Research reportRepetitive transcranial magnetic stimulation regulates L-type Ca2+ channel activity inhibited by early sevoflurane exposure

- The period of week 2 and week 3 was crucial for brain development.
- Early sevoflurane exposure inhibited L-type Ca2+ channel activity.
- Low-frequency rTMS regulated L-type Ca2+ channel activity inhibited by sevoflurane.

BackgroundSevoflurane might be harmful to the developing brain. Therefore, it is essential to reverse sevoflurane-induced brain injury.ObjectiveThis study aimed to determine whether low-frequency repetitive transcranial magnetic stimulation (rTMS) can regulate L-type Ca2+ channel activity, which is inhibited by early sevoflurane exposure.MethodsRats were randomly divided into three groups: control, sevoflurane, and rTMS groups. A Whole-cell patch clamp technique was applied to record L-type Ca2+ channel currents. The I-V curve, steady-state activation and inactivation curves were studied in rats of each group at different ages (1 week, 2 weeks, 3 weeks, 4 weeks and 5 weeks old).ResultsIn the control group, L-type Ca2+ channel current density significantly increased from week 2 to week 3. Compared with the control group, L-type Ca2+ channel currents of rats in the sevoflurane group were significantly inhibited from week 1 to week 3. Activation curves of L-type Ca2+ channel shifted significantly towards depolarization at week 1 and week 2. Moreover, steady-state inactivation curves shifted towards hyperpolarization from week 1 to week 3. Compared with the sevoflurane group, rTMS significantly increased L-type Ca2+ channel currents at week 2 and week 3. Activation curves of L-type Ca2+ channel significantly shifted towards hyperpolarization at week 2. Meanwhile, steady-state inactivation curves significantly shifted towards depolarization at week 2.ConclusionsThe period between week 2 and week 3 is critical for the development of L-type Ca2+ channels. Early sevoflurane exposure inhibits L-type Ca2+ channel activity and rTMS can regulate L-type Ca2+ channel activity inhibited by sevoflurane.