3.6.1 Impaired synaptic plasticity in NAc of depressed mice
Growing evidence supports the notion that synaptic adjustability in the NAc and its connected circuitry has a principal mission in many forms of reward-dependent learning(Grueter, Robison, Neve, Nestler, & Malenka, 2013). Furthermore, current studies have certified that synaptic molecular adaptability exist in the neurons of NAc that underlie susceptible and plasticity responses to chronic stress. Three forms of synaptic plasticity at prefrontal cortex-accumbal glutamatergic synapses—paired-pulse facilitation (PPF), input-output relationship(I-O) and LTD—were inspected in sagittal slices by us to identify the adjustment of synaptic plasticity by D-serine.
The PPF is a subtle estimate of the probability of transmitter liberation. Our results revealed that CSDS produced no outcomes on PPF, hinting the lack of obvious change in presynaptic action (Figure 6.1A and 6.1B). To determine whether the synaptic effectiveness was varied with chronic stress exposure and antidepressant administration, the input-output(I-O) relationships for field excitatory postsynaptic potentials amplitude were compared. Electrophysiological recordings showed an important reduction in the amplitude of field excitatory postsynaptic potentials in the CSDS group as compared with control group (Figure 6.1C and 6.1D). Moreover, chronic D-serine administration reversed the damage of basic prefrontal cortex-accumbal glutamatergic synapse transmission from CSDS mice (Figure 6.1C and 6.1D). It is suggested that D-serine can improve the basic synaptic damage in CSDS mice. As shown in Figure 6.1 E, F, G, H and I, NMDAR-dependent LTD of prefrontal cortex-accumbal glutamatergic synapse was impaired in CSDS mice, although it was normal in control mice. It is indicated that depressed mice’s synaptic plasticity in NAc was impaired.