We employed the autoradiographic deoxyglucose method to study metabolic whisker maps of the adult mouse somatosensory brainstem and thalamus after the neonatal removal of left whisker follicles C1, C2 and C3. Left whiskers B1-3 and D1-3 were deflected to metabolically activate the somatosensory pathway. Unoperated mice that were stimulated in the same fashion served as controls, Whisker stimulation resulted in an ipsilateral increase in metabolic activity in the three trigeminal brainstem structures in which the whiskers are represented topologically by segments of high cytochrome oxidase activity, i.e. subnucleus caudalis, subnucleus interpolaris and nucleus principalis. In the two subnuclei of mice with lesions and of controls, there was an increase in metabolic activity of the representations of the deflected whiskers, whereas the metabolic activity of representations A1-3 and E1-3 was low. Apart from these similarities, the metabolic activation of the representations originally representing whiskers C1-3 was remarkably greater in mice with lesions than in controls. This increase reached statistical significance in subnucleus caudalis and approached statistical significance in subnucleus interpolaris. In nucleus principalis the deprived territory was only partially activated and the degree of metabolic activation was less than in the subnuclei. In the thalamic ventrobasal complex of mice with lesions metabolic activity was unpatterned whereas two areas of metabolic activation were distinct in controls. Hence, the removal of whisker follicles in newborn mice resulted in the suppression of localized metabolic responses to whisker stimulation in the thalamus, whereas in the brainstem stimulus-related activity was prominent and the deprived territory became responsive to the stimulation of whisker follicles adjacent to the lesion. Apparently, the modification of the whisker representation at the first synapse of the pathway induces a diminution of localized responsivity in the thalamus.

In the murine somatosensory pathway, the metabolic whisker map in barrel cortex derived with the autoradiographic deoxyglucose method is spatially in register with the morphological whisker map represented by the barrels. The barrel cortex of adult mice, in which we had removed three whisker follicles from the middle row of whiskers shortly after birth, contained a disorganized zone surrounded by enlarged barrels with partially disrupted borders. With the fully quantitative autoradiographic deoxyglucose method, we investigated in barrel cortex of such mice the magnitude and the pattern of metabolic responses evoked by the deflection of whiskers. Most remarkably, the simultaneous deflection of six whiskers neighbouring the lesion activated not only the territory of the corresponding barrels, but also the unspecifiable area intercalated between the clearly identified barrels. This metabolic whisker map, unpredictable from the morphological 'barrel' map, may reflect a functional compensation for the deficit in input.

