Caudal brainstem res expression is restricted to periventricular catecholamine neuron-containing loci following intraventricular administration of 2-deoxy-D-glucose

Reports that food intake is stimulated by fourth ventricular administration of glucose antimetabolites or uptake inhibitors suggest that glucose deprivation within the periventricular caudal brainstem activates compensatory neural mechanisms that restore global metabolic stasis. In the present study, Fos immunocytochemistry was employed to characterize the distribution of neurons within this region of the male rat brain that undergo genomic activation in response to intraventricular delivery of the antiglycolytic agent, 2-deoxy-D-glucose (2DG). Fos immunoreactivity (-ir) was only detected in the locus coeruleus (LC), nucleus of the solitary tract (NTS), and area postrema (AP) following drug treatment, whereas immunostaining for Fos was absent from these structures in the vehicle-treated control group. Dual-label immunocytochemical processing of sections of these loci for Fos- and tyrosine hydroxylase (TH)-ir revealed that, in each site, a majority of TH-ir-positive neurons were co-labeled for this nuclear protein in response to this treatment paradigm. These results provide evidence for the transcriptional activation of catecholaminergic neurons in discrete periventricular caudal brainstem structures during central glucopenia. Taken together with pharmacological evidence for the initiation of glucoprivic regulatory signaling within neural tissue accessible from the fourth ventricle, the present findings suggest that LC A(6), NTS precommissural C-2 and commissural A(2). and AP TH-ir-positive neurons may function to monitor and/or signal alterations in periventricular glucose metabolism as a means of defending central substrate balance.