Large conductance calcium-voltage operated potassium (BK) channels are a diverse ion channel family that features in many cellular processes, mainly serving as regulators of Ca++ entry mediated processes such as neurotransmission and exocytosis. The pore forming α-subunit is coded for by the single gene KCNMA1 which undergoes extensive alternative splicing, imparting differential properties to the overall channel kinetics. One such splice variant, STREX greatly enhances channel Ca++ sensitivity thus increasing channel excitability and promoting cell excitability. Aberrant changes in spinal cord BK channel levels are now thought to contribute to development of pathological pain. In obesity, nociceptive responses and inflammatory pain are potentiated but the underlying mechanism is not known It is hypothesized that alterations in the relative expression of STREX in spinal cord may contribute to changes in nociceptive processing with obesity. The aim of this study was to investigate differential expression of BK and STREX channels in spinal cord and white adipose tissue (WAT) in the Zucker rat model of genetic obesity. WAT and spinal cord tissues from adult male and female lean (n = 10 and 9, respectively) and obese (n = 10 and 9, respectively) Zucker rats were collected after schedule 1 killing. Total RNA was extracted, reverse transcribed and using real-time PCR the relative expressions of BK, STREX mRNA were quantified. For relative quantitative analysis of target gene mRNA the comparative Ct method was utilized which normalizes the number of copies of the target gene to the reference gene cyclophilin. Data was analyzed using either a student’s t-test or ANOVA. Both BK and STREX mRNA were found to be constitutively expressed in WAT and spinal cord. BK and STREX mRNA was more highly expressed in spinal cord tissue compared to WAT (2 fold higher; p < 0.05). Levels of expression of BK and STREX mRNA were unchanged in obese rat spinal cord, and there was no difference between sexes. In WAT, BK and STREX mRNA expression were similar in obese and lean rats but were significantly down-regulated in both lean and obese females compared to lean and obese males (4.5 fold lower; p < 0.05). The current study failed to detect any alteration in BK or STREX mRNA levels in spinal cord from obese rats, suggesting that another mechanism is responsible for plasticity-related changes in spinal nociceptive processing. This is the first study to detect BK and STREX mRNA in WAT. Their functional role in this tissue is not known, but could influence the excitability of adipocytes to affect secretion rates of inflammatory adipokines. The finding that BK channel genes are suppressed in female white adipose tissues, suggests that these channels are under hormonal regulation and could underlie a sex specific mechanism of regulating adipokine release.