Gustatory Neural Circuitry in the Hamster Brain Stem

Abstract

Cho YK, Li C-S. Gustatory neural circuitry in the hamster brain stem. J Neurophysiol 100: 1007-1019. First published June 4, 2008 doi:10.1152/jn.01364.2007. The nucleus of the solitary tract (NST) and the parabrachial nuclei (PbN) are the first and second central relays for the taste pathway, respectively. Taste neurons in the NST project to the PbN, which further transmits taste information to the rostral taste centers. Nevertheless, details of the neural connections among the brain stem gustatory nuclei are obscure. Here, we investigated these relationships in the hamster brain stem. Three electrode assemblies were used to record the activity of taste neurons extracellularly and then to electrically stimulate these same areas in the order: left PbN, right PbN, and right NST. A fourth electrode, a glass micropipette, was used to record from gustatory cells in the left NST. Results showed extensive bilateral communication between brain stem nuclei at the same level: 1) 10% of 96 NST neurons projected to the contralateral NST and 58% received synaptic input from the contralateral NST; and 2) 12% of 43 PbN neurons projected to the contralateral PbN and 21% received synaptic input from the contralateral PbN. Results also showed extensive communication between levels: 1) as expected, the majority of 119 NST neurons, 82%, projected to the ipsilateral PbN, but 85% of the 20 NST neurons tested received synaptic input from the ipsilateral PbN, as did 59% of 22 NST neurons that did not project to the PbN; and 2) although few, 3%, of 119 NST cells projected to the contralateral PbN and 38% received synaptic input from the contralateral PbN. These results demonstrated that taste neurons in the NST not only project to, but also receive descending input from the bilateral PbN and that gustatory neurons in the NST and PbN also communicate with the corresponding nucleus on the contralateral side.

Gustatory neural responses to umami stimuli in the parabrachial nucleus of C57BL/6J mice

“…Although relatively low, the mean breadth of tuning values (0.59 Ϯ 0.04) found in the present study fall within the range of those obtained in previous studies in the PbN in rat and hamster (Van Buskirk and Smith 1981;Nishijo and Norgren 1997;Cho and Li 2008;Geran and Travers 2009; for review see Spector and Travers 2005). This value is much higher than those in the single CT fibers of mice, which range from 0.22 to 0.41 (Ninomiya et al 1982;.…”

“…Finally it should be also noted that the anesthetic used might have an influence on spontaneous neural activity. However, our spontaneous firing rate is still lower than those in other studies recording from the NST or PbN using the same anesthetic, urethane (Adachi and Aoyama 1991;Boughter and Smith 1998;Lemon and Margolskee 2009;Cho and Li 2008;Shimura et al 1997;Tokita et al 2004). Another potential limitation of urethane is that it causes hyperglycemia (Reinert 1964), which suppresses neural responses to sapid sugars (Giza and Scott 1983).…”

Integrative responses of neurons in parabrachial nuclei to a nauseogenic gastrointestinal stimulus and vestibular stimulation in vertical planes

“…PBN/KF neurons project to the hypothalamus, limbic system, and other forebrain regions (6,11,12,21,53) and receive visceral inputs directly from area postrema and nucleus tractus solitarius (NTS) (25,28,33,34,37,45,46,56). PBN/KF neurons respond to a variety of visceral inputs, including those from baroreceptors (27,30,31), pulmonary receptors (14,19,45), gastrointestinal (GI) receptors (2,35,60), and gustatory receptors (13,17,23). Some PBN/KF neurons also have respiratory related activity and modulate the respiratory cycle; these neurons are components of the pontine respiratory group (20).…”

Parabrachial and hypothalamic interaction in sodium appetite

“…These same areas also are connected to the PBN reciprocally, to one another (3,21), and to key components in a proposed reward system: the prefrontal cortex, ventral tegmental area, and nucleus accumbens (22,24,47). This anatomical complexity confounds any simple prediction about the mechanisms through which the hedonic sign of parabrachial gustatory activity is altered by body sodium deficit.…”