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. 2018 Jan 30;7:e32237. doi: 10.7554/eLife.32237

Figure 2. A single synapse can be modulated by different gliotransmitters.

(A) Schematic drawing depicting paired recordings from CA1 pyramidal neurons and the stimulating electrodes (S1 and S2). (B) Fluorescent image showing two pyramidal cells, one loaded with Texas Red (red) and the other one with Alexa 488 (green). Scale bar: 40 µm. (C) Representative EPSC traces (n = 20) and their average traces during basal conditions, after a neuronal depolarization (ND) and after a HFS. Scale bars: 5 pA, 10 ms. (D) Synaptic parameters vs time in control conditions. Open and filled arrows indicate ND and HFS, respectively. (E) Probability of release vs time in the presence of CPT (2 µM) or LY367385 (100 µM). Open and filled arrows indicate ND and HFS, respectively. (F) Percentage of cells that underwent synaptic potentiation, depression, both or no change in the different conditions. (G) Relative changes in synaptic parameters after ND and HFS in control conditions (n = 5) and in the presence of CPT (2 µM; n = 6) or LY367385 (100 µM; n = 4). (H) Schematic summary depicting the signaling pathways leading to eCB-mediated synaptic potentiation or heterosynaptic depression. Data are represented as mean ± s.e.m., *p<0.05, **p<0.01.

Figure 2.

Figure 2—figure supplement 1. eCBs mediate glutamate-induced synaptic potentiation but not heterosynaptic depression.

Figure 2—figure supplement 1.

(A) Schematic drawing depicting paired recordings from two CA1 pyramidal neurons and the stimulating electrode. (B) Representative EPSC traces before and after neuronal depolarization (ND) recorded from WT and GFAP-CB1-null mice. Scale bars: 5 pA, 20 ms. (C) Probability of release vs time. Zero time correspond with ND (arrow). (D) Relative changes in synaptic parameters after ND in WT (n = 8) and GFAP-CB1-null (n = 10) mice. (E) Schematic drawing depicting CA1 pyramidal neuron recording and the two stimulating electrodes. (F) Representative EPSC traces before and after neuronal high frequency stimulation (HFS) recorded from WT and GFAP-CB1-null mice. Scale bars: 5 pA, 20 ms. (G) Probability of release vs time. Zero time correspond with HFS (arrow). (H) Relative changes in synaptic parameters after HFS in WT (n = 9) and GFAP-CB1-null (n = 5) mice. Data are represented as mean ± s.e.m., *p<0.05, **p<0.01, ***p<0.001.
Figure 2—figure supplement 2. Astroglial specific GFAP-CB1-null mice shows impairments in astrocytic responsiveness to CB1 receptor agonists but not in the neuronal CB1 receptor dependent depolarization-induced suppression of inhibition (DSI).

Figure 2—figure supplement 2.

(A) Scheme depicting local application of WIN55,212–2 (500 µM) and ATP (2 mM) through glass pipettes. (B) Pseudocolor images showing the fluorescence intensities of Fluo4-AM of 2 astrocytes recorded from WT and GFAP-CB1-null mice before (basal) and after WIN55,212–2 or ATP application. Scale bars: 15 µm. (C) Calcium event probability in response to WIN55,212–2 and ATP recorded from WT (n = 90 astrocytes) and GFAP-CB1-null mice (n = 91 astrocytes). Note that astrocytes from GFAP-CB1-null mice still respond to ATP but not to WIN55,212–2. (D) Scheme depicting the recorded CA1 pyramidal neuron and the SC stimulating electrode. (E) IPSC amplitude vs time (left panel) and normalized IPSC change in response to neuronal depolarization (right panel) in WT (n = 5) and GFAP-CB1-null mice (n = 5). Zero time corresponds with the neuronal depolarization (arrow).