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Vazquez-Rosa, E.

Publications and source records attributed to Vazquez-Rosa, E..

2 recordsLinked to original sources

Longitudinal in vivo monitoring of axonal integrity after brain injury

Traumatic brain injury-induced axonal degeneration leads to acute and chronic neuropsychiatric impairment, neuronal death, and accelerated neurodegenerative diseases of aging, including Alzheimers and Parkinsons diseases. Thus, there is much interest in developing treatments that protect axons after injury. For this endeavor, extended comprehensive evaluation of axonal integrity in experimental systems is required to evaluate the efficacy of putative interventions in preclinical models. However, traditional histological tissue proccessing techniques are logistically prohibitive for assessments of long-term pathology. Here, we report a new method of longitudinally monitoring the functional activity of thalamocortical axons before and after injury in vivo in the same animal over an extended period of time. Specifically, we expressed an axonal-targeting genetically-encoded calcium indicator in the mouse dorsolateral geniculate nucleus and then recorded axonal activity patterns in the visual cortex in response to visual stimulation. We demonstrate the utility of this method for assessing in vivo aberrant axonal activity patterns after traumatic brain injury, as well as for evaluating the therapuetic efficacy of the neuroprotective P7C3-A20 pharmacologic agent in vivo. We found that P7C3-A20 treatment minimized most, but not all, of the pathological changes in axonal activity patterns after traumatic brain injury.

neuroscience↗

Multifactorial and closed head impact traumatic brain injuries cause distinct tactile hypersensitivity profiles

Chronic complications of traumatic brain injury (TBI) represent one of the greatest financial burdens and sources of suffering in society today. A substantial number of these patients suffer from post-traumatic headache (PTH), which is typically associated with tactile allodynia. Unfortunately, this phenomenon has been under-studied, in large part due to the lack of well-characterized laboratory animal models. We have addressed this gap in the field by characterizing the tactile sensory profile of two non-penetrating models of PTH. We show that multifactorial TBI, consisting of aspects of impact, acceleration/deceleration, and blast wave exposure, produces long term tactile hypersensitivity and central sensitization, phenotypes reminiscent of PTH in patients, in both cephalic and extracephalic regions. By contrast, closed head injury induces only transient cephalic tactile hypersensitivity, with no extracephalic consequences. Both models show more severe phenotype with repetitive daily injury for three days, compared to either one or three successive injuries in a single day, providing new insight into patterns of injury that may place patients at greater risk of developing PTH. Importantly, even after recovery from transient cephalic tactile hypersensitivity, mice subjected to closed head injury had persistent hypersensitivity to established migraine triggers, including calcitonin gene-related peptide (CGRP) and sodium nitroprusside, a nitric oxide donor. Our results offer new tools for studying PTH, as well as preclinical support for a pathophysiologic role of CGRP in this condition. SummaryTwo models of post-traumatic headache after traumatic brain injury provide novel laboratory tools and insights in relative risks of injury and therapeutic opportunities.

neuroscience↗