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Oxytocin (OXT)‐immunoreactive axons closely appose tyrosine hydroxylase (TH)‐immunoreactive neurons in the rat nucleus of the solitary tract (NTS) and dorsal vagal motor (DMV) neurons that supply the gastrointestinal tract
Author(s) -
LlewellynSmith Ida J.,
Travagli R. Alberto,
Browning Kirsteen N
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.624.2
Subject(s) - catecholaminergic , dorsal motor nucleus , solitary tract , biology , neuroscience , tyrosine hydroxylase , catecholaminergic cell groups , postsynaptic potential , cholinergic , vagus nerve , brainstem , receptor , catecholamine , dopamine , biochemistry , stimulation
It has long been known that catecholaminergic NTS neurons provide synaptic input to vagal preganglionic neurons of the DMV. Cholinergic and catecholaminergic DMV neurons, in turn, supply the motor innervation to the gastrointestinal tract, from the lower esophagus to the transverse colon Axons of paraventricular hypothalamic neurons release OXT that modulates DMV neurons via both pre‐ and postsynaptic sites of action. The aim of the present study was to investigate whether OXT inputs directly target DMV or NTS neurons. We used double (TH+OXT) and triple (TH+OXT+ChAT) immunoperoxidase labelling to determine whether OXT axons closely apposed catecholaminergic NTS and/or DMV neurons. We also assessed OXT input to DMV neurons retrogradely labelled with cholera toxin B subunit from the corpus or ileum. OXT axons were most numerous in the caudal DMV and in the lateral aspects of the rostral DMV, but were sparsely distributed in the NTS. Close appositions by OXT axons occurred on TH‐positive NTS neurons and DMV neurons, as well as on DMV neurons projecting to either the ileum or corpus. These results suggest a prominent role of OXT in controlling different subpopulations of neurons in the dorsal vagal complex circuitry that controls gut function. Support: NH&MRC of Australia and NIH grant DK55530