Neuropsychiatric disorders present a complex array of behavioral symptoms, often encompassing deficits in learning and memory. However, our comprehension of the synaptic and circuitry abnormalities underpinning these conditions remains somewhat constrained. Many of these disorders share genetic anomalies involving synaptic cell adhesion molecules, including neurexins (Nrxns), and their interactors, cerebellins (Cbln1-4), which have been implicated in synapse formation and plasticity. Of particular interest, Cbln4 is enriched in brain regions associated with the memory process, such as the prefrontal cortex and the basolateral amygdala. Despite this localisation, the precise synaptic mechanisms and behavioural implications of Cbln4 remain elusive. To probe the role of Cbln4, we employed Cbln4 conditional knockout mice, targeting the medial prefrontal cortex (mPFC) through viral injection of Cre-recombinases. Following Cbln4 deletion, synaptic properties within the mPFC circuits were altered. Notably, frequencies of miniature postsynaptic currents (mEPSCs and mIPSCs) were altered, while their amplitudes remained unaffected. Strikingly, deletion of Cbln4 resulted in impaired long-term contextual fear memory recall, while contextual fear acquisition and short-term recall were intact. This finding suggests a potential role for mPFC Cbln4 in the expression of long-term contextual memory. These discoveries underscore the significance of Cbln4 in maintaining synaptic transmission within the mPFC critical for learning and memory, with the observed behavioural deficits potentially contributing to the pathophysiology of neuropsychiatric disorders associated with Cbln4 mutations.