Parabrachial and hypothalamic interaction in sodium appetite

Abstract

Rats with bilateral lesions of the lateral hypothalamus (LH) fail to exhibit sodium appetite. Lesions of the parabrachial nuclei (PBN) also block salt appetite. The PBN projection to the LH is largely ipsilateral. If these deficits are functionally dependent, damaging the PBN on one side and the LH on the other should also block Na appetite. First, bilateral ibotenic acid lesions of the LH were needed because the electrolytic damage used previously destroyed both cells and axons. The ibotenic LH lesions produced substantial weight loss and eliminated Na appetite. Controls with ipsilateral PBN and LH lesions gained weight and displayed robust sodium appetite. The rats with asymmetric PBN-LH lesions also gained weight, but after sodium depletion consistently failed to increase intake of 0.5 M NaCl. These results dissociate loss of sodium appetite from the classic weight loss after LH damage and prove that Na appetite requires communication between neurons in the LH and the PBN.

Fig. 1.

Darkfield photomicrographs of coronal sections showing wheat germ agglutinin-horseradish peroxidase (WGA-HRP) reaction product in the ventral forebrain after an infusion of the tracer into the pontine parabrachial nuclei. Dorsal is up, medial to the left. Top: reaction product (orange) is visible in the lateral hypothalamus (LH) and the central nucleus of the amygdala (CNA). A: LH lesion. B: control. Note that the CNA is filled with reaction product in both brains. Bottom: higher power photomicrographs of the LH reveal a pattern of dots and haze. The dots represent retrogradely labeled cell bodies; the haze is a mixture of retrograde and anterogradely labeled neural processes, i.e., axons and preterminal arbors. C: LH lesion. D: control. The core of the LH lesion eliminated all retrograde and anterograde labels. More medially, in the perifornical region, considerable reaction product remains. F, fornix; IC, internal capsule; OT, optic tract.

Fig. 2.

Body weights of rats (means ± SE) with bilateral LH lesions (Bilat LHx) compared with their combined surgical and intact controls for 3 days before and 20 days following surgery (S). A: experiment 1A, LHx = 23, controls = 9. B: experiment 1B LHx = 18, controls = 7. *P ≤ 0.001.

Fig. 3.

Mean ± SE 24-h intake of 0.51 M NaCl across Na appetite trials. A: experiment 1A: rats with bilateral ibotenic acid LHx (n = 23) ingested less NaCl than controls (n = 9) in the second furosemide (Furo) trial (*P ≤ 0.05), but they did not differ during the saline trial. During the first Furo trial, the NaCl intake of the LHx rats was similar to that during the second Furo and saline trials (P = 0.14; 0.43). Control rats consumed more NaCl during the second Furo trial than the first (P ≤ 0.0001), but their intake during both Furo trials was more than the saline trial (P ≤ 0.03; 0.0001). B: experiment 1B: rats with larger bilateral LHx (n = 18) ingested less NaCl than the controls (n = 7) during the Furo trial (*P ≤ 0.05) but not during the saline trial. Rats with LHx consumed equivalent volumes of NaCl during both the Furo and saline trials (P = 0.51). The controls, however, ingested more NaCl after the Furo injection than after saline (P = 0.01). C: experiment 2: rats with asymmetric lesions of the parabrachial nuclei and the LH (n = 13, Asym) ingested less NaCl than their controls (n = 10) on each of 3 Furo trials but not after the saline test (*P ≤ 0.05). The Asym group actually ingested equivalent amounts of NaCl on 3 Furo and the saline trials. The controls, however, consumed more NaCl during the second and third Furo trials than the first. The saline test was done between the second and third Furo trials, but the results are depicted last in the graph for clarity.

Fig. 4.

Photomicrographs of coronal sections through the LH (top) and the parabrachial nuclei (PBN; bottom) in a rat (no. 06–17) with asymmetric lesions (NeuN stain). A: intact left LH. B: lesioned right LH. C: lesioned left PBN. D: intact right PBN. The acellular area in C extends into the supratrigeminal area above the motor trigeminal nucleus (MoV) and the locus coeruleus medial to the mesencephalic trigeminal nucleus (MesV). BC, brachium conjunctivum. Magnification in C and D is double that of A and B.