Pontine gustatory activity is altered by electrical stimulation in the central nucleus of the amygdala.
Visceral signals and experience modulate the responses of brain stem neurons to gustatory stimuli. Both behavioral and anatomical evidence suggests that this modulation may involve descending input from the forebrain. The present study investigates the centrifugal control of gustatory neural activity in the parabrachial nucleus (PBN). Extracellular responses were recorded from 51 single PBN neurons during application of sucrose, NaCl, NaCl mixed with amiloride, citric acid, and QHCl with or without concurrent electrical stimulation in the ipsilateral central nucleus of the amygdala (CeA). Based on the sapid stimulus that evoked the greatest discharge, 3 neurons were classified as sucrose-best, 32 as NaCl-best, and 16 as citric acid-best. In most of the neurons sampled, response rates to an effective stimulus were either inhibited or unchanged during electrical stimulation of the CeA. Stimulation in the CeA was without effect in two sucrose-best neurons, nine NaCl-best neurons, and one citric acid-best neuron. Suppression was evident in 1 sucrose-best neuron, 18 NaCl-best neurons, and 15 citric acid-best neurons. In NaCl-best neurons inhibited by CeA stimulation, the magnitude of the effect was similar for spontaneous activity and responses to the five taste stimuli. Nonetheless, the inhibitory modulation of gustatory sensitivity increased the relative effectiveness of NaCl resulting in narrower chemical selectivity. For citric acid-best neurons, the magnitude of inhibition produced by CeA activation increased with an increase in stimulus effectiveness. The responses to citric acid were inhibited significantly more than the responses to all other stimuli with the exception of NaCl mixed with amiloride. The overall effect was to change these CA-best neurons to CA/NaCl-best neurons. In a smaller subset of NaCl-best neurons (n = 5), CeA stimulation augmented the responsiveness to NaCl but was without effect on the other stimuli or on baseline activity. It appears that electrical stimulation in the CeA modulates response intensity, as well as the type of gustatory information that is transmitted in a subset of NaCl-best neurons. These findings provide an additional link between the amygdala and the PBN in the control of NaCl intake, modulating the response and the chemical selectivity of an amiloride-sensitive Na+ detecting input pathway.
Lundy
R F
RF
Department of Behavioral Science, Penn State College of Medicine, Hershey, Pennsylvania 17033, USA. rfl6@psu.edu
Norgren
R
R
D000584:Amiloride / Q000494:pharmacology; D000679:Amygdala / Q000502:physiology*; D000818:Animals; D001931:Brain Mapping; D019343:Citric Acid / Q000494:pharmacology; D004338:Drug Combinations; D004558:Electric Stimulation; D004594:Electrophysiology; D008297:Male; D009433:Neural Inhibition / Q000502:physiology; D009475:Neurons, Afferent / Q000187:drug effects / Q000502:physiology; D011149:Pons / Q000166:cytology / Q000502:physiology*; D011803:Quinine / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012965:Sodium Chloride / Q000494:pharmacology; D013649:Taste / Q000502:physiology*; D014059:Tongue / Q000502:physiology
D004338:Drug Combinations; D019343:Citric Acid; D012965:Sodium Chloride; D000584:Amiloride; D011803:Quinine