Journal of NeurochemistryVolume 34, Issue 1 p. 213-215 Activity-dependent Energy Metabolism in Rat Posterior Pituitary Primarily Reflects Sodium Pump Activity Marina Mata, Marina Mata Section on Functional Neurochemistry, Behavioral Biology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20014; and the Laboratory of Cerebral Metabolism, National Institute of Mental Health, Bethesda, Maryland 20014.Search for more papers by this authorDavid J. Fink, David J. Fink Section on Functional Neurochemistry, Behavioral Biology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20014; and the Laboratory of Cerebral Metabolism, National Institute of Mental Health, Bethesda, Maryland 20014.Search for more papers by this authorHarold Gainer, Harold Gainer Section on Functional Neurochemistry, Behavioral Biology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20014; and the Laboratory of Cerebral Metabolism, National Institute of Mental Health, Bethesda, Maryland 20014.Search for more papers by this authorCarolyn B. Smith, Corresponding Author Carolyn B. Smith Section on Functional Neurochemistry, Behavioral Biology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20014; and the Laboratory of Cerebral Metabolism, National Institute of Mental Health, Bethesda, Maryland 20014.Address reprint requests to Dr. C. B. Smith, Laboratory of Cerebral Metabolism, Building 36, Room 1A-27, National Institute of Mental Health, 9000 Rockville Pike, Bethesda, Maryland 20005.Search for more papers by this authorLeslie Davidsen, Leslie Davidsen Section on Functional Neurochemistry, Behavioral Biology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20014; and the Laboratory of Cerebral Metabolism, National Institute of Mental Health, Bethesda, Maryland 20014.Search for more papers by this authorHelen Savaki, Helen Savaki Section on Functional Neurochemistry, Behavioral Biology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20014; and the Laboratory of Cerebral Metabolism, National Institute of Mental Health, Bethesda, Maryland 20014.Search for more papers by this authorWilliam J. Schwartz, William J. Schwartz Section on Functional Neurochemistry, Behavioral Biology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20014; and the Laboratory of Cerebral Metabolism, National Institute of Mental Health, Bethesda, Maryland 20014.Search for more papers by this authorLouis Sokoloff, Louis Sokoloff Section on Functional Neurochemistry, Behavioral Biology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20014; and the Laboratory of Cerebral Metabolism, National Institute of Mental Health, Bethesda, Maryland 20014.Search for more papers by this author Marina Mata, Marina Mata Section on Functional Neurochemistry, Behavioral Biology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20014; and the Laboratory of Cerebral Metabolism, National Institute of Mental Health, Bethesda, Maryland 20014.Search for more papers by this authorDavid J. Fink, David J. Fink Section on Functional Neurochemistry, Behavioral Biology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20014; and the Laboratory of Cerebral Metabolism, National Institute of Mental Health, Bethesda, Maryland 20014.Search for more papers by this authorHarold Gainer, Harold Gainer Section on Functional Neurochemistry, Behavioral Biology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20014; and the Laboratory of Cerebral Metabolism, National Institute of Mental Health, Bethesda, Maryland 20014.Search for more papers by this authorCarolyn B. Smith, Corresponding Author Carolyn B. Smith Section on Functional Neurochemistry, Behavioral Biology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20014; and the Laboratory of Cerebral Metabolism, National Institute of Mental Health, Bethesda, Maryland 20014.Address reprint requests to Dr. C. B. Smith, Laboratory of Cerebral Metabolism, Building 36, Room 1A-27, National Institute of Mental Health, 9000 Rockville Pike, Bethesda, Maryland 20005.Search for more papers by this authorLeslie Davidsen, Leslie Davidsen Section on Functional Neurochemistry, Behavioral Biology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20014; and the Laboratory of Cerebral Metabolism, National Institute of Mental Health, Bethesda, Maryland 20014.Search for more papers by this authorHelen Savaki, Helen Savaki Section on Functional Neurochemistry, Behavioral Biology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20014; and the Laboratory of Cerebral Metabolism, National Institute of Mental Health, Bethesda, Maryland 20014.Search for more papers by this authorWilliam J. Schwartz, William J. Schwartz Section on Functional Neurochemistry, Behavioral Biology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20014; and the Laboratory of Cerebral Metabolism, National Institute of Mental Health, Bethesda, Maryland 20014.Search for more papers by this authorLouis Sokoloff, Louis Sokoloff Section on Functional Neurochemistry, Behavioral Biology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20014; and the Laboratory of Cerebral Metabolism, National Institute of Mental Health, Bethesda, Maryland 20014.Search for more papers by this author First published: January 1980 https://doi.org/10.1111/j.1471-4159.1980.tb04643.xCitations: 476Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. 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Citing Literature Volume34, Issue1January 1980Pages 213-215 ReferencesRelatedInformation

Physiological stimulation of the hypothalamo-neurohypophysial system by salt loading of rats resulted in a dramatically increased glucose utilization in the posterior pituitary but not in the paraventricular or supraoptic nuclei. The good correlation between glucose utilization and neural activity in the posterior pituitary (that is, nerve terminals) contrasted with the lack of correlation in the paraventricular and supraoptic nuclei (that is, the sites of the cell bodies of the same neurons). This difference in the metabolic response to functional activity between the two regions of these neurons can be explained by the differences in surface-to-volume ratios of these regions.