Through a vast array of experiments, FAU researchers have discovered that ceftriaxone (CEF) is a high affinity binding partner with MBLAC1 and may be responsible for its neuroprotective properties. Mice were genetically modified to lack the MBLAC1 gene and compared to normal mice after the administration of cocaine. The mice lacking MBLAC1 had significantly stronger locomotor responses to cocaine than the normal mice. Both groups of mice received doses of CEF to determine if it could reverse the locomotor effects of cocaine. With CEF treatment, locomotor effects in normal mice were completely lost; however, no changes were observed in the MBLAC1 knockout mice. Thus, this relationship indicates the importance of MBLAC1 and the stimulation of this gene by CEF can inhibit the locomotor effects of cocaine.