Abstract
Progesterone (P) stimulates prolactin secretion through an unknown neural mechanism in estrogen (E)-primed female monkeys. Serotonin is a stimulatory neurotransmitter in prolactin regulation, and this laboratory has shown previously that E induces progestin receptors (PR) in serotonin neurons. Therefore, we questioned whether E and/or E + P increased serotonin neural function. The expression of mRNA for tryptophan hydroxylase (TPH) was examined in ovariectomized (spayed) control, E-treated (28 d), and E+P- treated monkeys (14 d E and 14 d E+P) using in situ hybridization and a 249 bp TPH cRNA probe generated with RT-PCR (n = 5 animals/group). Densitometric analysis of film autoradiographs revealed a ninefold increase in TPH mRNA in E-treated macaques compared to spayed animals (p <0.05). With supplemental P treatment, TPH mRNA signal was increased fivefold over spayed animals (p <0.05), but was not significantly different compared to E-treated animals. These results were verified by grain counts from photographic emulsion- coated slides. There were significantly higher single-cell levels of TPH mRNA in serotonergic neurons of the dorsal raphe in E- and E+P-treated groups (p <0.05). These data indicate that E induces TPH gene expression in nonhuman primates and that the addition of P has little additive effect on TPH gene expression. Thus, the action of P on prolactin secretion is probably not mediated at the level of TPH gene transcription. However, because P increases raphe serotonin content in E-primed rodents, the possibility remains that P may have other actions on post-translational processing or enzyme activity.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 7021-7029 |
| Number of pages | 9 |
| Journal | Journal of Neuroscience |
| Volume | 16 |
| Issue number | 21 |
| State | Published - Nov 1 1996 |
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Keywords
- dorsal raphe
- estrogen
- monkey
- progesterone
- serotonin
- tryptophan hydroxylase mRNA
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Ovarian steroid regulation of tryptophan hydroxylase mRNA expression in rhesus macaques. / Pecins-Thompson, Melanie; Brown, Nancy A.; Kohama, Steven; Bethea, Cynthia.
In: Journal of Neuroscience, Vol. 16, No. 21, 01.11.1996, p. 7021-7029.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Ovarian steroid regulation of tryptophan hydroxylase mRNA expression in rhesus macaques
AU - Pecins-Thompson, Melanie
AU - Brown, Nancy A.
AU - Kohama, Steven
AU - Bethea, Cynthia
PY - 1996/11/1
Y1 - 1996/11/1
N2 - Progesterone (P) stimulates prolactin secretion through an unknown neural mechanism in estrogen (E)-primed female monkeys. Serotonin is a stimulatory neurotransmitter in prolactin regulation, and this laboratory has shown previously that E induces progestin receptors (PR) in serotonin neurons. Therefore, we questioned whether E and/or E + P increased serotonin neural function. The expression of mRNA for tryptophan hydroxylase (TPH) was examined in ovariectomized (spayed) control, E-treated (28 d), and E+P- treated monkeys (14 d E and 14 d E+P) using in situ hybridization and a 249 bp TPH cRNA probe generated with RT-PCR (n = 5 animals/group). Densitometric analysis of film autoradiographs revealed a ninefold increase in TPH mRNA in E-treated macaques compared to spayed animals (p <0.05). With supplemental P treatment, TPH mRNA signal was increased fivefold over spayed animals (p <0.05), but was not significantly different compared to E-treated animals. These results were verified by grain counts from photographic emulsion- coated slides. There were significantly higher single-cell levels of TPH mRNA in serotonergic neurons of the dorsal raphe in E- and E+P-treated groups (p <0.05). These data indicate that E induces TPH gene expression in nonhuman primates and that the addition of P has little additive effect on TPH gene expression. Thus, the action of P on prolactin secretion is probably not mediated at the level of TPH gene transcription. However, because P increases raphe serotonin content in E-primed rodents, the possibility remains that P may have other actions on post-translational processing or enzyme activity.
AB - Progesterone (P) stimulates prolactin secretion through an unknown neural mechanism in estrogen (E)-primed female monkeys. Serotonin is a stimulatory neurotransmitter in prolactin regulation, and this laboratory has shown previously that E induces progestin receptors (PR) in serotonin neurons. Therefore, we questioned whether E and/or E + P increased serotonin neural function. The expression of mRNA for tryptophan hydroxylase (TPH) was examined in ovariectomized (spayed) control, E-treated (28 d), and E+P- treated monkeys (14 d E and 14 d E+P) using in situ hybridization and a 249 bp TPH cRNA probe generated with RT-PCR (n = 5 animals/group). Densitometric analysis of film autoradiographs revealed a ninefold increase in TPH mRNA in E-treated macaques compared to spayed animals (p <0.05). With supplemental P treatment, TPH mRNA signal was increased fivefold over spayed animals (p <0.05), but was not significantly different compared to E-treated animals. These results were verified by grain counts from photographic emulsion- coated slides. There were significantly higher single-cell levels of TPH mRNA in serotonergic neurons of the dorsal raphe in E- and E+P-treated groups (p <0.05). These data indicate that E induces TPH gene expression in nonhuman primates and that the addition of P has little additive effect on TPH gene expression. Thus, the action of P on prolactin secretion is probably not mediated at the level of TPH gene transcription. However, because P increases raphe serotonin content in E-primed rodents, the possibility remains that P may have other actions on post-translational processing or enzyme activity.
KW - dorsal raphe
KW - estrogen
KW - monkey
KW - progesterone
KW - serotonin
KW - tryptophan hydroxylase mRNA
UR - http://www.scopus.com/inward/record.url?scp=0029916026&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0029916026&partnerID=8YFLogxK
M3 - Article
VL - 16
SP - 7021
EP - 7029
JO - Journal of Neuroscience
JF - Journal of Neuroscience
SN - 0270-6474
IS - 21
ER -