Linked from

The 39 pages that link to GABA, each with the reason it gives.

• NeurotransmitterBroader topic: Its signaling counterbalances excitation and helps regulate neural circuit activity.

• BenzodiazepineNarrower topic: Benzodiazepines amplify signaling initiated by this neurotransmitter rather than replacing it.

• AcetylcholineCompared with: GABA commonly suppresses neural activity, contrasting with acetylcholine's varied receptor-dependent effects.

• GlutamateCompared with: GABA often counterbalances the excitation produced by glutamate.

• Basal gangliaRelated: Inhibitory GABAergic connections link many basal ganglia nuclei and shape their output.

• GABA receptorBroader topic: It is the signaling molecule that activates GABA receptors.

• GABA-A receptorRelated: Binding of this neurotransmitter opens the receptor’s ion channel.

• BarbiturateRelated: Barbiturates strengthen signaling through receptors activated by this neurotransmitter.

• DiazepamRelated: Diazepam enhances signaling at receptors activated by this neurotransmitter.

• FlumazenilRelated: Benzodiazepines alter receptor responses to GABA; flumazenil does not replace or directly block GABA.

• Alcohol withdrawal syndromeRelated: Alcohol enhances GABA-mediated inhibition; chronic exposure leads the brain to compensate.

• Antiseizure medicationRelated: Some medicines strengthen GABA-mediated inhibition to reduce seizure activity.

• Benzodiazepine dependenceNarrower topic: Benzodiazepines enhance signaling at GABA receptors, linking their calming effects to adaptation.

• ValproateRelated: Valproate can increase brain GABA levels, strengthening inhibitory signaling.

• CarbamazepineRelated: Its inhibitory signaling complements the reduction in excitation caused by sodium-channel blockade.

• Alcohol intoxicationRelated: Alcohol enhances some GABA-mediated signaling, contributing to sedation and slowed responses.

• SedativeRelated: Many sedatives enhance GABA signaling, increasing inhibition across neural circuits.

• TetanusRelated: Blocking its release helps explain the loss of inhibition behind tetanic spasms.

• CatatoniaRelated: Reduced GABA activity is one proposed contributor to catatonic symptoms and benzodiazepine response.

• Glutamic acidCompared with: It contrasts with glutamate's predominantly excitatory signaling and is synthesized from glutamate.

• GabapentinCompared with: Despite its name and structural resemblance, gabapentin does not act as a direct GABA receptor agonist.

• LevetiracetamRelated: Levetiracetam's antiseizure action is not explained by directly enhancing GABA signaling.

• SevofluraneRelated: Sevoflurane enhances inhibitory signaling involving GABA receptors, contributing to unconsciousness.

• Absence seizureRelated: GABA signaling in thalamic circuits is implicated in rhythms associated with absence seizures.

• MidazolamNarrower topic: Midazolam amplifies signaling initiated by this neurotransmitter rather than replacing it.

• ZolpidemRelated: Zolpidem amplifies the inhibitory effects of GABA rather than activating its receptor by itself.

• Clostridium tetaniRelated: Blocking its release removes signals that restrain motor-neuron activity.

• Delirium tremensRelated: Chronic alcohol exposure enhances GABA signaling; withdrawal removes that compensating inhibition.

• PregabalinCompared with: Despite its structural resemblance to GABA, pregabalin does not act directly at GABA receptors.

• TemazepamRelated: Temazepam amplifies the effects of this neurotransmitter rather than replacing it.

• AnticonvulsantRelated: Some anticonvulsants strengthen GABA-mediated inhibition to reduce seizure-prone activity.

• ClonazepamRelated: Clonazepam enhances the inhibitory signaling that GABA produces through GABA-A receptors.

• AnestheticRelated: Many general anesthetics enhance GABA-mediated inhibition in the brain.

• OxazepamRelated: Oxazepam strengthens GABA-mediated inhibition through benzodiazepine-sensitive receptors.

• ParaldehydeRelated: Paraldehyde’s central nervous system depression is associated with enhanced inhibitory signaling.

• DepressantRelated: Many depressants enhance signaling through GABA receptors, reducing neuronal activity.

• Stiff-person syndromeRelated: Reduced inhibitory control helps explain the persistent muscle activity and spasms.

• BromazepamRelated: Bromazepam increases the effectiveness of GABA at its receptors rather than replacing it.

• Gamma-hydroxybutyric acidCompared with: GHB is chemically related to GABA but is a distinct molecule with different distribution and effects.