PFC inactivation or disinhibition induces delay-independent impairments in delayed-responding. Non-selective antagonism of PFC NMDA receptors impairs delayed responding in a more delay-dependent manner. PFC GluN2B subunit-containing NMDA receptors do not appear to mediate delayed-responding. PFC NMDA and GABA-A receptors may differentially regulate components of working memory in rodents. Deficiencies in PFC GABA and NMDA receptor signalling may both contribute to working memory impairments in schizophrenia.