Catecholamines and Recovery of Function after Brain Damage

Feeney, Dennis M.; Sutton, Richard L.

doi:10.1007/978-1-4613-0927-7_7

Cited by 33 publications

(12 citation statements)

References 29 publications

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“…Widespread metabolic depression similar to that obtained in our model has been reported following unilateral ablation of sensorimotor cortex in rats and interpreted within the context of von Mona kow's theory of diaschisis (Feeney et a!., 1985;Feeney and Baron, 1986;Feeney and Sutton, 1988). In apparent contrast to our results, these authors found that after cortical injury, catecholamine acti vation with amphetamine alleviated what they call the metabolic remote functional depression, which was accelerated by LC lesions and exacerbated by catecholamine blockade with haloperidol.…”

Section: Discussionsupporting

confidence: 77%

The Effect of α-Adrenergic Receptor Blockers Prazosin and Yohimbine on Cerebral Metabolism and Biogenic Amine Content of Traumatized Brain

Inoue

McHugh

Pappius

1991

J Cereb Blood Flow Metab

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Widespread decrease in local cerebral glucose utilization (LCGU) previously shown to occur 3 days after a local freezing lesion was interpreted as reflecting a depression of functional activity in the affected areas. In parallel experiments, cortical norepinephrine (NE) content of traumatized brain was found to be decreased. The effects of prazosin (PZ), an alpha 1-adrenergic receptor blocker, and yohimbine (YOH), an alpha 2-blocker, on glucose use and biogenic amine content of lesioned rat brain were studied to determine if the changes in the noradrenergic system associated with injury are of functional importance, to identify the receptors that may be involved in mediating the action of NE in injured brain, and to look for evidence of interaction between the noradrenergic and the serotonergic systems in traumatized brain. PZ (1 mg/kg) given 30 min before the lesion ameliorated the subsequent metabolic cortical depression seen in untreated animals. PZ given for 3 days starting before the lesion (3 mg/kg/day) was also effective in normalizing LCGU in areas where it was depressed by lesioning, despite the fact that this regimen induced significant global decrease in LCGU in normal animals. Once cortical metabolic depression had developed 3 days after the lesion, it could not be modified by PZ. YOH was less effective than PZ and was so only when given for 3 days (22.5 mg/kg/day in three divided doses). PZ (3 mg/kg/day in three divided doses) slightly but significantly decreased the accumulation of the serotonin (5-HT) metabolite 5-hydroxyindoleacetic acid in the traumatized hemisphere. These results provide evidence that blockage of alpha 1-adrenergic receptors prevents the development of cortical dysfunction associated with brain trauma. This implies that the noradrenergic system plays a role in the functional consequences of injury and that this effect is, at least in part, mediated by alpha 1-adrenergic receptors. Furthermore, alpha 1-adrenergic receptor blockage appears to modulate cortical turnover of 5-HT, previously also implicated in functional consequences of brain injury. The data are compatible with inhibitory effects of NE in the cortex and suggest a potential of alpha 1-adrenergic blockage in development of novel therapeutic approaches to brain injury.

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Section: Discussionsupporting

confidence: 77%

The Effect of α-Adrenergic Receptor Blockers Prazosin and Yohimbine on Cerebral Metabolism and Biogenic Amine Content of Traumatized Brain

Inoue

McHugh

Pappius

1991

J Cereb Blood Flow Metab

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“…However, the rate of recovery was enhanced in rats that were required to traverse the beam while under the influence of D ‐AMP. A number of subsequent studies have extended these results 39, 40, 42, 43, 45, 63, 64, 66, 87, 197, 210. The results indicate that a tight coupling between behavioral experience and D ‐AMP intoxication is necessary for optimal recovery.…”

