PMID- 2394993
OWN - NLM
STAT- MEDLINE
DCOM- 19901011
LR  - 20131121
IS  - 0022-3034 (Print)
IS  - 0022-3034 (Linking)
VI  - 21
IP  - 5
DP  - 1990 Jul
TI  - Role of postnatal androgens in sexual differentiation of the lordosis-inhibiting 
      effect of central injections of cholecystokinin.
PG  - 796-807
AB  - The neuropeptide cholecystokinin (CCK) inhibits lordosis behavior when infused 
      into the ventromedial nucleus of the hypothalamus (VMN) of female rats and has no 
      effect when infused into the VMN of male rats. To test whether this sex 
      difference develops under the control of perinatal steroids, male rats were 
      castrated or given sham surgeries within 3 h of birth and female rats were 
      injected with either 0 or 100 micrograms testosterone propionate on postnatal day 
      5. As adults, these rats were castrated as necessary, implanted with unilateral 
      cannulae directed at the VMN, and tested for their ability to display female 
      sexual behavior and to respond to CCK. Neonatal castration of males prevented 
      defeminization of this response. When treated with 5 micrograms estradiol 
      benzoate (EB), neonatally castrated males showed both lordosis behavior and a 
      profound inhibition of that behavior after infusions of CCK. Neonatally castrated 
      males did not display lordosis behavior when treated with 2 micrograms EB. 
      Control males showed no lordosis behavior and, therefore, no response to CCK. 
      Both doses of EB induced lordosis behavior in neonatally androgenized females. 
      Significantly, these neonatally androgenized females were less responsive to 
      CCK's inhibition of lordosis and were also anovulatory. These results imply that 
      androgens alter the development of CCK responsive circuits as well as defeminize 
      cyclic gonadotropin release. Levels of 125I-sCCK-8 binding in the VMN were 
      correlated closely with an individual's ability to respond to sCCK-8. In summary, 
      the inhibition of female sexual behavior caused by exogenously administered CCK 
      in normal adult female rats appears to be controlled at least partially by levels 
      of CCK receptors in the VMN and to differentiate under the control of perinatally 
      present testosterone.
FAU - Ulibarri, C
AU  - Ulibarri C
AD  - Department of Anatomy and Cell Biology, UCLA School of Medicine, 90024-1763.
FAU - Popper, P
AU  - Popper P
FAU - Micevych, P E
AU  - Micevych PE
LA  - eng
GR  - NS 21220/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurobiol
JT  - Journal of neurobiology
JID - 0213640
RN  - 0 (Androgens)
RN  - 4TI98Z838E (Estradiol)
RN  - 9011-97-6 (Cholecystokinin)
SB  - IM
MH  - Androgens/*pharmacology
MH  - Animals
MH  - Animals, Newborn
MH  - Brain/*physiology
MH  - Cholecystokinin/*pharmacology
MH  - Estradiol
MH  - Female
MH  - Injections
MH  - Male
MH  - Posture
MH  - Rats
MH  - Rats, Inbred Strains
MH  - *Sex Characteristics
MH  - *Sexual Behavior, Animal
EDAT- 1990/07/01 00:00
MHDA- 1990/07/01 00:01
CRDT- 1990/07/01 00:00
PHST- 1990/07/01 00:00 [pubmed]
PHST- 1990/07/01 00:01 [medline]
PHST- 1990/07/01 00:00 [entrez]
AID - 10.1002/neu.480210513 [doi]
PST - ppublish
SO  - J Neurobiol. 1990 Jul;21(5):796-807. doi: 10.1002/neu.480210513.