Smith D V, Liu H, Vogt M B
Department of Otolaryngology, Head and Neck Surgery, University of Cincinnati College of Medicine, OH 45267.
Physiol Behav. 1994 Dec;56(6):1189-96. doi: 10.1016/0031-9384(94)90365-4.
There is increasing evidence, both electrophysiological and behavioral, that bitter and sweet stimuli drive parallel pathways in the gustatory brainstem. Here we report two lines of investigation that suggest significant interactions among these parallel systems. First, responses recorded from single cells in the hamster's parabrachial nuclei (PbN) show that quinine hydrochloride (QHCl) produces a substantial suppression (> 40%) of the responses of PbN cells to sucrose. Sucrose stimulation has a reciprocal suppressive effect on the response to QHCl. These results imply that aversive and appetitive stimuli produce mutual inhibition in the gustatory system; studies of the chorda tympani nerve response suggest that this inhibition likely arises within the brainstem. A second line of investigation, using both an in vitro brainstem slice preparation and in vivo pharmacological manipulations of cells in the hamster NST, has demonstrated an inhibitory network within the rostral NST that plays a role in the modulation of taste activity. Patch-clamp and extracellular recording studies in vitro show that cells within the rostral central subdivision of the NST are inhibited by gamma-aminobutyric acid (GABA); this mediation is largely through the GABAA receptor subtype. Here we show that responses to taste stimulation recorded extracellularly from NST cells in vivo can be inhibited by local microinjections of GABA; this inhibition is blocked by the GABAA receptor antagonist bicuculline methiodide. Responses to sucrose are significantly more inhibited than those to NaCl or KCl. These combined lines of evidence show that appetitive and aversive stimuli activate mutually inhibitory systems within the brainstem and suggest that the basis for this interaction is a GABAergic inhibitory network within the NST.(ABSTRACT TRUNCATED AT 250 WORDS)
越来越多的电生理和行为学证据表明,苦味和甜味刺激在味觉脑干中驱动平行通路。在此,我们报告两项研究,提示这些平行系统之间存在显著相互作用。首先,从仓鼠臂旁核(PbN)的单细胞记录显示,盐酸奎宁(QHCl)对PbN细胞对蔗糖的反应产生显著抑制(>40%)。蔗糖刺激对QHCl反应有反向抑制作用。这些结果表明,厌恶和喜好刺激在味觉系统中产生相互抑制;鼓索神经反应研究表明,这种抑制可能起源于脑干内。第二项研究,使用体外脑干切片制备和对仓鼠孤束核(NST)细胞的体内药理学操作,已证明在头端NST内存在一个抑制性网络,其在味觉活动调节中起作用。体外膜片钳和细胞外记录研究表明,NST头端中央亚区的细胞受到γ-氨基丁酸(GABA)抑制;这种介导主要通过GABAA受体亚型。我们在此表明,体内从NST细胞细胞外记录的味觉刺激反应可被局部微量注射GABA抑制;这种抑制被GABAA受体拮抗剂甲硫酸荷包牡丹碱阻断。对蔗糖的反应比NaCl或KCl的反应受到的抑制显著更强。这些综合证据表明,喜好和厌恶刺激在脑干内激活相互抑制系统,并提示这种相互作用的基础是NST内的GABA能抑制网络。(摘要截短于250字)