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. 2021 Jul 8;2021:7806370. doi: 10.1155/2021/7806370

Figure 5.

Figure 5

Optogenetically activated astrocytes induced excitatory response in SF-1 neurons, mainly via NMDA receptor. (a) Schematic representing viral construct of ChR2 specifically expressed in astrocytes. (b) Whole-cell recording of VMH neurons near ChR2-expressing astrocytes. (c) Representative recordings illustrating VMH SF-1 neurons depolarized by optical stimulation of astrocytes. (d) Application of glutamatergic receptor antagonists NBQX (50 μM) and D-APV (50 μM) suppressed action potential firing caused by optical stimulation of astrocytes, which was recovered after aCSF washout (n = 6). (e) Application of D-APV significantly diminished membrane potential depolarization induced by astrocyte activation (n = 5, ∗∗p < 0.01; paired t-test). (f) NBQX did not influence interaction between astrocytes and SF-1 neurons (n = 5, ∗p < 0.05; paired t-test). (g) Schematic showing that manipulation of astrocytes in VMH could bidirectionally regulate chronic stress-induced anxiety and bone loss by affecting neural excitatory through NMDA receptors.