Cerebellar norepinephrine infusions facilitate recovery after sensorimotor cortex injury

Boyeson, Michael G.; Krobert, Kurt A.

doi:10.1016/0361-9230(92)90080-h

Cited by 54 publications

(31 citation statements)

References 12 publications

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“…33 Taken together, these findings suggest that amphetamine-accelerated recovery may be mediated by noradrenergic rather than dopaminergic neurotransmission. -33 appear to recover by the first testing session, it is improbable that the behavioral recovery is due to structural changes proximal to the site of injury.…”

Section: -32mentioning

confidence: 71%

Amphetamine promotes recovery from sensory-motor integration deficit after thrombotic infarction of the primary somatosensory rat cortex.

Hurwitz

Dietrich

McCabe

et al. 1991

Stroke

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The present studies were undertaken to examine 1) whether (/-amphetamine sulfate administered to rats well after thrombotic infarction of the vibrissal cortical barrel-field within the primary somatosensory cortex affected the rate and completeness of behavioral recovery and 2) whether a dose-response relation exists between (/-amphetamine sulfate dose and recovery of function. In a learning task requiring sensory-motor integration, 41 rats were trained to perform a motor response in a T-maze consequent to the detection of a vibrissal deflection cue. Once training was complete, unilateral (ft=29) or sham (n = 12) infarction was produced by a noninvasive photochemical technique. After infarction, T-maze performance was assessed repeatedly in rats receiving 2 (n = 10) or4(n=10) mg/kg J-amphetamine sulfate or saline (/i=9) 24 hours prior to testing on days 4, 6, 9, and 11. The sham-operated control rats received (/-amphetamine sulfate (n-1) or no injections (n-5). All three infarcted groups displayed a reliable and sustained behavioral deficit in performance that was not present in the shamoperated control animals. Although the performance of each infarcted group improved over the testing sessions after the first injection, the amphetamine-treated groups improved at a faster rate than the saline-injected group. The results further demonstrated a dose-response effect, with the 4 mg/kg amphetamine group recovering to within preinfarction levels 6-8 days earlier than the 2 mg/kg amphetamine and saline-injected groups. Moreover, both amphetaminetreated groups recovered more completely than the saline-injected group. Quantification of the chronic infarct area revealed no differences among the amphetamine-treated and saline-injected groups. These data provide further evidence of the facilitatory effect of (/-amphetamine sulfate on recovery from brain injury and extend this effect to the enhancement of recovery subsequent to thrombotic infarction of the primary somatosensory cortex. (Stroke 1991^22:648-654) S ince the turn of this century, the remarkable capacity for the brain to recover from cerebral injury, such as stroke, has spurred interest in the use of animal models to study mechanisms of functional recovery and apply them in the clinical setting.1 In recent years, data from animal studies Received August 27, 1990; accepted January 29, 1991. and preliminary clinical findings indicate that some pharmacologic manipulations that alter neurotransmitter (e.g., acetylcholine, •y-amino butyric acid, serotonin, dopamine, and norepinephrine [NE]) function may markedly promote recovery of function following brain injury. 2 One promising agent, the catecholamine agonist amphetamine, has been consistently shown during the past 20 years to reinstate locomotor, righting, and other postural reflexes and enhance recovery from learning and memory deficits induced by electrolytic brain lesions. 2^1 In particular, one recent study found that a single dose of amphetamine given to cats 10 days after unilateral motor cortex ablation...

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Section: -32mentioning

confidence: 71%

Amphetamine promotes recovery from sensory-motor integration deficit after thrombotic infarction of the primary somatosensory rat cortex.

