Neural Correlates of Tasting Concentrated Quinine and Sugar Solutions

Journal of Neurophysiology - Tập 87 Số 2 - Trang 1068-1075 - 2002
David H. Zald1, Mathew C. Hagen2,3, José V. Pardo2,3
1Department of Psychology, Vanderbilt University, Nashville, Tennessee 37240.
2Cognitive Neuroimaging Unit, Psychiatry Service, Veterans Affairs Medical Center, Minneapolis 55417; and
3Division of Neuroscience Research, Department of Psychiatry, University of Minnesota, Minneapolis, Minnesota 55455

Tóm tắt

Behavioral, ethological, and electrophysiological evidence suggests that the highly unpleasant, bitter taste of a concentrated quinine hydrochloride (QHCL) should activate the human amygdala. In the present study, healthy subjects tasted 0.02 M QHCL or water while regional cerebral blood flow (rCBF) was assayed with H2 15O PET. Subjects were also studied while tasting a pleasant sucrose solution and resting with eyes closed (ECR). Tasting QHCL significantly increased rCBF within the left amygdala relative to control conditions of tasting water and ECR. Sucrose and water caused small to moderate rCBF increases in the amygdala relative to ECR, but sucrose did not significantly increase activity within either amygdalae relative to water. In the frontal lobe, QHCL and sucrose both activated the right posterior orbitofrontal cortex (OFC) relative to water, but portions of the anterior OFC and inferior frontal pole showed valence specific responses to QHCL. These data indicate that the left amygdala responds robustly to QHCL and more moderately to nonaversive sapid stimuli, both pleasant and unpleasant gustatory stimuli activate the right posterior OFC, and the left inferior frontal pole/anterior OFC demonstrates valence-specific responses to aversive gustatory stimuli.

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Tài liệu tham khảo

10.1007/BF00237437

Bartoshuk LM, 1978, Handbook of Behavioral Neurobiology. Sensory Integration, 1, 503

10.1016/0306-4522(94)00449-F

10.1097/00001756-199804200-00048

10.1016/0031-9384(84)90010-6

10.1002/(SICI)1096-9861(19960722)371:2<179::AID-CNE1>3.0.CO;2-#

10.1093/brain/82.4.483

10.1016/S0304-3940(99)00881-2

10.1038/jcbfm.1988.111

10.1097/00001756-199902250-00003

10.1046/j.1460-9568.1999.00738.x

10.1016/0031-9384(94)90369-7

10.1093/brain/110.2.339

Henkin RI, 1977, Trans Am Neurol Assoc, 102, 146

10.1097/00001756-199607290-00014

Katz DB, 2000, Soc Neurosci Abstr, 26, 1974

10.1109/23.34585

10.1016/0006-8993(94)90890-7

10.1016/S0028-3932(97)00070-5

Minoshima S, 1992, J Nucl Med, 33, 1579

Minoshima S, 1994, J Nucl Med, 35, 1528

Minoshima S, 1993, J Nucl Med., 34, 322

10.1037/h0036973

10.1152/jn.1998.79.1.21

10.1152/jn.2001.85.3.1315

Pfaffmann C, 1964, Am Scientist, 52, 187

10.1152/jn.1990.64.4.1055

10.1152/jn.1993.69.6.1810

10.1152/jn.1986.56.3.876

10.1038/jcbfm.1993.80

10.1097/00001756-199712220-00014

10.1523/JNEUROSCI.17-13-05136.1997

10.1097/00001756-199901180-00002

10.1093/brain/124.9.1720

10.1093/chemse/26.4.425

10.1152/jn.1991.66.4.1156

10.1006/nimg.1998.0356

10.1016/0006-8993(90)90546-N

10.1038/jcbfm.1992.127

10.1176/jnp.8.2.125

10.1093/brain/121.6.1143

10.1073/pnas.94.8.4119

10.1002/1531-8249(199909)46:3<281::AID-ANA2>3.0.CO;2-L

Zald DH, 2000, Soc Neurosci Abstr, 26, 1072

10.1093/chemse/25.3.267

Zald DH, 1998, Soc Neurosci Abstr, 24, 1508

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Journal of Neurophysiology

Tập 87 Số 2

1068-1075

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