GABA potentiation: a logical pharmacological approach for the treatment of acute ischaemic stroke

  title={GABA potentiation: a logical pharmacological approach for the treatment of acute ischaemic stroke},
  author={A Richard Green and Atticus H. Hainsworth and David M. Jackson},
Coactivation of GABAA and GABAB Receptor Results in Neuroprotection During In Vitro Ischemia
Antiepileptic drugs targeting GABAergic transmission can exert neuroprotective effects against ischemia by increasing endogenous GABA levels and via the activation of both GABAA and GABAB receptors.
The Role of Peri-synaptic GABA Receptors After Stroke
D dampening tonic GABA inhibition from 3 days poststroke can afford an early and robust improvement in functional recovery after stroke and boosting tonic inhibition early after a stroke can afford significant protection and minimize the extent of neuronal cell loss.
Perisynaptic GABA Receptors The Overzealous Protector
  • A. Clarkson
  • Biology, Psychology
    Advances in pharmacological sciences
  • 2012
Substantial evidence suggests that local inhibitory and excitatory currents are altered after stroke and modulation of these networks to enhance excitability during the repair phase can facilitate functional recovery after stroke.
g-Aminobutyric acidA neurotransmission and cerebral ischemia
Evidence for the role of g-aminobutyric acid (GABA) neurotransmission in cerebral ischemia-induced neuronal death and how dysfunction of GABA neurotransmission may contribute to neuronal death are presented and how neuronal death can be prevented by GABAergic drugs are discussed.
Protection of Malonate-Induced GABA But Not Dopamine Loss by GABA Transporter Blockade in Rat Striatum
GABA transporter blockade during mitochondrial impairment in the striatum provides protection to GABAergic neurons and points to fundamental differences between immature and adult neurons in the downstream involvement of GABA receptors during metabolic insult.
The Gliopeptide ODN, a Ligand for the Benzodiazepine Site of GABAA Receptors, Boosts Functional Recovery after Stroke
It is proposed that octadecaneuropeptide (ODN), an endogenous allosteric modulator of the GABAAR synthesized by astrocytes, influences the outcome of ischemic brain tissue and subsequent functional recovery and can be used as a delayed treatment to safely correct cortical excitability and facilitate sensorimotor recovery after stroke.


Effect of gamma-aminobutyric acid modulation on neuronal ischemia in rabbits.
Pharmacological manipulation of the GABA-A receptor may offer another avenue of therapy for central nervous system ischemia, possibly with less severe associated physiological side effects than other effective drugs.
Protection against ischaemic neuronal damage by drugs acting on excitatory neurotransmission.
  • B. Meldrum
  • Medicine, Biology
    Cerebrovascular and brain metabolism reviews
  • 1990
The availability of competitive and noncompetitive antagonists acting at the NMDA receptor has permitted the demonstration of cerebroprotective effects of these compounds in animal models of global, focal, neonatal, and secondary cerebral ischaemia.
Combination Therapy Protects Ischemic Brain in Rats: A Glutamate Antagonist Plus a γ‐Aminobutyric Acid Agonist
Combination therapy, using a glutamate antagonist and a GABA-A agonist, appeared to protect the brain and ameliorate a defect in learning behavior after stroke and may have been more effective than either agent used alone, although further study of higher doses is needed.
GABA Agonist "Muscimol" Is Neuroprotective in Repetitive Transient Forebrain Ischemia in Gerbils
The study shows that potentiation of inhibitory mechanisms may be important mechanisms of neuronal protection from the effects of repetitive ischemia and the effects are not limited to the SNr.
NMDA antagonists: their role in neuroprotection.
Postischemic inhibition of GABA reuptake by tiagabine slows neuronal death in the gerbil hippocampus
It is suggested that tiagabine slows the development of hippocampal degeneration following ischemia, and that mild, postischemic hypothermia is responsible, in large part, for the neuroprotective actions of this drug.
Long-Term Neuroprotection by Benzodiazepine: Full Versus Partial Agonists after Transient Cerebral Ischemia in the Gerbil
If given early enough during reperfusion, both benzodiazepine full and partial agonists are neuroprotective for at least 35 days, but the lack of sedating side effects of imidazenil must be weighed against its reduced efficacy.