Leptin and the control of food intake: neurons in the nucleus of the solitary tract are activated by both gastric distension and leptin.

摘要: Leptin reduces food intake by an unspecified mechanism. Studies show that forebrain ventricular leptin delivery increases the inhibitory effects of gastrointestinal (GI) stimulation on and amplifies electrophysiological response to gastric distension in neurons medial subnucleus nucleus tractus solitarius (mNTS). However, leaves neuroanatomical site(s) mediating leptin's effect intake. Detailed anatomical analysis rats mice phosphorylated signal transducer activator transcription 3 immunohistochemistry shows hindbrain leptin-responsive are located exclusively within mNTS. Here, we investigate 1) whether affect same mNTS 2) intake-inhibitory action is potentiated delivery. Twenty-five minutes after balloon or sham distension, were injected with vehicle killed 35 min later. Double-fluorescent for c-Fos revealed about 40% cells also respond distension. A paradigm was then developed examine relationship between volume inhibition. At subthreshold levels, without effect. When combined, interaction occurred significantly reduced We conclude primarily at level area postrema, a key vagal afferent projection zone GI system; significant proportion activated stomach distension; 3) delivered sufficient potentiate intake-suppressive otherwise ineffective These results consistent hypothesis acts directly reduce through processing.