Follicle-stimulating hormone is required for the initial phase of spermatogenic restoration in adult rats following gonadotropin suppression

The role of follicle‐stimulating hormone (FSH) in adult rat spermatogenesis is unclear. Although exogenous testosterone (T) restores spermatogenesis following gonadotropin‐releasing hormone (GnRH) immunization or T plus estradiol (TE) treatments, an assessment of the independent action of T and FSH...

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Published in:Journal of andrology 1998-11, Vol.19 (6), p.725-735
Main Authors: Meachem, S. J, Wreford, N. G, Stanton, P. G, Robertson, D. M, McLachlan, R. I
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Follicle Stimulating Hormone - immunology
Follicle Stimulating Hormone - physiology
Fundamental and applied biological sciences. Psychology
germ cell
Gonadotropins - antagonists & inhibitors
Hormone metabolism and regulation
Immunization, Passive
Male
Mammalian male genital system
optical disector
Organ Size
Rats
Rats, Sprague-Dawley
Spermatogenesis - physiology
spermatogonia
Spermatozoa - cytology
stereology
Testis - metabolism
Testis - physiology
Testosterone
Testosterone - blood
Testosterone - metabolism
Vertebrates: reproduction
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cited_by cdi_FETCH-LOGICAL-c5482-811dcaeea52281596c28e7475d175318c412a228b1c862705fd449bd3ba6092e3
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McLachlan, R. I
description The role of follicle‐stimulating hormone (FSH) in adult rat spermatogenesis is unclear. Although exogenous testosterone (T) restores spermatogenesis following gonadotropin‐releasing hormone (GnRH) immunization or T plus estradiol (TE) treatments, an assessment of the independent action of T and FSH was not possible, as exogenous T treatment maintains serum FSH levels. We have used passive immunization against FSH to determine whether T alone is capable of reinitiating spermatogenesis after chronic and acute FSH withdrawal. Adult rats received T‐filled Silastic implants 6 cm (T6) or 8 cm (T24) in length for 7 days in combination with either a polyclonal sheep antisera raised against rat FSH (FSHAb, 2 mg/kg SC daily) or control sheep immunoglobulin (ConAb) after either GnRH immunization (12 weeks) or TE treatment (9 weeks). The neutralizing capacity of the FSHAb was determined using a FSH in vitro bioassay; this analysis demonstrated that administration of FSHAb in vivo reduced FSH levels by >90%. Testes were fixed and germ cell number per testis quantified using the optical dissector. GnRH immunization reduced spermatogonia, pachytene spermatocytes, and round spermatids to 50,13, and
doi_str_mv 10.1002/j.1939-4640.1998.tb02082.x
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J ; Wreford, N. G ; Stanton, P. G ; Robertson, D. M ; McLachlan, R. I</creator><creatorcontrib>Meachem, S. J ; Wreford, N. G ; Stanton, P. G ; Robertson, D. M ; McLachlan, R. I</creatorcontrib><description>The role of follicle‐stimulating hormone (FSH) in adult rat spermatogenesis is unclear. Although exogenous testosterone (T) restores spermatogenesis following gonadotropin‐releasing hormone (GnRH) immunization or T plus estradiol (TE) treatments, an assessment of the independent action of T and FSH was not possible, as exogenous T treatment maintains serum FSH levels. We have used passive immunization against FSH to determine whether T alone is capable of reinitiating spermatogenesis after chronic and acute FSH withdrawal. Adult rats received T‐filled Silastic implants 6 cm (T6) or 8 cm (T24) in length for 7 days in combination with either a polyclonal sheep antisera raised against rat FSH (FSHAb, 2 mg/kg SC daily) or control sheep immunoglobulin (ConAb) after either GnRH immunization (12 weeks) or TE treatment (9 weeks). The neutralizing capacity of the FSHAb was determined using a FSH in vitro bioassay; this analysis demonstrated that administration of FSHAb in vivo reduced FSH levels by &gt;90%. Testes were fixed and germ cell number per testis quantified using the optical dissector. GnRH immunization reduced spermatogonia, pachytene spermatocytes, and round spermatids to 50,13, and &lt;1% of normal, respectively. T6 and T24 Silastic implants with the inclusion of the FSHAb did not increase the number of spermatogonia, pachytene spermatocytes, and round spermatids (50, 15, and 1% of normal, respectively). T6+ConAb treatment increased spermatogonial, pachytene spermatocyte, and round spermatid numbers to 74, 30, and 3% of normal, respectively (P &lt; 0.05). No further increases were seen with T24 implants. TE treatment suppressed pachytene spermatocytes and round spermatids to 33 and 1% of normal, respectively (P &lt; 0.05). T6+FSHAb treatment did not increase the number of pachytene spermatocytes and round spermatids (36 and 8%, respectively), whereas T6+ConAb treatment increased pachytene spermatocyte and round spermatid number to 50 and 28% of normal, respectively (P &lt; 0.05). T24+FSHAb treatment increased the number of pachytene spermatocyte and round spermatids (56 and 22% of normal, respectively; P &lt; 0.05), whereas T24+ConAb treatment increased these cells forms to 79 and 31% of normal, respectively. In conclusion, T alone is unable to restore spermatogenic cell populations in the setting of chronic FSH withdrawal. 