David Spanswick

TL;DR: It is shown that leptin hyperpolarizes glucose-receptive hypothalamic neurons of lean Sprague–Dawley and Zucker rats, but is ineffective on neurons of obese Zucker (fa/fa ) rats, and single-channel recordings demonstrate that leptin activates an ATP-sensitive potassium (KATP) channel.

TL;DR: It is demonstrated that insulin, like leptin, hyperpolarizes lean rat hypothalamic glucose-responsive neurons by opening KATP channels, which suggest hypothalamic KatP channel function is crucial to physiological regulation of food intake and body weight.

TL;DR: Rat ARC neurons containing neuropeptide Y and agouti-related protein, which are conditional pacemakers, are activated by orexigens and inhibited by the anorexigen leptin to propose a neuron-specific signaling mechanism through which central and peripheral signals engage the central neural anabolic drive.

TL;DR: It is demonstrated that leptin couples changes in weight to changes in BP in mammalian species, and humans with loss-of-function mutations in leptin and the LepR have low BP despite severe obesity.

TL;DR: A working model for the involvement of glutamate and GABA in the regulation of LH release in teleost fish is proposed and it is suggested that it is a receptor similar to the GABA(A) type which mediates the effects of GABA on LHRelease in fish, at least partially acting on the GnRH neuron, but likely directly acting at the gonadotroph as well.