Lab resourceMechanism of neuronal activity and synaptic transmission in rostral ventrolateral medulla

- AMPA and NMDA promote spontaneous firing of neurons in RVLM.
- GABA inhibits spontaneous firing of neurons in RVLM.
- GABAA receptor antagonist increases sEPSPs and sIPSPs of neurons in RVLM.
- GABAA receptor agonist and glutamate receptor antagonist decrease sEPSPs and sIPSPs of neurons in RVLM.

Rostral ventrolateral medulla (RVLM) plays an essential role in blood pressure homeostasis. This study was aimed to investigate the mechanism of neuronal activity and synaptic transmission in the RVLM. Medulla oblongata slices were carefully obtained from brainstem of rats. With continues perfusion of artificial cerebrospinal fluid (ACSF), the spontaneous firing of slices and amplitudes were assayed by conventional whole cell patch-clamp recording after addition of gamma-aminobutyric acid (GABA), α-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) and N-methyl d-aspartate (NMDA). Furthermore, the effects of agonist or antagonist targeted Type-A GABA (GABAA) or glutamate receptors on spontaneous excitatory postsynaptic potential (sEPSP) and spontaneous inhibitory postsynaptic potential (sIPSP) of neurons in RVLM were determined. The spontaneous firing of neurons in RVLM were inhibited by GABA (P < 0.001) while were promoted by NMDA or AMPA (P < 0.01 or P < 0.001). In terms of sEPSP and sIPSP, the numbers of firing neurons in RVLM were both improved by GABAA receptor antagonist (P < 0.01 or P < 0.001) while were both decreased by GABAA receptor agonist or glutamate receptor antagonist (P < 0.05, P < 0.01 or P < 0.001). The corresponding effects of agonist and antagonist on amplitudes were the same as the effects on number of firing neurons in RVLM. The spontaneous firing, sEPSP and sIPSP of neurons in RVLM were all activated by GABAA receptor antagonist while were all suppressed by GABAA receptor agonist or glutamate receptor antagonist.