Figure 1. Lateral radioventriculograph showing the location of the fourth ventricle in a sheep and determination of the target for fourth ventricular cannulation.

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Figure 1. Lateral radioventriculograph showing the location of the fourth ventricle in a sheep and determination of the target for fourth ventricular cannulation. This picture was taken during a preliminary surgery using an animal different from the experimental ones. A straight line is drawn between the frontal edge of chiasmatic sulcus (p; black arrowhead) and dorsal edge of squamous part of the occipital bone (q; white arrowhead) on the x-ray film, and the fourth ventricle (arrow) is located at a distance 0.65d from p on the line, where d was the distance between p and q (see also Materials and Methods). The dottedline indicates the direction of the cannula assembly to the fourth ventricle at the cannula placement. 3V, Third ventricle; 4V, fourth ventricle; LV, lateral ventricle. Central, But Not Peripheral, Glucose-Sensing Mechanisms Mediate Glucoprivic Suppression of Pulsatile Luteinizing Hormone Secretion in the Sheep**This work was supported by the U.S.-Japan Cooperative Science Program from NSF (National Science Foundation) and JSPS (Japan Society for the Promotion of Science) (INT-9603310); a grant-in-aid for International Scientific Research from the Ministry of Education, Science, Sports, and Culture, Japan (Joint Research 09044215); and research grants from the NIH (HD-18258 and HD-18394). A preliminary report of this work was presented at the 29th Annual Meeting of the Society for Neuroscience, Miami Beach, FL, October 1999 (Abstract 166.13). Endocrinology. 2000;141(12):4472-4480. doi:10.1210/endo.141.12.7853 Endocrinology | Copyright © 2004 by the Endocrine Society

Figure 2. Profiles of plasma LH concentrations in three representative ovariectomized sheep before and after 2DG (250 or 50 mg/kg) or xylose (250 mg/kg) infusion (4–6 h; shadedperiods) into the hepatic portal (H2DG or HXyl) or jugular vein (J2DG). Each row represents same animal with a different treatment. Arrowheads represent LH pulses identified by Cluster analysis. Central, But Not Peripheral, Glucose-Sensing Mechanisms Mediate Glucoprivic Suppression of Pulsatile Luteinizing Hormone Secretion in the Sheep**This work was supported by the U.S.-Japan Cooperative Science Program from NSF (National Science Foundation) and JSPS (Japan Society for the Promotion of Science) (INT-9603310); a grant-in-aid for International Scientific Research from the Ministry of Education, Science, Sports, and Culture, Japan (Joint Research 09044215); and research grants from the NIH (HD-18258 and HD-18394). A preliminary report of this work was presented at the 29th Annual Meeting of the Society for Neuroscience, Miami Beach, FL, October 1999 (Abstract 166.13). Endocrinology. 2000;141(12):4472-4480. doi:10.1210/endo.141.12.7853 Endocrinology | Copyright © 2004 by the Endocrine Society

Figure 3. Mean (±sem) LH pulse frequencies and LH concentrations 3 h before and after 2DG (250 or 50 mg/kg) or xylose (250 mg/kg) infusion into the hepatic portal (H2DG or HXyl) or jugular vein (J2DG). Numbers in a column indicate the number of animals used. *, P < 0.05 vs. pretreated values. Values with different letters are significantly different from each other (P < 0.05). Central, But Not Peripheral, Glucose-Sensing Mechanisms Mediate Glucoprivic Suppression of Pulsatile Luteinizing Hormone Secretion in the Sheep**This work was supported by the U.S.-Japan Cooperative Science Program from NSF (National Science Foundation) and JSPS (Japan Society for the Promotion of Science) (INT-9603310); a grant-in-aid for International Scientific Research from the Ministry of Education, Science, Sports, and Culture, Japan (Joint Research 09044215); and research grants from the NIH (HD-18258 and HD-18394). A preliminary report of this work was presented at the 29th Annual Meeting of the Society for Neuroscience, Miami Beach, FL, October 1999 (Abstract 166.13). Endocrinology. 2000;141(12):4472-4480. doi:10.1210/endo.141.12.7853 Endocrinology | Copyright © 2004 by the Endocrine Society

