CIP seminars are held on Fridays at 12.30pm, in the Hugh Robson lecture theatre, unless otherwise indicated.
Our seminars are sponsored in part by The Physiological Society.
Frid 6th December
Ancient behavioral modulation by oxytocin/vasopressin-related peptidesFriday 6 December 2013, 12.30pm
- 1.30pmDr Isabel Beets (Department of Biology, Leuven, Belgium)
Neuropeptidergic signaling plays an important role in modulating the behavioral output of neuronal circuits according to environmental and internal state cues. This potential for modulation is supported by the diversity of neuropeptides and their receptors that, however, often show strong evolutionary conservation. In mammals, neuropeptides of the oxytocin and vasopressin family are key modulators of social behavior and cognitive processes, but the evolutionary origin of these effects remains elusive. We have characterized a related signaling system and its neuromodulatory function in the nematode C. elegans, and shed light on the underlying cellular and molecular circuit. In the worm, oxytocin/vasopressin-related signaling regulates associative learning, suggesting that this peptide family is an ancient modulator of neural circuits underlying behavioral plasticity.
Host: Dr Emanuel Busch
Wednesday 11th December
Ventromedial nucleus of the hypothalamus (VMH) projecting lateral parabrachial (LPBN) cholecystokinin neurons regulate glucose homeostasisWednesday 11 December 2013, 2pm
- 3pmDr Alastair Garfield (CIP/Harvard)
The lateral parabrachial nucleus (LPBN) forms part of an assimilatory forebrain-projecting viscerosensory relay that subserves physiological and behavioural responses to a number of viseroceptive modalities, including nociceptive processing, thermostasis, malaise, energy homeostasis and metabolism. As an archetypal visceral stressor, hypoglycaemia is known to induce neural activity within the LPBN, yet a definitive function for the LPBN within this context remains to be determined. Here we identify cholecystokinin (CCK) expressing neurons as the cellular basis for LPBN mediated glucoregulation. Specifically, LPBN CCK neurons are reactive to states of glucoprivation and are able to promote elevations in blood glucose levels when artificially stimulated. Furthermore, we find that via a specific LPBN ventromedial nucleus of the hypothalamus (VMH) microcircuit these CCK neurons form part of the counter-regulatory machinery required for physiological responses to hypoglycaemia.
Host: Prof Mike Shipston
This article was published on Dec 2, 2013