چکیده:
Background: Glutamate plays a major role in synaptic plasticity that is important for learning and memory. Astrocyte is important neuroglia, involves in the neuroinflammation and plays a key role in maintaining glutamine/glutamate homeostasis. As astrocytes provide a vital support to neurons in pathological conditions. Hence, in this study, we aimed to evaluate the effect of hippocampal astrocytes ablation induced by microinjection of L-α-aminoadipic acid (L-α-AAA) on memory, anxiety and the density of GFAP-ir astrocytes in the hippocampus.
Methods: Adult male Wistar rats were randomly assigned to control, vehicle, and experimental group. L-α-AAA was injected into the hippocampal CA1 subfield for 3 days. Memory was evaluated by inhibitory passive avoidance test and anxiety-related behavior was assessed by elevated plus maze apparatus. Hippocampal sections were immunostained for GFAP and the density of GFAP-ir astrocytes were counted.
Results: Microinjection of L-α-AAA into the CA1 subfield of the hippocampus significantly decreased the step-through latency time in passive avoidance test and significantly decreased time spent in open arm and increased time spent in closed arm in elevated plus maze test. Also, administration of L-α-AAA significantly declined the density of GFAP-ir astrocytes in the hippocampus.
Conclusion: Inhibition of astrocytes impaired the memory and increased the anxiety-like behavior in male rats. Hence, the current study confirmed hippocampal astrocyte’s key role in memory and anxiety-like behavior which can be considered in future therapeutic strategies.
Methods: Adult male Wistar rats were randomly assigned to control, vehicle, and experimental group. L-α-AAA was injected into the hippocampal CA1 subfield for 3 days. Memory was evaluated by inhibitory passive avoidance test and anxiety-related behavior was assessed by elevated plus maze apparatus. Hippocampal sections were immunostained for GFAP and the density of GFAP-ir astrocytes were counted.
Results: Microinjection of L-α-AAA into the CA1 subfield of the hippocampus significantly decreased the step-through latency time in passive avoidance test and significantly decreased time spent in open arm and increased time spent in closed arm in elevated plus maze test. Also, administration of L-α-AAA significantly declined the density of GFAP-ir astrocytes in the hippocampus.
Conclusion: Inhibition of astrocytes impaired the memory and increased the anxiety-like behavior in male rats. Hence, the current study confirmed hippocampal astrocyte’s key role in memory and anxiety-like behavior which can be considered in future therapeutic strategies.
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