Background:Although progress has been made in the detection and characterization of neural plasticity in depression, it has not been fully understood in individual synaptic changes in the neural circuits under chronic stress and antidepressant treatment.Methods:Using electron microscopy and Western-blot analyses, the present study quantitatively examined the changes in the Gray’s Type I synaptic ultrastructures and the expression of synapse-associated proteins in the key brain regions of rats’ depressive-related neural circuit after chronic unpredicted mild stress and/or escitalopram administration. Meanwhile, their depressive behaviors were also determined by several tests.Results:The Type I synapses underwent considerable remodeling after chronic unpredicted mild stress, which resulted in the changed width of the synaptic cleft, length of the active zone, postsynaptic density thickness, and/or synaptic curvature in the subregions of medial prefrontal cortex and hippocampus, as well as the basolateral amygdaloid nucleus of the amygdala, accompanied by changed expression of several synapse-associated proteins. Chronic escitalopram administration significantly changed the above alternations in the chronic unpredicted mild stress rats but had little effect on normal controls. Also, there was a positive correlation between the locomotor activity and the maximal synaptic postsynaptic density thickness in the stratum radiatum of the Cornu Ammonis 1 region and a negative correlation between the sucrose preference and the length of the active zone in the basolateral amygdaloid nucleus region in chronic unpredicted mild stress rats.Conclusion:These findings strongly indicate that chronic stress and escitalopram can alter synaptic plasticity in the neural circuits, and the remodeled synaptic ultrastructure was correlated with the rats’ depressive behaviors, suggesting a therapeutic target for further exploration.

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Genetic polymorphisms in the glutamatergic and GABAergic systems and certain genetic interactions, as well as gene-environment interactions, are associated with antidepressant response.

NEURORADIOLOGYC ollateral status is an important predictor of radiologic and clinical outcome in patients with acute ischemic stroke (AIS) due to anterior circulation occlusions (1,2). Blood flow can reach the ischemic territory through collaterals and may contribute to prolonged penumbral sustenance (3,4). Although digital subtraction angiography is considered the standard modality with which to assess collateral flow (4), it is impractical to use for assessment in an acute setting since it is essential to shorten the time to reperfusion.With the development of mechanical thrombectomy, advanced imaging modalities have been developed for use in baseline assessment. CT perfusion imaging is routinely used in many stroke centers as an additional tool to assess tissue at risk. However, CT perfusion is time consuming in terms of acquisition, postprocessing, and interpretation. It is highly dependent on different postprocessing methods and software and is easily affected by motion artifacts (5-7). By comparison, CT angiography takes less time and can yield information on collateral status using appropriate methods of acquisition and reconstruction. Singlephase CT angiography depicts the cerebral circulation at a single snapshot which depends on the timing of CT angiography acquisition after contrast material injection; this may lead to inaccurate estimation of the circulation (1,8). Multiphase CT angiography has already been routinely used for patient selection and outcome prediction in clinical research (9). When compared with single-phase

Our results support a definite role for CRHR1 in the pharmacogenetics of antidepressant drugs. This may contribute to interpatient differences in their responses to antidepressant drugs.