title: Taste responses of neurons in the hamster solitary nucleus are modulated by the central nucleus of the amygdala.
abstract: Previous studies have shown a modulatory influence of forebrain gustatory areas, such as the gustatory cortex and lateral hypothalamus, on the activity of taste-responsive cells in the nucleus of the solitary tract (NST). The central nucleus of the amygdala (CeA), which receives gustatory afferent information, also exerts descending control over taste neurons in the parabrachial nuclei (PbN) of the pons. The present studies were designed to investigate the role of descending amgydaloid projections to the NST in the modulation of gustatory activity. Extracellular action potentials were recorded from 109 taste-responsive cells in the NST of urethan-anesthetized hamsters and analyzed for a change in excitability following electrical and chemical stimulation of the CeA. Electrical stimulation of the CeA orthodromically modulated 36 of 109 (33.0%) taste-responsive NST cells. An excitatory response was observed in 33 (30.28%) cells. An initial decrease in excitability to electrical stimulation of the CeA, suggestive of postsynaptic inhibition, was observed in three (2.75%) NST taste cells. NST cells modulated by the CeA were significantly less responsive to taste stimuli than cells that were not. Many of these cells were under the modulatory influence of the contralateral CeA (28/36 = 77.8%) as well as the ipsilateral (22/36 = 61.1%); 14 (38.9%) were excited bilaterally. Latencies for excitation were longer after ipsilateral than after contralateral CeA stimulation. Microinjection of DL-homocysteic acid (DLH) into the CeA mimicked the effect of electrical stimulation on each of the nine cells tested: DLH excited eight and inhibited one of these electrically activated NST cells. Application of subthreshold electrical stimulation to the CeA during taste trials increased the taste responses of every CeA-responsive NST cell (n = 7) tested with this protocol. These effects would enhance taste discriminability by increasing the signal-to-noise ratio of taste-evoked activity.
authors.affiliation: Department of Anatomy and Neurobiology and Program in Neuroscience, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.
authors.forename: Cheng-Shu
authors.initials: CS
authors.lastname: Li
authors.forename: Young K
authors.initials: YK
authors.lastname: Cho
authors.forename: David V
authors.initials: DV
authors.lastname: Smith
mesh_terms: D000679:Amygdala / Q000502:physiology*; D000818:Animals; D006224:Cricetinae; D004525:Efferent Pathways / Q000502:physiology; D004558:Electric Stimulation; D006710:Homocysteine / Q000031:analogs & derivatives* / Q000494:pharmacology; D008297:Male; D008647:Mesocricetus; D009475:Neurons, Afferent / Q000187:drug effects / Q000502:physiology*; D017552:Solitary Nucleus / Q000166:cytology / Q000502:physiology*; D013649:Taste / Q000502:physiology*
chemical_list: D006710:Homocysteine; C007956:homocysteic acid