv4 subunits shapes the action potential phenotypes of principal neurons and interneurons in the cortex.
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Abnormalities in Hippocampal Functioning with Persistent Pain
Amelia A. Mutso,Daniel Radzicki,Marwan N. Baliki,Lejian Huang,Ghazal Banisadr,Maria Virginia Centeno,Jelena Radulovic,Marco Martina,Richard J. Miller,A. Vania Apkarian +9 more
TL;DR: The results indicate that hippocampus-mediated behavior, synaptic plasticity, and neurogenesis are abnormal in neuropathic rodents, and these abnormalities may underlie learning and emotional deficits commonly observed in chronic pain patients.
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Morphological and functional reorganization of rat medial prefrontal cortex in neuropathic pain.
TL;DR: The results not only provide evidence that neuropathic pain leads to rearrangement of the mPFC, which may help defining the cellular basis for cognitive impairments associated with chronic pain, but also show pain-associated morphological changes in the cortex at single neuron level.
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Distal initiation and active propagation of action potentials in interneuron dendrites.
TL;DR: Simultaneous recordings from dendrites and somata suggested that action potential initiation occurs preferentially in the axon with long threshold stimuli, but can be shifted to somatodendritic sites when brief stimuli are applied.
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Scapuloperoneal spinal muscular atrophy and CMT2C are allelic disorders caused by alterations in TRPV4.
Han Xiang Deng,Christopher J. Klein,Jianhua Yan,Yong Shi,Yanhong Wu,Faisal Fecto,Hau Jie Yau,Yi Yang,Hong Zhai,Nailah Siddique,E. Tessa Hedley-Whyte,Robert DeLong,Marco Martina,Peter J. Dyck,Teepu Siddique +14 more
TL;DR: It is reported that SPSMA and CMT2C are allelic disorders caused by mutations in the gene encoding the transient receptor potential cation channel, subfamily V, member 4 (TRPV4), implying a pathogenic mechanism and possible options for therapy for these disorders.