1996 Fiscal Year Final Research Report Summary
Investigation of neurotransmitters responsible for the expression of salt appetite.
| Project/Area Number |
07680873
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neuroscience in general
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| Research Institution | Osaka University |
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Principal Investigator |
SHIMURA Tsuyoshi Osaka University, Faculty of Human Sciences, Assistant Professor -> 大阪大学, 人間科学部, 講師 (80150332)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAMOTO Takashi Osaka University, Faculty of Human Sciences, Professor, 人間科学部, 教授 (60028793)
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| Project Period (FY) |
1995 – 1996
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| Keywords | taste / salt appetite / acetylcholine / microdialysis / glutamate / dopamine / rat / motivation |
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| Research Abstract |
When animals are deficient in body sodium, they ingest excessive amounts of salty solutions and consume considerable quantities of concentrated salty solutions that are normally avoided at such high concentrations. To clarify the neurochemical mechanisms responsible for the expression of salt appetite, we conducted neurochemical, behavioral and electrophysiological experiments. 1) We measured acetylcholine release in response to intraoral infusion of concentrated NaCl (0.5M) in the insular gustatory cortex of freely behaving rats using the microdialysis technique. Acetylcholine release of acutely sodium-deprived rats by injections of furosemide was greater than that of normal rats. This result indicates that acetylcholine in the gustatory cortex is involved in the behavioral expression of salt appetite. 2) Using a recently developed dialysis-biosensor, we measured real-time glutamate level in response to various taste stimuli in the globus pallidus of freely behaving rats. Palatable ta
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ste stimuli such as sucrose and milk facilitated glutamate release compared with aversive or neutral solutions. This result suggests that glutamate in the globus pallidus is related to processing of palatability. 3) Electrolytic lesions of midbrain ventral tegmental area disturbed salt appetite. Lesioned animals consumed lower amounts of hedonically positive solutions than normal animals did. More selective, neurotoxic lesions, however, revealed that dopamine is not primarily concerned with salt appetite. 4) We compared parabrachial unit responses to taste stimuli between sodium-deprived and non-deprived rats under urethane anesthesia. Response magnitudes to NaCl were lower in deprived rats than in non-deprived rats. Responses to other tastes were not different between groups. These results suggest that interactions between gustatory relays in the lower brainstem and several forebrain structures are necessary for the expression of salt appetite. Acetylcholine and glutamate, but not dopamine, are suggested to be involved in salt appetite. Less
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Research Products
(15 results)
