Brainstem activation of GABA receptors in the nucleus tractus solitarius increases gastric motility.

Background And Aim: Local GABAergic signaling in the dorsal vagal complex (DVC) is essential to control gastric function. While the inhibitory GABA receptor action on motility in the DVC is well-documented, the role of the GABA receptor on gastric function is less well-established. Microinjection of baclofen, a selective GABA receptor agonist, in the dorsal motor nucleus of the vagus (DMV) increases gastric tone and motility, while the effect on motility in the nucleus tractus solitarius (NTS) needs to be investigated.

Interactions between Brainstem Neurons That Regulate the Motility to the Stomach.

Activity in the dorsal vagal complex (DVC) is essential to gastric motility regulation. We and others have previously shown that this activity is greatly influenced by local GABAergic signaling, primarily because of somatostatin (SST)-expressing GABAergic neurons. To further understand the network dynamics associated with gastric motility control in the DVC, we focused on another neuron prominently distributed in this complex, neuropeptide-Y (NPY) neurons.

Somatostatin Neurons in the Mouse Pontine Nucleus Activate GABA Receptor Mediated Synaptic Currents in Locus Coeruleus Neurons.

The pontine nuclei comprising the locus coeruleus (LC) and Barrington's nucleus (BRN) amongst others form the neural circuitry(s) that coordinates arousal and voiding behaviors. However, little is known about the synaptic connectivity of neurons within or across these nuclei. These include corticotropin-releasing factor (CRF) expressing neurons in the BRN that control bladder contraction and somatostatin expressing (SST) neurons whose role in this region has not been discerned.

Predicting and validating a model of suppressor of IKKepsilon through biophysical characterization.

Suppressor of IKKepsilon (SIKE) is a 207 residue protein that is implicated in the TLR3-TANK-binding kinase-1-mediated response to viral infection. SIKE's function in this pathway is unknown, but SIKE forms interactions with two distinct cytoskeletal proteins, α-actinin and tubulin, and SIKE knockout reduces cell migration. As structure informs function and in the absence of solved structural homologs, our studies were directed toward creating a structural model of SIKE through biochemical and biophysical characterization to probe and interrogate SIKE function.