Figure 4. Changes in mean (±sem) plasma 2DG (a), cortisol (b), glucose (c), and insulin (d) concentrations after 2DG (250 or 50 mg/kg) or xylose (250 mg/kg) infusion into the hepatic portal (H2DG or HXyl) or jugular vein (J2DG). The shaded bar represents the period of infusion. *, H2DG/250; †, H2DG/50; #, J2DG/250 [P < 0.05 vs. pretreated values (time zero)]. §, H2DG/250 vs. J2DG/250 (P < 0.05). Central, But Not Peripheral, Glucose-Sensing Mechanisms Mediate Glucoprivic Suppression of Pulsatile Luteinizing Hormone Secretion in the Sheep**This work was supported by the U.S.-Japan Cooperative Science Program from NSF (National Science Foundation) and JSPS (Japan Society for the Promotion of Science) (INT-9603310); a grant-in-aid for International Scientific Research from the Ministry of Education, Science, Sports, and Culture, Japan (Joint Research 09044215); and research grants from the NIH (HD-18258 and HD-18394). A preliminary report of this work was presented at the 29th Annual Meeting of the Society for Neuroscience, Miami Beach, FL, October 1999 (Abstract 166.13). Endocrinology. 2000;141(12):4472-4480. doi:10.1210/endo.141.12.7853 Endocrinology | Copyright © 2004 by the Endocrine Society

Figure 5. Profiles of plasma LH concentrations in three representative ovariectomized sheep before and after 2DG (5 mg/kg) or saline infusion (4–4.5 h; shaded periods) into the fourth (4V/2DG or 4V/Saline) or lateral (LV/2DG) ventricle. Arrowheads represent LH pulses identified by Cluster analysis. Central, But Not Peripheral, Glucose-Sensing Mechanisms Mediate Glucoprivic Suppression of Pulsatile Luteinizing Hormone Secretion in the Sheep**This work was supported by the U.S.-Japan Cooperative Science Program from NSF (National Science Foundation) and JSPS (Japan Society for the Promotion of Science) (INT-9603310); a grant-in-aid for International Scientific Research from the Ministry of Education, Science, Sports, and Culture, Japan (Joint Research 09044215); and research grants from the NIH (HD-18258 and HD-18394). A preliminary report of this work was presented at the 29th Annual Meeting of the Society for Neuroscience, Miami Beach, FL, October 1999 (Abstract 166.13). Endocrinology. 2000;141(12):4472-4480. doi:10.1210/endo.141.12.7853 Endocrinology | Copyright © 2004 by the Endocrine Society

Figure 6. Mean (±sem) LH pulse frequencies and LH concentrations 2 h before and after 2DG (5 mg/kg) or saline infusion into the fourth (4V/2DG or 4V/Saline) or lateral (LV/2DG) ventricles. Numbers in a column indicate the number of animals used. *, P < 0.05 vs. pretreated values. Values with different letters are significantly different from each other (P < 0.05). Central, But Not Peripheral, Glucose-Sensing Mechanisms Mediate Glucoprivic Suppression of Pulsatile Luteinizing Hormone Secretion in the Sheep**This work was supported by the U.S.-Japan Cooperative Science Program from NSF (National Science Foundation) and JSPS (Japan Society for the Promotion of Science) (INT-9603310); a grant-in-aid for International Scientific Research from the Ministry of Education, Science, Sports, and Culture, Japan (Joint Research 09044215); and research grants from the NIH (HD-18258 and HD-18394). A preliminary report of this work was presented at the 29th Annual Meeting of the Society for Neuroscience, Miami Beach, FL, October 1999 (Abstract 166.13). Endocrinology. 2000;141(12):4472-4480. doi:10.1210/endo.141.12.7853 Endocrinology | Copyright © 2004 by the Endocrine Society

Figure 7. Changes in mean (±sem) plasma 2DG (a), cortisol (b), glucose (c), and insulin (d) concentrations after 2DG (5 mg/kg) or saline infusion into the fourth (4V/2DG or 4V/Saline) or lateral (LV/2DG) ventricles. The shaded bar represents the period of infusion. *, 4V/2DG; #, LV/2DG[ P < 0.05 vs. pretreated values (time zero)]. §, 4V/2DG vs. LV/2DG (P < 0.05). Central, But Not Peripheral, Glucose-Sensing Mechanisms Mediate Glucoprivic Suppression of Pulsatile Luteinizing Hormone Secretion in the Sheep**This work was supported by the U.S.-Japan Cooperative Science Program from NSF (National Science Foundation) and JSPS (Japan Society for the Promotion of Science) (INT-9603310); a grant-in-aid for International Scientific Research from the Ministry of Education, Science, Sports, and Culture, Japan (Joint Research 09044215); and research grants from the NIH (HD-18258 and HD-18394). A preliminary report of this work was presented at the 29th Annual Meeting of the Society for Neuroscience, Miami Beach, FL, October 1999 (Abstract 166.13). Endocrinology. 2000;141(12):4472-4480. doi:10.1210/endo.141.12.7853 Endocrinology | Copyright © 2004 by the Endocrine Society