Section: Modulation Of Motor Recovery By Pharmacologic Treatmentmentioning

confidence: 76%

Role of adaptive plasticity in recovery of function after damage to motor cortex

2001

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Based upon neurophysiologic, neuroanatomic, and neuroimaging studies conducted over the past two decades, the cerebral cortex can now be viewed as functionally and structurally dynamic. More specifically, the functional topography of the motor cortex (commonly called the motor homunculus or motor map), can be modified by a variety of experimental manipulations, including peripheral or central injury, electrical stimulation, pharmacologic treatment, and behavioral experience. The specific types of behavioral experiences that induce long-term plasticity in motor maps appear to be limited to those that entail the development of new motor skills. Moreover, recent evidence demonstrates that functional alterations in motor cortex organization are accompanied by changes in dendritic and synaptic structure, as well as alterations in the regulation of cortical neurotransmitter systems. These findings have strong clinical relevance as it has recently been shown that after injury to the motor cortex, as might occur in stroke, post-injury behavioral experience may play an adaptive role in modifying the functional organization of the remaining, intact cortical tissue.

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“…Prior studies using cortical freezing lesion, ablation, concussion, contusion, or stroke-injury models have also reported a depression of both cerebral oxidative (Dail et al, 1981;Hovda et al, 1991;Hovda, 1996;) and glycolytic (Pappius, 1981;Colleet al, 1986;Pappius et al, 1988;Sutton et al, 1989a;Dielrich et al, 1990;Yoshino et al, 1991;Queen et al, 1997) metabolism. As with the current findings, such injury-induced metabolic depressions are most evident within the ipsilateral cortical and/or subcortical regions during the first few days post injury. The physiological consequences of these injuryinduced metabolic depressions may be functionally related to the neurobehavioral deficits in the contralateral limbs that are exhibited during this same time period post injury (Feeney et al, 1982; Feeney & Sutton, , 1988Gilman et al, 1987;Sutton et al, 1987;.…”

Section: Effect Of Amphetamine In Sham Operatesmentioning

confidence: 99%

Alleviation of Brain Injury‐Induced Cerebral Metabolic Depression by Amphetamine: A Cytochrome Oxidase Histochemistry Study

Sutton

Hovda²,

Chen

et al. 2000

Neural Plasticity

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Measurements of oxidative metabolic capacity following the ablation of rat sensorimotor cortex and ,he administration of amphetamine were examined to determine their effects on the metabolic dysfunction that follows brain injury. Twenty-four hours after surgery, rats sustaining either sham operations or unilateral cortical ablation were administered a single injection of D-amphetamine (2 mg/kg; i.p.) or saline and then sacrificed 24 h later. Brain tissue was processed for cytochrome oxidase histochemistry, and 12 bilateral cerebral areas were measured, using optical density as an index of the relative amounts of the enzyme. Compared with that of the control groups, cytochrome oxidase in the injured animals was significantly reduced throughout the cerebral cortex and in 5 of II subcortical structures. This injury-induced depression of oxidative capacity was most pronounced in regions of the hemisphere ipsilateral to the ablation. Animals given D-amphetamine had less depression of oxidative capacity, which was most pronounced bilaterally in the cerebral cortex, red nucleus, and superior colliculus; and in the nucleus accumbens, caudateputamen, and globus pallidus ipsilaterai to the ablation. The ability of D-amphetamine to alleviate depressed cerebral oxidative metabolism following cortical injury may be one mechanism by which drugs increasing noradrenaline release accelerate functional recovery in both animals and humans.

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Catecholamines and Recovery of Function after Brain Damage

Cited by 33 publications

References 29 publications

The Effect of α-Adrenergic Receptor Blockers Prazosin and Yohimbine on Cerebral Metabolism and Biogenic Amine Content of Traumatized Brain

The Effect of α-Adrenergic Receptor Blockers Prazosin and Yohimbine on Cerebral Metabolism and Biogenic Amine Content of Traumatized Brain

Role of adaptive plasticity in recovery of function after damage to motor cortex

Alleviation of Brain Injury‐Induced Cerebral Metabolic Depression by Amphetamine: A Cytochrome Oxidase Histochemistry Study

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