Anatomical and Functional Evidence for a Neural Hypothalamic-Testicular Pathway that Is Independent of the Pituitary
| Autor: | Catherine Rivier, Soon Lee, Richard R. Miselis |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
Male
endocrine system medicine.medical_specialty Pituitary gland Corticotropin-Releasing Hormone Central nervous system Hypothalamus Biology Axonal Transport Chorionic Gonadotropin Human chorionic gonadotropin Rats Sprague-Dawley Corticotropin-releasing hormone Endocrinology Internal medicine Neural Pathways Testis medicine Animals Testosterone Receptor Spinal Cord Injuries Injections Intraventricular Staining and Labeling Leydig cell Brain Leydig Cells Luteinizing Hormone Spinal cord Herpesvirus 1 Suid Rats medicine.anatomical_structure Spinal Cord Pituitary Gland Brain Stem Interleukin-1 |
| Zdroj: | Endocrinology. 143:4447-4454 |
| ISSN: | 1945-7170 0013-7227 |
| DOI: | 10.1210/en.2002-220392 |
| Popis: | Testosterone (T) secretion is classically considered to be under the primary control of pituitary LH, itself regulated by the hypothalamic peptide LH-releasing hormone. Secretagogues present in the general circulation and/or manufactured in the testis can also alter Leydig cell activity independently of the pituitary. Finally, spanchnic innervation regulates testicular LH receptors and blood flow. In the present work, we provide evidence that, in addition, there may be a neural brain-testicular circuit that regulates T release function independently of LH release. We had recently reported that the intracerebroventricular injection of IL-1β, corticotropin-releasing factor, or β-adrenergic agonists significantly interfered with the T response to human chorionic gonadotropin through mechanisms that did not involve LH. Here, we show that the injection of the transganglionic retrograde tracer pseudorabies virus into the testes caused viral staining in the spinal cord, the brain stem, and the hypothalamus. This observation indicates the presence of a neural pathway between the central nervous system and the testis. We then demonstrated that spinal cord injury significantly interfered with this staining, thus supporting the hypothesis that the proposed circuit travels through the cord. Finally, we showed that spinal cord injury completely abolished the ability of intracerebroventricularly injected IL-1β or corticotropin-releasing factor to blunt the T response to human chorionic gonadotropin, which suggests that these two secretagogues act within the brain to stimulate a neural pathway that interferes with Leydig cell function independently of the pituitary. The hitherto unsuspected brain-testicular circuit that these experiments have uncovered may play a role in pathologies, so far unexplained, that are characterized by decreased T levels despite normal LH production. |
| Databáze: | OpenAIRE |
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