Strain in the Midbrain: Impact of Traumatic Brain Injury on the Central Serotonin System.

Traumatic brain injury (TBI) is a pervasive public health crisis that severely impacts the quality of life of affected individuals. Like peripheral forms of trauma, TBI results from extraordinarily heterogeneous environmental forces being imparted on the cranial space, resulting in heterogeneous disease pathologies. This has made therapies for TBI notoriously difficult to develop, and currently, there are no FDA-approved pharmacotherapies specifically for the acute or chronic treatment of TBI.

Increased Carbon Dioxide Respiration Prevents the Effects of Acceleration/Deceleration Elicited Mild Traumatic Brain Injury.

Acceleration/deceleration forces are a common component of various causes of mild traumatic brain injury (mTBI) and result in strain and shear forces on brain tissue. A small quantifiable volume dubbed the compensatory reserve volume (CRV) permits energy transmission to brain tissue during acceleration/deceleration events. The CRV is principally regulated by cerebral blood flow (CBF) and CBF is primarily determined by the concentration of inspired carbon dioxide (CO).

Effect of driver gas composition on production of scaled Friedlander waveforms in an open-ended shock tube model.

With the evolution of modern warfare and the increased use of improvised explosive devices (IEDs), there has been an increase in blast-induced traumatic brain injuries (bTBI) among military personnel and civilians. The increased prevalence of bTBI necessitates bTBI models that result in a properly scaled injury for the model organism being used. The primary laboratory model for bTBI is the shock tube, wherein a compressed gas ruptures a thin membrane, generating a shockwave.