“
“The peptide cholecystokinin (CCK) is a short-term satiety signal released from the gastrointestinal tract during food intake. From the periphery, CCK signalling travels via the vagus nerve to reach the brainstem from which it is relayed higher into the brain. The hypothalamus is a key integrator of appetite-related stimuli and the ventromedial nucleus of the hypothalamus (VMN) is thought to have an important role in the regulation of satiety. We investigated Crizotinib datasheet the effect of intravenous injections of CCK on the spontaneous firing activity of single VMN neurons in urethane-anaesthetised rats in vivo. We found that the predominant effect of CCK on the electrical activity

in the VMN is inhibitory. We analysed the responses to CCK according to electrophysiologically distinct subpopulations of VMN neurons and found that four of these VMN subpopulations

were inhibited by CCK, while five were not significantly affected. Finally, CCK-induced inhibitory response in VMN neurons was not altered by pre-administration of intravenous leptin. “
“Converging lines of evidence suggest that synaptic plasticity at auditory inputs to the lateral amygdala (LA) is critical for the formation and storage of auditory fear memories. Auditory information reaches the LA from both thalamic and cortical areas, raising the question of whether they make distinct contributions to fear memory storage. Here we address this by comparing the induction of long-term potentation (LTP) at the CP-868596 datasheet two inputs in vivo in anesthetized rats. We first show, using field potential measurements, that different patterns and frequencies of high-frequency stimulation (HFS) consistently elicit stronger LTP at cortical inputs than at thalamic inputs.

Field potential responses elicited during HFS of thalamic inputs were also smaller than responses during HFS of cortical inputs, suggesting less effective postsynaptic depolarization. Pronounced differences in the short-term plasticity profiles of the two inputs were also observed: Glycogen branching enzyme whereas cortical inputs displayed paired-pulse facilitation, thalamic inputs displayed paired-pulse depression. These differences in short- and long-term plasticity were not due to stronger inhibition at thalamic inputs: although removal of inhibition enhanced responses to HFS, it did not enhance thalamic LTP and left paired-pulse depression unaffected. These results highlight the divergent nature of short- and long-term plasticity at thalamic and cortical sensory inputs to the LA, pointing to their different roles in the fear learning system. “
“The H+ hypothesis of lateral feedback inhibition in the outer retina predicts that depolarizing agents should increase H+ release from horizontal cells. To test this hypothesis, self-referencing H+-selective microelectrodes were used to measure extracellular H+ fluxes from isolated goldfish horizontal cells.