TRPV1 enhances cholecystokinin signaling in primary vagal afferent neurons and mediates the central effects on spontaneous glutamate release in the NTS.

The gut peptide cholecystokinin (CCK) is released during feeding and promotes satiation by increasing excitation of vagal afferent neurons that innervate the upper gastrointestinal tract. Vagal afferent neurons express CCK1 receptors (CCK1Rs) in the periphery and at central terminals in the nucleus of the solitary tract (NTS). While the effects of CCK have been studied for decades, CCK receptor signaling and coupling to membrane ion channels are not entirely understood.

The relationship of alliance, cohesion, and climate with outcome among college counseling populations.

It is not yet fully understood how alliance, cohesion, and climate differentially correlate with client outcome in group therapy, especially when assessed simultaneously. This study aims to elucidate these relationships through an archival analysis of continuous Group Questionnaire (GQ) and Outcome Questionnaire-45 (OQ-45) data from 412 group therapy clients at college counseling centers, which were originally collected by Burlingame, Whitcomb, et al. (2018).

Alliance Rupture Detection and Repair in Group Therapy: Using the Group Questionnaire--GQ.

The identification of relationship ruptures in group therapy coupled with repair efforts by the group leader are addressed from a measurement-based care (MBC) perspective. Several MBC systems are now recognized as evidence-based treatments, and these systems typically use self-report assessment of both outcome and relationship measures. After laying a brief foundation of alliance rupture and repair from an individual therapy perspective, the complexity of applying alliance and repair across the multiple therapeutic relationships and constructs found in the group treatment literature is considered.

TRPM3 expression and control of glutamate release from primary vagal afferent neurons.

Vagal afferent fibers contact neurons in the nucleus of the solitary tract (NTS) and release glutamate via three distinct release pathways: synchronous, asynchronous, and spontaneous. The presence of TRPV1 in vagal afferents is predictive of activity-dependent asynchronous glutamate release along with temperature-sensitive spontaneous vesicle fusion. However, pharmacological blockade or genetic deletion of TRPV1 does not eliminate the asynchronous profile and only attenuates the temperature-dependent spontaneous release at high temperatures (>40°C), indicating additional temperature-sensitive calcium conductance(s) contributing to these release pathways.

Corticosterone inhibits vagal afferent glutamate release in the nucleus of the solitary tract via retrograde endocannabinoid signaling.

Circulating blood glucocorticoid levels are dynamic and responsive to stimuli that impact autonomic function. In the brain stem, vagal afferent terminals release the excitatory neurotransmitter glutamate to neurons in the nucleus of the solitary tract (NTS). Vagal afferents integrate direct visceral signals and circulating hormones with ongoing NTS activity to control autonomic function and behavior.