γ-Aminobutyric acid-induced potentiation of cortical hemiplegia

Brailowsky, Simón; Knight, Robert T.; Blood, Katherine; Scabini, Donatella

doi:10.1016/0006-8993(86)90457-9

Cited by 90 publications

(32 citation statements)

References 27 publications

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“…GABA-mimetic drugs, such as clomethiazole or muscimol, are neuroprotective in animal models, and combination therapy with NMDA antagonists (eg, MK-801) may be more effective, but GABA agonists are associated with a high incidence of respiratory depression. 22,23 Like the NMDA antagonists, they act on membrane receptors and should be administered within the same time window and over the same period.…”

Section: Mechanisms Of Actionmentioning

confidence: 99%

Duration of Neuroprotective Treatment for Ischemic Stroke

Dyker

Lees

1998

Stroke

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Background-The therapeutic time window for thrombolysis appears to be extremely short, probably because of the hemorrhagic complications associated with late reperfusion of ischemic brain tissue. Other neuroprotective forms of treatment continue to be developed, although their efficacy has yet to be conclusively proved in patients. The duration of treatment in recent phase 3 trials ranges from a single bolus injection to 12 weeks of oral therapy. Summary of Review-In this article we discuss the factors that should influence the choice of route and duration of treatment.Excitotoxic injury following stroke evolves over at least 4 hours in rodents and possibly beyond 48 hours in humans. In addition, autoregulation and local cerebral perfusion are deranged for approximately 72 hours in patients with stroke. Neuroprotection should provide cover during this critical time. Conclusions-Important considerations influencing drug administration should include the pharmacology of the compound (pharmacokinetics, mechanism of action, preclinical toxicity, and pharmaceutical properties), its safety and tolerability in patients, and the likelihood of continuing or recurrent cerebral ischemia, along with practical issues such as ease of administration and interactions with early rehabilitation and other therapies. Optimization of treatment will be possible only when neuroprotection is confirmed to be effective. (Stroke. 1998;29:535-542.)

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Section: Mechanisms Of Actionmentioning

confidence: 99%

Duration of Neuroprotective Treatment for Ischemic Stroke

Dyker

Lees

1998

Stroke

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“…No previous study has infused muscimol into the ipsilateral or contralateral VNC during compensation. Furthermore, only one study has infused muscimol (62.5 and 250 ng/h) via a mini-osmotic pump into brain tissue (Martin et al, 2000); therefore, the muscimol dose used was based on previous studies that have delivered either muscimol or GABA into the brain via a mini-osmotic pump (Brailowsky et al, 1986;SilvaBarrat et al, 1989). Brailowsky and colleagues have used a high GABA dose (1000 g/h) that induces a "GABA withdrawal syndrome" characterized by spontaneous epileptic activity in the area surrounding the infusion.…”

Section: Methodsmentioning

confidence: 99%

Effects of Chronic Infusion of a GABA_A Receptor Agonist or Antagonist into the Vestibular Nuclear Complex on Vestibular Compensation in the Guinea Pig

Gliddon

Darlington²,

Smith³

2005

J Pharmacol Exp Ther

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The aim of this study was to determine the effects of chronic infusion of a GABA A receptor agonist/antagonist into the ipsilateral or contralateral vestibular nuclear complex (VNC) on vestibular compensation, the process of behavioral recovery that occurs after unilateral vestibular deafferentation (UVD). This was achieved by a mini-osmotic pump that infused, over 30 h, muscimol or gabazine into the ipsilateral or contralateral VNC. Spontaneous nystagmus (SN), yaw head tilt (YHT), and roll head tilt (RHT) were measured. Infusion of muscimol or gabazine into either the ipsilateral or the contralateral VNC had little effect on SN compensation. In contrast, infusion of muscimol (250, 500, and 750 ng) into the contralateral VNC and gabazine (31.25, 62.5, and 125 ng) into the ipsilateral VNC significantly affected YHT and RHT (p Ͻ 0.05), but not their rate of compensation (p Ͼ 0.05). Interestingly, the effects of muscimol and gabazine on YHT and RHT were consistent throughout the first 30 h post-UVD. Infusion of muscimol (62.5, 125, and 250 ng) into the ipsilateral VNC and gabazine (125, 375, and 750 ng) into the contralateral VNC had little effect on YHT and RHT or their rate of compensation. These results suggest that the ipsilateral gabazine and contralateral muscimol infusions are modifying the expression of the symptoms without altering the mechanism of compensation. Furthermore, the neurochemical mechanism responsible for vestibular compensation can cope with the both the GABA A receptor-mediated and the UVD-induced decrease in resting activity.

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“…73 Intracortical infusion of the inhibitory neurotransmitter increases the hemiparesis produced by a small motor cortex lesion in rats. 74 Diazepam, an indirect GABA agonist, impedes recovery from the sensory asymmetry caused by anterior-medial neocortex damage in the rat. 75 Amphetamine administration influences the activity of GABAergic neurons, leading to lower extracellular GABA concentrations.…”

Section: Other Neurotransmitters and Motor Recoverymentioning

confidence: 99%

Neurotransmitters and motor activity: Effects on functional recovery after brain injury

Goldstein

2006

NeuroRX

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Summary: There are complex relationships among behavioral experience, brain morphology, and functional recovery of an animal before and after brain injury. A large series of experimental studies have shown that exogenous manipulation of central neurotransmitter levels can directly affect plastic changes in the brain and can modulate the effects of experience and training. These complex relationships provide a formidable challenge for studies aimed at understanding neurotransmitter effects on the recovery process. Experiments delineating norepinephrine-modulated locomotor recovery after injury to the cerebral cortex illustrate the close relationships among neurotransmitter levels, brain plasticity, and behavioral recovery. Understanding the neurobiological processes underlying recovery, and how they might be manipulated, may lead to novel strategies for improving recovery from stroke-related gait impairment in humans.

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γ-Aminobutyric acid-induced potentiation of cortical hemiplegia

Cited by 90 publications

References 27 publications

Duration of Neuroprotective Treatment for Ischemic Stroke

Duration of Neuroprotective Treatment for Ischemic Stroke

Effects of Chronic Infusion of a GABA_A Receptor Agonist or Antagonist into the Vestibular Nuclear Complex on Vestibular Compensation in the Guinea Pig

Neurotransmitters and motor activity: Effects on functional recovery after brain injury

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γ-Aminobutyric acid-induced potentiation of cortical hemiplegia

Cited by 90 publications

References 27 publications

Duration of Neuroprotective Treatment for Ischemic Stroke

Duration of Neuroprotective Treatment for Ischemic Stroke

Effects of Chronic Infusion of a GABAA Receptor Agonist or Antagonist into the Vestibular Nuclear Complex on Vestibular Compensation in the Guinea Pig

Neurotransmitters and motor activity: Effects on functional recovery after brain injury

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Product

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Effects of Chronic Infusion of a GABA_A Receptor Agonist or Antagonist into the Vestibular Nuclear Complex on Vestibular Compensation in the Guinea Pig