Journal of neurotrauma
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Journal of neurotrauma · Jan 1988
Controlled cortical impact: a new experimental brain injury model.
A new experimental model of mechanical brain injury was produced in the laboratory ferret (Mustela putorius furo) using a stroke-constrained pneumatic impactor. Cortical impacts were made on vertex to the intact dura mater overlying the cerebral cortex with contact velocities ranging from 2.0 to 4.0 m/sec and with deformations of 2.0 to 5.0 mm. The dwell time of the impact and the stability of the skull during impact were verified with high speed (1000 to 3000 frames/sec) cineradiography. ⋯ The spectrum of anatomic injury and systemic physiologic responses closely resembled aspects of closed head injury seen clinically. This procedure complements and improves on existing techniques by allowing independent control of contact velocity and level of deformation of the brain to facilitate biomechanical and analytic modeling of brain trauma. Graded cortical contusions and subcortical injury are produced by precisely controlled brain deformations, thereby allowing questions to be addressed regarding the influence of contact velocity and level of deformation on the anatomic and functional severity of brain injury.
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Journal of neurotrauma · Jan 1988
The effects of scopolamine and traumatic brain injury on central cholinergic neurons.
This study examined the effects of scopolamine and fluid percussion traumatic brain injury (TBI) on the activity of cholinergic neurons in specific areas of the rat brain 12 min, 4 h, and 24 h after injury. Acetylcholine (ACh) turnover, used as an index of cholinergic neuronal activity, was determined using gas chromatography-mass fragmentography. ⋯ The responses of thalamic, hippocampal, and amygdaloid cholinergic neurons to TBI did not differ substantially in scopolamine-pretreated rats from those studied previously in untreated fluid-percussion-injured rats. However, cholinergic neurons in the cingulate-frontal cortex of rats receiving TBI did respond in a different manner to scopolamine than those of rats receiving sham injury, suggesting a disruption of regulation of cortical cholinergic neurons following this model of TBI.