“…Studies comparing the potencies of NMB to GRP as well as binding studies or antagonist studies provide evidence that the BB 1 receptor can stimulate contraction of urogenital and gastrointestinal smooth muscle (esophageal, gastric, colon, and gallbladder) (Regoli et al, 1988;von Schrenck et al, 1989von Schrenck et al, , 1990Severi et al, 1991;Kilgore et al, 1993;Parkman et al, 1994;Milusheva et al, 1998), potently inhibit thyrotropin release from the pituitary gland by acting as an autocrine and paracrine regulator (Rettori et al, 1992;Pazos-Moura et al, 1996;Ortiga-Carvalho et al, 2003), and have potent CNS effects including inhibiting food intake independent of BB 2 stimulation (Ladenheim et al, 1994(Ladenheim et al, , 1996b(Ladenheim et al, , 1997bMerali et al, 1999;Ladenheim and Knipp, 2007) and mediating aspects of the stress and fear responses as well as various behaviors such as spontaneous activity (Merali et al, 2002(Merali et al, , 2006. BB 1 receptor knockout mice are now available and have undergone a limited number of investigations for actions of NMB Oeffner et al, 2000;Yamada et al, 2002bYamada et al, , 2003Yamano et al, 2002) (Table 1). In these mice the hypothermic effect of NMB was reduced by 50% without a change in the GRP response, supporting a possible BB 1 receptor-mediated role in thermoregulation: NMB-mediated gastric smooth muscle contraction was not affected, suggesting this is mediated not through BB 1 receptors, and no effect on feeding could be confirmed, although NMB did not have an effect in the control animals (Ohki- .…”