Both of them show spontaneous seizures, hyperalgesia and severe memory impairment [24], [25], suggesting that heterodimerization between GABABR1 and GABABR2 subunits is critical for elicitation of most functions mediated by GABABR. In GABABR2-deficient mice, but not in GABABR1-deficient mice, however, atypical electrophysiological GABAB responses are still seen, suggesting that GABABR1 subunit plays a functional role even in the absence of the dimerization partner, GABABR2 subunit [25]. The gene discussed is GABBR1; the disease is memory impairment.