INTRODUCTION: Stress-related elevated glucocorticoid level disrupts performance of motor tests in rats but underlying neuronal mechanisms remain unknown. Repeated corticosterone injections serve as an animal model of prolonged stress. Recently we have shown that treatment with corticosterone influences both the electrophysiology and morphology of pyramidal neurons of rat primary motor cortex (M1). It enhances spontaneous glutamate release and has no effect on dendritic spine density in superficial layers of M1, whereas in deep layers it increases spine density but does not affect electrophysiology AIM(S): The current study aimed at identification of spine types in different layers of M1 and consequent judgment on their ability to form functional synapses. Investigating the density of various spine types would clarify the apparent discrepancy between our previous electrophysiological and morphological data. METHOD(S): Rats were injected with corticosterone for 7 days, twice-daily (control group received the vehicle) and then decapitated. Brains were removed and stained using the Golgi-Cox method. Images of layer II/III and V M1 pyramidal neurons were obtained and deconvolved. Mushroom, stubby and thin spines and filopodia were counted manually on representative dendrites from the apical and basal part of the neurons. RESULTS: In layer II/III of M1 the density of each morphological spine type remained unaltered by corticosterone treatment, however, it significantly elevated the density of thin spines in layer V neurons. Other spine types were not affected. CONCLUSIONS: These data suggest that previously observed increase in M1 layer V spine density was caused exclusively by thin spine number upsurge. Thin spines are considered immature and do not form functional synaptic connections, what further validates our previous electrophysiological data. Lack of morphological changes in layer II/III is congruent with the proposed corticosterone-induced pre-synaptic mechanism of enhanced glutamate release.
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