The control of glutamate level in the synaptic gap is crucial for neuronal communication, as it prevents excitotoxicity from excessive receptor activation. Glutamate transporters GLT-1 are mainly localized in astrocytes and its expression is particularly abundant in the hippocampus (Hp). In this study, explored the role of GLT-1 in consolidation, expression and reconsolidation of memory, using contextual fear conditioning (CFC) task. Dihydrokainic acid (DHK), a selective GLT-1 inhibitor, was injected into the dorsal Hp of male rats at different times around aversive learning. DHK administration 15 minutes after weak CFC training session promoted long-term memory (LTM) formation. However, DHK administration around strong CFC training session did not affect memory consolidation. Moreover, DHK infusion 15 minutes before test session impaired CFC memory expression. Importantly, if applied 15 minutes after a reactivation session, DHK impairs CFC reconsolidation. This study complements previous findings in females rats by covering the full dynamics of aversive memory and confirms the lack of sexual dimorphism in the role of GLT-1. In conclusion, our findings indicate that inhibition of hippocampal astroglial glutamate uptake impairs the expression and reconsolidation of aversive memory without impairing its consolidation, and highlight potential therapeutic avenues for neuropsychiatric conditions, including phobias, post-traumatic stress disorder, and cognitive deficits.