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Interaction of Taste and Ingestion
Published in Robert H. Cagan, Neural Mechanisms in Taste, 2020
Pontine gustatory neurons send axons through the central tegmental tract to terminate in the wedge-shaped medial tip of the ventrobasal complex.48–51 This small, densely packed parvocellular nucleus contains the fourth-order neurons of taste. Although the most medial cells are responsive purely to chemical stimulation of the oral cavity, a lateral progression of the recording electrode quickly identifies multimodal cells sensitive to taste and temperature, to taste and oral touch, and, then, still only a millimeter from the medial border, solely to touch.
Mechanisms of Fluid Homeostasis Mediated by the Brainstem
Published in I. Robin A. Barraco, Nucleus of the Solitary Tract, 2019
Neural connections between the NTS and higher CNS levels have been explored by electrophysiological and neuroanatomical methods. Rogers et al.31 verified by means of the both techniques that hepatically activated neurons are localized to the parabrachial nucleus (PB) and the ventrobasal complex (VB) known to relay gustatory input, and also a path between the NTS, the PB, and the VB certainly exists. Thus, they suggested that this pathway is responsible for the physiological and the behavioral consequences of hepatic Na+ or osmotic stimulation. Convergence of vagal and gustatory afferent inputs to the PB neurons32 provide further evidence for their suggestion.
Specific Synonyms
Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
Ventral posterior nucleus4 (K&S, p. 334) Ventrobasal complex (ibid.)This is in the thalamus. See, also, D: Nucleus vs. subnucleus vs. nuclear complex.
Brain circuits and neurochemical systems in essential tremor: insights into current and future pharmacotherapeutic approaches
Published in Expert Review of Neurotherapeutics, 2018
Sara M Schaefer, Ana Vives Rodriguez, Elan D Louis
Agonist activity at GABAA receptors with those subunits that are widely expressed, most notably α1 and γ subunits, is likely to produce far-reaching clinical effects. Given the many different types of GABAergic neurons even within the cerebellum (i.e. basket cells, PCs, Golgi cells, stellate cells, projection neurons from the DCN to the ION), one may posit that a diffusely GABAergic effect, as seen with nonselective GABAA receptor agonists and GABA reuptake inhibitors, would lead to competing/canceling effects, and that this would not have an overall inhibitory influence on cerebellar outflow. Based on the fact that pathological tremor occurred in α1GABAAR KO mice, we may presume that agonist activity at GABAA receptors with α1 subunits would lessen tremor. Those receptor subunits with more focal predominance lend themselves better to speculation with regards to clinical effects. GABAA receptors with α3 subunits are expressed in the cerebellar dentate nucleus and ION, among other locations [16]; an inhibitory effect on the dentate nucleus in particular would decrease cerebellar output, thus potentially reducing tremor. Agonist effects on receptors with α4 subunits include analgesia (through inhibition of the ventrobasal complex in the thalamus) and amnesia (through hippocampal inhibition); ataxia has also been shown to be related to agonist activity to receptors with α4 subunits, but it is unclear which localization of α4 subunits may account for this [18]. A KO mouse model of α4 subunits did not induce tremor, but otherwise the impact of α4 subunits on tremor is not known [18]. α5 Subunits are found in the hippocampus, and therefore their effects are amnestic, which does not influence tremor but could account for the amnestic side effect of some tremor-reducing medications (e.g. benzodiazepines) [17]. α6-Containing GABAA receptors are found almost exclusively in cerebellar granule cells, whose excitatory parallel fibers synapse with PCs in the molecular layer of the cerebellum [15]. One could infer that agonist activity at GABAA receptors with α6 subunits would inhibit granule cells and thereby worsen tremor, as PC GABAergic output would be downregulated. We do know that α6 subunit activation causes motor incoordination [35], but we do not know its direct impact on tremor. δ Subunits tend to couple with α4 and α6 subunits [36]. As we have discussed, agonism at receptors with either α4 or α6 subunits has been shown to induce motor incoordination, but specific effects on tremor are not known.