GABA is the major inhibitory neurotransmitter in the mature CNS. When GABA A receptors
are activated the membrane potential is driven towards hyperpolarization due to chloride …

Seizures are thought to originate from a failure of inhibition to quell hyperactive neural
circuits, but the nature of this failure remains unknown. Here we combine high-speed two …

Altered inhibitory function is an important facet of epileptic pathology. A key concept is that
GABAergic activity can become excitatory if intraneuronal chloride rises. However, it has …

GABAergic synaptic inhibition, which is a critical regulator of neuronal excitability, is closely
involved in epilepsy. Interestingly, fast GABAergic transmission mediated by Cl− permeable …

Highlights•Ionic plasticity of GABA signaling relies on short-term and long term changes in E
GABA.•Cl− transport and carboanhydrases play a key role in ionic plasticity and …

Highlights•Small changes in the neuronal Cl− gradient significantly impact
excitability.•Relatively minor perturbations in Cl− homeostasis degrade neuronal …

Abstract Changes in neuronal chloride homeostasis affect GABAA receptor-mediated
transmission and may contribute to epileptic activities. Work on human epileptic tissue …

Excitation and inhibition are at the core of brain function and malfunction. To sustain the
activity of neuronal networks over time and space, glutamatergic excitation is balanced by …

Synapses mediated by γ-aminobutyric acid (GABA) A receptors are notoriously altered
during periods of enhanced activity. Since a loss of inhibitory tone is a basic cause of …

Chloride ions play an important role in controlling excitability of principal neurons in the
central nervous system. When neurotransmitter GABA is released from inhibitory …