Regulation of gonadotropin subunit gene transcription
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Figure 1
The effects of GnRH antagonist (A) and testosterone (T) on pituitary β-subunit primary transcripts (PT) in CAST male rats. Rats (n=5–10/group) were CAST only or CAST and treated with GnRH antagonist LRF-147 (200 μg, s.c.) every 12 h with and without silastic T implants (designed to achieve T levels of 3.5 ng/ml). Rats were killed 0, 8 and 24 h later. All data are presented as percent 0-h (±s.e.) controls. Bars with different letters are significantly different (P<0.05). Reproduced with permission from Burger et al. 2004.
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Figure 2
Disappearance rates for the gonadotropin subunit primary transcripts (PT) in 7-day CAST rats. PT concentration (fmol PT/100 μg RNA) is shown on the vertical axis, and time after GnRH antagonist treatment (h) is shown along the horizontal axis. The shaded areas represent the range observed in intact animals. The calculated t1/2 for the LHβ and FSHβ subunits is displayed on the respective curves. Reproduced with permission from Dalkin et al. 2001.
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Figure 3
The changes in gonadotropin subunit primary transcript (PT) concentrations following OVX. Pituitaries were collected from intact rats or rats OVX for the indicated times. n=5–9/group. Each bar represents the mean±s.e. Bars with different letters are significantly (P < 0.05) different. Reproduced with permission from Burger et al. 2001.
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Figure 4
The effects of GnRH antagonist on gonadotropin subunit primary transcript (PT) concentrations after OVX. Pituitaries were collected from intact rats, and 12- and 72-h OVX rats treated either with the GnRH antagonist LRF-147 (+) or vehicle (−, BSA-saline) n=5–7/group. Each bar represents the mean±s.e. * Indicates means are significantly different (P<0.05) from intact rats. ** Indicates antagonist-treated group is significantly different (P<0.05) from OVX (vehicle, –) at the same time point. Reproduced with permission from Burger et al. 2001.
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Figure 5
The effects of GnRH antagonist on β-subunit primary transcript (PT) half-disappearance times (t1/2). Pituitaries were collected from 7-day OVX rats treated with the GnRH antagonist LRF-147 (30 μg i.v.) and then killed 0, 30, 60 or 120 min later (n=5–6/time). Each point represents the mean±s.e. The shaded areas represent the mean ±s.e. observed in intact rats. The calculated t1/2 for LHβ and FSHβ primary transcripts is displayed on the respective curves. Reproduced with permission from Burger et al. 2001.
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Figure 6
The effects of fast- and slow-frequency GnRH pulses over 24 h on gonadotropin subunit primary transcripts (PT). CAST plus testosterone-replaced male rats were i.v. pulsed with 25 ng GnRH every 30 (fast) or 240 (slow) min for 1–24 h (n=4–8 rats/observation). Data are expressed as fold change versus controls (0 h). * Indicates significant differences (P<0.05) versus untreated, CAST plus testosterone (T) controls (0 h). ** Indicates significant differences between GnRH pulse regimens at 24 h. Reproduced with permission from Burger et al. 2002.
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Figure 7
Effect of the calcium channel activator Bay K 8644 (BK) pulse interval (15, 60 or 180 min) on LHβ, and FSHβ primary transcript (PT) levels. Pulse treatments were given for 6 h, and a GnRH pulse group (60-min interval) was included for comparison. Results are expressed as the percent change versus vehicle-pulsed controls (Con). Means±s.e.m. are shown; note the different scale for each panel. The number of chambers per group was 10–12, derived from four or five separate experiments. *P<0.05 versus control, #P<0.05 versus 15′ pulse BK group; +P<0.05 versus peak BK treatment group. Reproduced with permission from Haisenleder et al. 2001.
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Figure 8
α, LHβ and FSHβ primary transcript (PT) responses to pulsatile GnRH with and without the Ca/CAMK II-specific inhibitor, KN-93 (10 μM). Rat pituitary cells received pulses of GnRH (200 pM, 60-min intervals) for 24 h. Results are expressed as the percent change versus medium-pulsed controls (Con). Note the different scale for each panel. Groups marked with different letters (a, b or c) are statistically different (P<0.05). Reproduced with permission from Haisenleder et al. 2003a.
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Figure 9
ERK responses to pulsatile or continuous GnRH after 1, 2, 4 or 8 h. GnRH was administered to adult male rats either in a pulsatile (50 ng/pulse, 60-min interval) or continuous manner (25 ng/min; this dose was selected to provide sustained levels of circulating GnRH similar to peak levels obtained after a single 50-ng pulse (that is, 200 pg/ml)). Controls (C) received BSA-saline pulses or a continuous infusion for 8 h. The means±s.e.m. are shown (n=3/group, except in the pulsatile control group, in which n=4. * P<0.05 versus controls. Reproduced with permission from Haisenleder et al. 1998.
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Figure 10
Gonadotrope mRNA responses to pulsatile GnRH (peak chamber concentration, 100 pg/ml) given every 60 min for 24 h in the presence of PD-098059 (PD) or vehicle in perifused male pituitary cells (n=4/group). The data are presented as the percent change versus medium-pulsed controls (Con). Reproduced with permission from Haisenleder et al. 1998.
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Figure 11
The time course of testosterone (T) action on pituitary β-subunit primary transcripts (PT) and mRNAs in GnRH antagonist (GnRH-A)-treated CAST male rats. Castrated rats (n=4−7/group) were treated with GnRH-A LRF-147 (100 μg, s.c.) every 12 h. Four days after CAST, rats received T implants and were killed 0, 3, 8, 24 and 48 later. All data are presented as percent 0-h T (±s.e.) controls. Intact rat (±s.e.) control values are represented by shading. Points with different letters are significantly different (P<0.05).
- © 2004 Society for Endocrinology
