Research Paper Volume 13, Issue 7 pp 9522—9541

EGB761 ameliorates chronic cerebral hypoperfusion-induced cognitive dysfunction and synaptic plasticity impairment

EGB761 could improve LTP impairment, synaptic transmission dysfunction and the synchronization of neural circuit signals between the entorhinal cortex and CA1 of hippocampus after CCH. After finishing behavior tests, the stimulating and recording electrodes were implanted in entorhinal cortex and CA1 of hippocampus. The rats received the HFS in entorhinal cortex and the excitable postsynaptic potentials during pre-HFS and post-HFS were recording and analyzed (A, B). The average population spikes potential were recorded and the potential slopes were counted (C). The paired pulse potential (20ms, 60ms, 80ms, 120ms, 160, 200ms time interval) were recorded (D). The electrical signals in cortex and CA1 of hippocampus were recorded and phase locking values were calculated (E) and analyzed (F).

Figure 2. EGB761 could improve LTP impairment, synaptic transmission dysfunction and the synchronization of neural circuit signals between the entorhinal cortex and CA1 of hippocampus after CCH. After finishing behavior tests, the stimulating and recording electrodes were implanted in entorhinal cortex and CA1 of hippocampus. The rats received the HFS in entorhinal cortex and the excitable postsynaptic potentials during pre-HFS and post-HFS were recording and analyzed (A, B). The average population spikes potential were recorded and the potential slopes were counted (C). The paired pulse potential (20ms, 60ms, 80ms, 120ms, 160, 200ms time interval) were recorded (D). The electrical signals in cortex and CA1 of hippocampus were recorded and phase locking values were calculated (E) and analyzed (F).