PMID- 16556770
OWN - NLM
STAT- MEDLINE
DCOM- 20060622
LR  - 20181201
IS  - 0013-7227 (Print)
IS  - 0013-7227 (Linking)
VI  - 147
IP  - 6
DP  - 2006 Jun
TI  - Role played by brainstem neurons in regulating testosterone secretion via a 
      direct neural pathway between the hypothalamus and the testes.
PG  - 3070-5
AB  - We previously reported anatomical and functional evidence for a direct, 
      inhibitory neural pathway that regulates testosterone (T) secretion independently 
      of the pituitary. This pathway is activated by the intracerebroventricular (icv) 
      administration of agents that stimulate stress responses, such as IL-1beta, 
      corticotropin-releasing factor (CRF), and norepinephrine (NE), which results in a 
      blunted T response to the administration of human chorionic gonadotropin (hCG). 
      Blunting of the T response is mediated by central beta-adrenergic receptor 
      stimulation. CRF, but not ethanol (EtOH) or IL-1beta, acts directly on the 
      paraventricular nucleus of the hypothalamus to activate the pathway. Here we 
      explored the role played by brain areas hypothesized to be part of this pathway, 
      such as neurons in the dorsal pons [including the locus coeruleus (LC) of the 
      brainstem], where NE is produced. Microinfusion of EtOH or IL-1beta, but not CRF, 
      into these neurons activated the pathway. Electrolytic lesions of this region 
      significantly reversed the inhibitory effect of icv-administered EtOH on 
      hCG-induced T release, while having no effect on the ability of IL-1beta or CRF 
      to do so. However, the icv administration of IL-1beta, EtOH, or CRF, in doses 
      that rapidly inhibit the T response to hCG, all caused a significant depletion of 
      NE from the LC. Collectively, these results indicate that in addition to the 
      paraventricular nucleus, the brainstem area containing the LC is part of a neural 
      pathway that connects the brain to the testes independently of the pituitary. We 
      also speculate that EtOH may stimulate this pathway through NE-dependent 
      activation of the dorsal pons.
FAU - Selvage, Daniel J
AU  - Selvage DJ
AD  - The Clayton Foundation Laboratories for Peptide Biology, The Salk Institute, La 
      Jolla, California 92037, USA.
FAU - Parsons, Loren
AU  - Parsons L
FAU - Rivier, Catherine
AU  - Rivier C
LA  - eng
GR  - AA-12294/AA/NIAAA NIH HHS/United States
GR  - AA-12810/AA/NIAAA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20060323
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (Chorionic Gonadotropin)
RN  - 0 (Interleukin-1)
RN  - 3K9958V90M (Ethanol)
RN  - 3XMK78S47O (Testosterone)
RN  - 9015-71-8 (Corticotropin-Releasing Hormone)
RN  - X4W3ENH1CV (Norepinephrine)
SB  - IM
MH  - Animals
MH  - Chorionic Gonadotropin/pharmacology
MH  - Corticotropin-Releasing Hormone/pharmacology
MH  - Ethanol/pharmacology
MH  - Frontal Lobe/drug effects
MH  - Hypothalamus/*physiology
MH  - Interleukin-1/pharmacology
MH  - Locus Coeruleus/*physiology
MH  - Male
MH  - Neural Pathways/*physiology
MH  - Norepinephrine/analysis
MH  - Pons/drug effects/physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Testis/*innervation
MH  - Testosterone/*metabolism
EDAT- 2006/03/25 09:00
MHDA- 2006/06/23 09:00
CRDT- 2006/03/25 09:00
PHST- 2006/03/25 09:00 [pubmed]
PHST- 2006/06/23 09:00 [medline]
PHST- 2006/03/25 09:00 [entrez]
AID - en.2005-1358 [pii]
AID - 10.1210/en.2005-1358 [doi]
PST - ppublish
SO  - Endocrinology. 2006 Jun;147(6):3070-5. doi: 10.1210/en.2005-1358. Epub 2006 Mar 
      23.