No hay notas en la diapositiva.
The effects of gamma-aminobutyric acid (GABA), the main inhibitory neurotransmitter in the brain, are mediated through receptors which have a close functional relationship with benzodiazepine (BZD) receptors in the modulation of chloride ion channel activity. Benzodiazepines potentiate GABA transmission, leading to suppression of neuronal firing and inhibition or regulation of other neurotransmitters, including serotonin and norepinephrine.
Patients with GAD are reported to have impaired BZD receptor function as evidenced by a reduction in peripheral BZD receptors in untreated patients, and a rise in the number of these receptors following treatment. Furthermore, sacchadic eye movement velocity, an indicator of the functional integrity of the BZD system, is reduced in patients with GAD.
The consequence of impaired BZD function could be reduced GABA-mediated effects in the brain, and subsequent dysregulation of other neurotransmitters.
Connor KM, Davidson JRT. Generalized anxiety disorder: neurobiological and pharmacotherapeutic perspectives. Biol Psychiatry 1998;44:1286-1294.