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J</creatorcontrib><creatorcontrib>Wreford, N. G</creatorcontrib><creatorcontrib>Stanton, P. G</creatorcontrib><creatorcontrib>Robertson, D. M</creatorcontrib><creatorcontrib>McLachlan, R. I</creatorcontrib><title>Follicle-stimulating hormone is required for the initial phase of spermatogenic restoration in adult rats following gonadotropin suppression</title><title>Journal of andrology</title><addtitle>J Androl</addtitle><description>The role of follicle‐stimulating hormone (FSH) in adult rat spermatogenesis is unclear. Although exogenous testosterone (T) restores spermatogenesis following gonadotropin‐releasing hormone (GnRH) immunization or T plus estradiol (TE) treatments, an assessment of the independent action of T and FSH was not possible, as exogenous T treatment maintains serum FSH levels. We have used passive immunization against FSH to determine whether T alone is capable of reinitiating spermatogenesis after chronic and acute FSH withdrawal. Adult rats received T‐filled Silastic implants 6 cm (T6) or 8 cm (T24) in length for 7 days in combination with either a polyclonal sheep antisera raised against rat FSH (FSHAb, 2 mg/kg SC daily) or control sheep immunoglobulin (ConAb) after either GnRH immunization (12 weeks) or TE treatment (9 weeks). The neutralizing capacity of the FSHAb was determined using a FSH in vitro bioassay; this analysis demonstrated that administration of FSHAb in vivo reduced FSH levels by &gt;90%. Testes were fixed and germ cell number per testis quantified using the optical dissector. GnRH immunization reduced spermatogonia, pachytene spermatocytes, and round spermatids to 50,13, and &lt;1% of normal, respectively. T6 and T24 Silastic implants with the inclusion of the FSHAb did not increase the number of spermatogonia, pachytene spermatocytes, and round spermatids (50, 15, and 1% of normal, respectively). T6+ConAb treatment increased spermatogonial, pachytene spermatocyte, and round spermatid numbers to 74, 30, and 3% of normal, respectively (P &lt; 0.05). No further increases were seen with T24 implants. TE treatment suppressed pachytene spermatocytes and round spermatids to 33 and 1% of normal, respectively (P &lt; 0.05). T6+FSHAb treatment did not increase the number of pachytene spermatocytes and round spermatids (36 and 8%, respectively), whereas T6+ConAb treatment increased pachytene spermatocyte and round spermatid number to 50 and 28% of normal, respectively (P &lt; 0.05). T24+FSHAb treatment increased the number of pachytene spermatocyte and round spermatids (56 and 22% of normal, respectively; P &lt; 0.05), whereas T24+ConAb treatment increased these cells forms to 79 and 31% of normal, respectively. In conclusion, T alone is unable to restore spermatogenic cell populations in the setting of chronic FSH withdrawal. 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Psychology</subject><subject>germ cell</subject><subject>Gonadotropins - antagonists &amp; inhibitors</subject><subject>Hormone metabolism and regulation</subject><subject>Immunization, Passive</subject><subject>Male</subject><subject>Mammalian male genital system</subject><subject>optical disector</subject><subject>Organ Size</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Spermatogenesis - physiology</subject><subject>spermatogonia</subject><subject>Spermatozoa - cytology</subject><subject>stereology</subject><subject>Testis - metabolism</subject><subject>Testis - physiology</subject><subject>Testosterone</subject><subject>Testosterone - blood</subject><subject>Testosterone - metabolism</subject><subject>Vertebrates: reproduction</subject><issn>0196-3635</issn><issn>1939-4640</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><recordid>eNqVUc1u1DAQthCoLIVHQLIQcMtiO4kTc2pVWn5UwQXOluM4G6-cOLUdpX0HHroTbVTOnDye72dG8yH0jpI9JYR9Ou6pyEVW8AIaQtT71BBGara_f4Z2T9BztCNU8CznefkSvYrxCFpCq_wMnYm64oQVO_T3xjtntTNZTHaYnUp2PODeh8GPBtuIg7mbbTAt7nzAqYfeaJNVDk-9igb7DsfJhEElfzCj1cCPyQew8SNQsWpnlzD8Ixg455fV_uBH1foU_ASMOE8TiCIIXqMXnXLRvNnec_Tn5vr31bfs9tfX71eXt5kui5plNaWtVsaokrGaloJrVpuqqMqWVmVOa11QpgBqqK45q0jZtUUhmjZvFCeCmfwcfTz5TsHfzbCwHGzUxjk1Gj9HyQWlFeMMiJ9PRB18jMF0cgp2UOFBUiLXKORRrveW673lGoXcopD3IH67TZmbwbRP0u32gL_fcBW1cl1Qo7bx3wSei5IRoF2caIt15uE_FpA_Ln9-WUuw-HCy6O2hXyBNGQflHOxF5bIsVEguK1bmjwrPtuk</recordid><startdate>199811</startdate><enddate>199811</enddate><creator>Meachem, S. 