Gastric modulation of gustatory afferent activity

Glenn, John F.; Erickson, Robert P.

doi:10.1016/0031-9384(76)90216-x

Cited by 126 publications

(41 citation statements)

References 23 publications

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“…Changes in such variables as blood glucose and insulin and gastric distension associated with satiety appear to specifically decrease the response to sweet stimuli Scott 1983, 1987;Glenn and Erickson 1976). However, the present data suggest that global activation of the LH has a more general excitatory effect on taste responses in the NST.…”

Section: Taste Response Modulation By the Lhmentioning

confidence: 47%

“…Gustatory responses of NST neurons can be inhibited by physiological factors associated with satiety, including blood insulin and glucose levels and gastric distension Scott 1983, 1987;Giza et al 1992Giza et al , 1993Glenn and Erickson 1976). These data suggest that taste activity may vary between states of hunger and satiety.…”

Section: Discussionmentioning

confidence: 97%

“…The responsiveness of some gustatory neurons in the nucleus of the solitary tract (NST) is altered by physiological factors associated with satiety, such as blood insulin and glucose levels Scott 1983, 1987;Giza et al 1992Giza et al , 1993 and gastric distension (Glenn and Erickson 1976), and by taste aversion (Chang and Scott 1984) or preference (Giza et al 1997) learning. However, the underlying neural substrates for these modulatory effects are not known.…”

Section: Introductionmentioning

confidence: 99%

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Taste Responses of Neurons of the Hamster Solitary Nucleus Are Enhanced by Lateral Hypothalamic Stimulation

Cho

Smith

2002

Journal of Neurophysiology

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. Taste responses of neurons of the hamster solitary nucleus are enhanced by lateral hypothalamic stimulation. J Neurophysiol 87: 1981-1992, 2002; 10.1152/jn.00765.2001. Gustatory responses in the brain stem are modifiable by several physiological factors, including blood insulin and glucose, intraduodenal lipids, gastric distension, and learning, although the neural substrates for these modulatory effects are not known. Stimulation of the lateral hypothalamus (LH) produces increases in food intake and alterations in taste preference behavior, whereas damage to this area has opposite effects. In the present study, we investigated the effects of LH stimulation on the neural activity of taste-responsive cells in the nucleus of the solitary tract (NST) of the hamster. Bipolar stimulating electrodes were bilaterally implanted in the LH, and the responses of 99 neurons in the NST, which were first characterized for their taste sensitivities, were tested for their response to both ipsilateral and contralateral LH stimulation. Half of the tasteresponsive cells in the NST (49/99) were modulated by LH stimulation. Contralateral stimulation was more often effective (41 cells) than ipsilateral (13 cells) and always excitatory; 10 cells were excited bilaterally. Six cells were inhibited by ipsilateral stimulation. A subset of these cells (n ϭ 13) was examined for the effects of microinjection of DL-homocysteic acid (DLH), a glutamate receptor agonist, into the LH. The effects of electrical stimulation were completely mimicked by DLH, indicating that cell somata in and around the LH are responsible for these effects. Other cells (n ϭ 14) were tested for the effects of electrical stimulation of the LH on the responses to stimulation of the tongue with 0.032 M sucrose, NaCl, and quinine hydrochloride, and 0.0032 M citric acid. Responses to taste stimuli were more than doubled by the excitatory influence of the LH. These data show that the LH, in addition to its role in feeding and metabolism, exerts descending control over the processing of gustatory information through the brain stem.

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Section: Taste Response Modulation By the Lhmentioning

confidence: 47%

Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

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Taste Responses of Neurons of the Hamster Solitary Nucleus Are Enhanced by Lateral Hypothalamic Stimulation

Cho

Smith

2002

Journal of Neurophysiology

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“…This extensive neural substrate no doubt underlies the modulation of taste activity by physiological and experiential factors. Further research should be directed toward determining how these pathways are engaged by alterations in blood glucose (Giza and Scott 1983), gastric distension (Glenn and Erickson 1976), intraduodenal lipids (Hajnal et al 1999), CTA learning (Chang and Scott 1984), and other physiological conditions known to alter taste sensitivity. …”

Section: Forebrain Modulation Of Taste Responsesmentioning

confidence: 99%

Modulation of Parabrachial Taste Neurons by Electrical and Chemical Stimulation of the Lateral Hypothalamus and Amygdala

Cho²,

Smith³

2005

Journal of Neurophysiology

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The lateral hypothalamus (LH) and the central nucleus of the amygdala (CeA) exert an influence on ingestive behavior and are reciprocally connected to gustatory and viscerosensory areas, including the nucleus of the solitary tract (NST) and the parabrachial nuclei (PbN). We investigated the effects of LH and CeA stimulation on the activity of 101 taste-responsive neurons in the hamster PbN. Eighty three of these neurons were antidromically activated by stimulation of these sites; 57 were antidromically driven by both. Of these 83 neurons, 21 were also orthodromically activated-8 by the CeA and 3 by the LH. Additional neurons were excited (n ϭ 5) or inhibited (n ϭ 8) by these forebrain nuclei but not antidromically activated. Taste stimuli were: 0.032 M sucrose, 0.032 M sodium chloride (NaCl), 0.032 M quinine hydrochloride (QHCl), and 0.0032 M citric acid. Among the 34 orthodromically activated neurons, more sucrose-best neurons were excited than inhibited, whereas the opposite occurred for citric-acidand QHCl-best cells. Neurons inhibited by the forebrain responded significantly more strongly to citric acid and QHCl than cells excited by these sites. The effects of electrical stimulation were mimicked by microinjection of DL-homocysteic acid, indicating that cells at these forebrain sites were responsible for these effects. These data demonstrate that many individual PbN gustatory neurons project to both the LH and CeA and that these areas modulate the gustatory activity of a subset of PbN neurons. This neural substrate is likely involved in the modulation of taste activity by physiological and experiential factors.

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“…17,18 Additionally, satiety factors serve to modify NTS responses in a specific way. 18,[19][20][21] Therefore, it is clear that alterations in digestive physiology have a significant effect on taste responses in neurons located at the first synaptic relay along the taste system. This, in turn, may have significant effects on other physiological systems such as cardiovascular function due to the anatomical proximity of associated neural structures and their circuits with the NTS.…”

Section: Plasticity Of Brainstem Gustatory Neurons In Adult Mammalsmentioning

confidence: 99%

Neural Plasticity in the Gustatory System

Hill¹

2004

Nut. Rev.

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Sensory systems adapt to changing environmental influences by coordinated alterations in structure and function. These alterations are referred to as plastic changes. The gustatory system displays numerous plastic changes even in receptor cells. This review focuses on the plasticity of gustatory structures through the first synaptic relay in the brain. Unlike other sensory systems, there is a remarkable amount of environmentally induced changes in these peripheral-most neural structures. The most consistent and largest changes occur to stimuli that also impact on homeostatic systems, especially when the environmental manipulation is instituted during early development.

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Gastric modulation of gustatory afferent activity

Cited by 126 publications

References 23 publications

Taste Responses of Neurons of the Hamster Solitary Nucleus Are Enhanced by Lateral Hypothalamic Stimulation

Taste Responses of Neurons of the Hamster Solitary Nucleus Are Enhanced by Lateral Hypothalamic Stimulation

Modulation of Parabrachial Taste Neurons by Electrical and Chemical Stimulation of the Lateral Hypothalamus and Amygdala

Neural Plasticity in the Gustatory System

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