More sensitivity of cortical GABAergic neurons than glutamatergic neurons in response to acidosis.
Acidosis impairs brain functions. Neuron-specific mechanisms underlying acidosis-induced brain dysfunction remain elusive. We studied the sensitivity of cortical GABAergic neurons and glutamatergic neurons to acidosis by whole-cell recording in brain slices. The acidification to the neurons was induced by perfusing artificial cerebral spinal fluid with lower pH. This acidification impairs excitability and synaptic transmission in the glutamatergic and GABAergic neurons. Acidosis impairs spiking capacity in the GABAergic neurons more than in the glutamatergic neurons. Acidosis also strengthens glutamatergic synaptic transmission and attenuates GABAergic synaptic transmission on the GABAergic neurons more than the glutamatergic neurons, which results in the functional impairment of these GABAergic neurons. This acidosis-induced dysfunction predominantly in the cortical GABAergic neurons drives the homeostasis of neuronal networks toward overexcitation and exacerbates neuronal impairment.
aDepartment of Neurology, The First Affiliated Hospital of Harbin Medical University bDepartment of Neurology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Hua
H
Liu
Fang
F
Li
Chunyan
C
Wang
Zhiqiang
Z
Su
D000138:Acidosis / Q000378:metabolism*; D000818:Animals; D059330:GABAergic Neurons / Q000378:metabolism*; D018698:Glutamic Acid / Q000378:metabolism*; D051379:Mice; D009474:Neurons / Q000378:metabolism*; D018408:Patch-Clamp Techniques; D066191:Sensorimotor Cortex / Q000378:metabolism*
D018698:Glutamic Acid