Hurwitz

Dietrich

McCabe

et al. 1991

Stroke

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“…In general, treatments that enhance the synaptic effects of NE improve the rate or amount of recovery following brain injury (Meyer et al, 1963;Feeney et al, 1981;Feeney et al, 1982;Feeney and Hovda, 1983;Hovda et al, 1987;1989;Boyeson et al, 1992;Feeney et al, 1993;Queen et al, 1997;Kikuchi et al, 1999;Kikuchi et al, 2000). Furthermore, amphetamine and NE reuptake inhibitors have been demonstrated to improve function in humans following stroke (Boyeson, 1996).…”

Section: Vns In Cns Injurymentioning

confidence: 99%

Increased extracellular concentrations of norepinephrine in cortex and hippocampus following vagus nerve stimulation in the rat

Roosevelt¹,

et al. 2006

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The vagus nerve is an important source of afferent information about visceral states and it provides input to the locus coeruleus (LC), the major source of norepinephrine (NE) in the brain. It has been suggested that the effects of electrical stimulation of the vagus nerve on learning and memory, mood, seizure suppression, and recovery of function following brain damage are mediated, in part, by the release of brain NE. The hypothesis that left vagus nerve stimulation (VNS) at the cervical level results in increased extracellular NE concentrations in the cortex and hippocampus was tested at four stimulus intensities 0.0, 0.25, 0.5, and 1.0 mA. Stimulation at 0.0 and 0.25 mA had no effect on NE concentrations, while the 0.5 mA stimulation increased NE concentrations significantly in the hippocampus (23%), but not the cortex. However, 1.0 mA stimulation significantly increased NE concentrations in both the cortex (39%) and hippocampus (28%) bilaterally. The increases in NE were transient and confined to the stimulation periods. VNS did not alter NE concentrations in either structure during the inter-stimulation baseline periods. No differences were observed between NE levels in the initial baseline and the post-stimulation baselines. These findings support the hypothesis that VNS increases extracellular NE concentrations in both the hippocampus and cortex.

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“…This theory may presently also apply to denervation supersensitivity and collateral sprouting, both occurring before the development of significant anatomical rewiring. Several authors have found, after permanent unilateral sensorimotor lesions in the rat and cat, that contralateral motor deficits recover in about 2 weeks in the rat [13,14], within 2 months in the cat [12] and after 2-3 months after anatomical hemispherectomy in monkeys [17]. In the present study, we have tried to determine the role of the cerebellum in the motor recovery after anatomical microsurgical cerebral hemispherectomy in rats, using this procedure as an experimental model of the routine clinical neurosurgical hemispherectomies.…”

Section: Introductionmentioning

confidence: 99%

“…Recent research has provided data that reveal several forms of brain plasticity [9][10][11], including changes in neurotransmitter sensitivity [12][13][14], collateral sprouting [15], and von Monakow's diaschisis phenomenon [5,6,10], as an increasing evidence that not only function but also structure in the lesioned nervous system can be partially recovered. A large portion of recovery is ascribable to taking over of functions by redundant circuitry, but it is presently clear that neuronal regeneration may also be involved [15,16].…”

Section: Introductionmentioning

confidence: 99%

Functional Recovery after Combined Cerebral and Cerebellar Hemispherectomy in the Rat

Marino

Machado

Timo-Iaria

2001

Stereotact Funct Neurosurg

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The cerebellum seems to be one of the structures responsible for early neurological improvement after cerebral hemispherectomy and its consequent deficits. Considered as an accessory brain, the cerebellum may constitute a neurobiological substrate for the recovery of such extensive cortical and subcortical lesions. It may compensate for the injury by structural remodeling and plasticity. The authors observed that, indeed, rats submitted to contralateral hemicerebellectomy before cerebral hemispherectomy do not recover as well as those submitted to hemicerebellectomy 2 weeks after cerebral hemispherectomy.

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Cerebellar norepinephrine infusions facilitate recovery after sensorimotor cortex injury

Cited by 54 publications

References 12 publications

Amphetamine promotes recovery from sensory-motor integration deficit after thrombotic infarction of the primary somatosensory rat cortex.

Amphetamine promotes recovery from sensory-motor integration deficit after thrombotic infarction of the primary somatosensory rat cortex.

Increased extracellular concentrations of norepinephrine in cortex and hippocampus following vagus nerve stimulation in the rat

Functional Recovery after Combined Cerebral and Cerebellar Hemispherectomy in the Rat

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