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Psychology</topic><topic>germ cell</topic><topic>Gonadotropins - antagonists &amp; inhibitors</topic><topic>Hormone metabolism and regulation</topic><topic>Immunization, Passive</topic><topic>Male</topic><topic>Mammalian male genital system</topic><topic>optical disector</topic><topic>Organ Size</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Spermatogenesis - physiology</topic><topic>spermatogonia</topic><topic>Spermatozoa - cytology</topic><topic>stereology</topic><topic>Testis - metabolism</topic><topic>Testis - physiology</topic><topic>Testosterone</topic><topic>Testosterone - blood</topic><topic>Testosterone - metabolism</topic><topic>Vertebrates: reproduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Meachem, S. J</creatorcontrib><creatorcontrib>Wreford, N. G</creatorcontrib><creatorcontrib>Stanton, P. G</creatorcontrib><creatorcontrib>Robertson, D. M</creatorcontrib><creatorcontrib>McLachlan, R. 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We have used passive immunization against FSH to determine whether T alone is capable of reinitiating spermatogenesis after chronic and acute FSH withdrawal. Adult rats received T‐filled Silastic implants 6 cm (T6) or 8 cm (T24) in length for 7 days in combination with either a polyclonal sheep antisera raised against rat FSH (FSHAb, 2 mg/kg SC daily) or control sheep immunoglobulin (ConAb) after either GnRH immunization (12 weeks) or TE treatment (9 weeks). The neutralizing capacity of the FSHAb was determined using a FSH in vitro bioassay; this analysis demonstrated that administration of FSHAb in vivo reduced FSH levels by &gt;90%. Testes were fixed and germ cell number per testis quantified using the optical dissector. GnRH immunization reduced spermatogonia, pachytene spermatocytes, and round spermatids to 50,13, and &lt;1% of normal, respectively. T6 and T24 Silastic implants with the inclusion of the FSHAb did not increase the number of spermatogonia, pachytene spermatocytes, and round spermatids (50, 15, and 1% of normal, respectively). T6+ConAb treatment increased spermatogonial, pachytene spermatocyte, and round spermatid numbers to 74, 30, and 3% of normal, respectively (P &lt; 0.05). No further increases were seen with T24 implants. TE treatment suppressed pachytene spermatocytes and round spermatids to 33 and 1% of normal, respectively (P &lt; 0.05). T6+FSHAb treatment did not increase the number of pachytene spermatocytes and round spermatids (36 and 8%, respectively), whereas T6+ConAb treatment increased pachytene spermatocyte and round spermatid number to 50 and 28% of normal, respectively (P &lt; 0.05). T24+FSHAb treatment increased the number of pachytene spermatocyte and round spermatids (56 and 22% of normal, respectively; P &lt; 0.05), whereas T24+ConAb treatment increased these cells forms to 79 and 31% of normal, respectively. In conclusion, T alone is unable to restore spermatogenic cell populations in the setting of chronic FSH withdrawal. Although acute FSH withdrawal markedly impairs the restoration process, higher doses of T can partially compensate for the lack of FSH. These data suggest that FSH is important for the initial phase of spermatogenic restoration.</abstract><cop>Oxford, UK</cop><pub>Am Soc Andrology</pub><pmid>9876024</pmid><doi>10.1002/j.1939-4640.1998.tb02082.x</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record>
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subjects Animals
Biological and medical sciences
Follicle Stimulating Hormone - immunology
Follicle Stimulating Hormone - physiology
Fundamental and applied biological sciences. Psychology
germ cell
Gonadotropins - antagonists & inhibitors
Hormone metabolism and regulation
Immunization, Passive
Male
Mammalian male genital system
optical disector
Organ Size
Rats
Rats, Sprague-Dawley
Spermatogenesis - physiology
spermatogonia
Spermatozoa - cytology
stereology
Testis - metabolism
Testis - physiology
Testosterone
Testosterone - blood
Testosterone - metabolism
Vertebrates: reproduction
title Follicle-stimulating hormone is required for the initial phase of spermatogenic restoration in adult rats following gonadotropin suppression
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