Effects of scopolamine treatment on long-term behavioral deficits following concussive brain injury to the rat

Lyeth, Bruce G.; Dixon, C. Edward; Jenkins, Larry W.; Hamm, Robert J.; Alberico, Anthony; Young, Harold F.; Stonnington, Henry H.; Hayes, Ronald L.

doi:10.1016/0006-8993(88)90006-6

Cited by 110 publications

(27 citation statements)

References 42 publications

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“…Traumatized animals showed full recovery of function for vibrissae-evoked forelimb placing and lateral stepping by 21 days after injury (Figs. 4B,C), a result that is in agree- ment with previous studies on controlled cortical impact (Hamm et al, 1992a;Hoffman et al, 1994;Smith et al, 1995;Dixon et al, 1999;Clark et al, 2000), fluid percussion injury (Lyeth et al, 1988(Lyeth et al, , 1990McIntosh et al, 1989;Hamm et al, 1992b) and impact-acceleration injury (Beaumont et al, 1999). In these reports, similar time courses of neurological deficits were found, namely a functional impairment in the first 7 to 10 days after injury followed by a relatively rapid recovery.…”

Section: Discussionsupporting

confidence: 80%

Upregulation of ICAM-1 and MCP-1 but not of MIP-2 and sensorimotor deficit in response to traumatic axonal injury in rats

et al. 2001

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Section: Discussionsupporting

confidence: 80%

Upregulation of ICAM-1 and MCP-1 but not of MIP-2 and sensorimotor deficit in response to traumatic axonal injury in rats

et al. 2001

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“…The delivery of the pressure pulse was associated with brief (Ͻ120 -200 sec), transient traumatic unconsciousness (as assessed by the duration of the suppression of the righting reflex). Although the injured animals in this study, subjected only to mild or moderate impacts, did not exhibit any obvious lasting behavioral deficit or seizure activity, fluid percussion head injury, especially at higher impact forces, can lead to detectable motor and memory deficits that last for days (Lyeth et al, 1988;McIntosh et al, 1989;Povlishock et al, 1994). Before and during each experiment, great care was taken to ensure that no air bubble was trapped or had formed in the device.…”

Section: Methodsmentioning

confidence: 95%

“…At mild to moderate impact forces, there is minimal cortical injury, similar to that which occurs in humans after mild to moderate closed head injury. Fluid percussion injury leads to neurological and behavioral features similar to mild to moderate head injury in humans, including hyperexcitability and memory and motor deficits (Lyeth et al, 1988;Dixon et al, 1989;Lowenstein et al, 1992). Specifically, we sought to answer the following questions.…”

mentioning

confidence: 99%

Instantaneous Perturbation of Dentate Interneuronal Networks by a Pressure Wave-Transient Delivered to the Neocortex

et al. 1997

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Whole-cell patch-clamp recordings and immunocytochemical experiments were performed to determine the short-and longterm effects of lateral fluid percussion head injury on the perisomatic inhibitory control of dentate granule cells in the adult rat, with special reference to the development of traumainduced hyperexcitability. One week after the delivery of a single, moderate (2.0-2.2 atm) mechanical pressure wave to the neocortex, the feed-forward inhibitory control of dentate granule cell discharges was compromised, and the frequency of miniature IPSCs was decreased. Consistent with the electrophysiological data, the number of hilar parvalbumin (PV)-and cholecystokinin (CCK)-positive dentate interneurons supplying the inhibitory innervation of the perisomatic region of granule cells was decreased weeks and months after head injury. The initial injury to the hilar neurons took place instantaneously after the impact and did not require the recruitment of active physiological processes. Furthermore, the decrease in the number of PV-and CCK-positive hilar interneurons was similar to the decrease in the number of the AMPA-type glutamate receptor subunit 2/3-immunoreactive mossy cells, indicating that the pressure wave-transient causes injurious physical stretching and bending of most cells that are large and not tightly packed in a cell layer.These results reveal for the first time that moderate pressure wave-transients, triggered by traumatic head injury episodes, impact the dentate neuronal network in a unique temporal and spatial pattern, resulting in a net decrease in the perisomatic control of granule cell discharges.

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“…These processes result in depolarization of traumatically deformed axons and propagation of action potentials to synaptic terminals. When cholinergic or glutamatergic neurons are traumatically activated and release these neurotransmitters in excess, they are, alone or in combination, excitotoxic to postsynaptic targets and also presynaptic afferents [7,[31][32][33][34]. Given the co-localization of these systems within cerebral areas important to attention, memory, and executive function (ie, hippocampus, thalamus, frontal cortex) [21], excessive activation of cholinergic or glutamatergic neurons predictably results in acute and chronic dysfunction of these areas and the cognitive functions they serve.…”

Section: Cholinergic Dysfunction After Traumatic Brain Injury: Animalmentioning

confidence: 97%

The cholinergic hypothesis of cognitive impairment caused by traumatic brain injury

Arciniegas

2003

Curr Psychiatry Rep

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Cognitive impairments are among the most common neuropsychiatric sequelae of traumatic brain injury at all levels of severity. Cerebral cholinergic neurons and their ascending projections are particularly vulnerable to acute and chronic traumatically mediated dysfunction. In light of the important role of acetylcholine in arousal, attention, memory, and other aspects of cognition, cerebral cholinergic systems contribute to and may also be a target for pharmacologic remediation among individuals with post-traumatic cognitive impairments. This article will review the evidence in support of this hypothesis. Evidence of relatively selective damage to cholinergic injury, the development of persistent anticholinergic sensitivity, and the effects of cholinergic augmentation on memory performance are presented first. Thereafter, neuropathologic, electrophysiologic, and pharmacologic evidence of cholinergic dysfunction after traumatic brain injury in humans is reviewed. Finally, future directions for investigation of the cholinergic hypothesis and possible clinical applications of this information are discussed.

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Effects of scopolamine treatment on long-term behavioral deficits following concussive brain injury to the rat

Cited by 110 publications

References 42 publications

Upregulation of ICAM-1 and MCP-1 but not of MIP-2 and sensorimotor deficit in response to traumatic axonal injury in rats

Upregulation of ICAM-1 and MCP-1 but not of MIP-2 and sensorimotor deficit in response to traumatic axonal injury in rats

Instantaneous Perturbation of Dentate Interneuronal Networks by a Pressure Wave-Transient Delivered to the Neocortex

The cholinergic hypothesis of cognitive impairment caused by traumatic brain injury

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