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.