Abstract
Orchidectomy produced a rise in plasma gonadotropin levels after 16 h, which was completely prevented by an intraperitoneal injection of DL α methyltyrosine (α MT). When α MT was injected 18 h after castration, a sharp fall in plasma LH, but not of FSH, followed. L dihydroxyphenylalanine (L DOPA) and dihydroxyphenylserine (DOPS) were given to restore catecholamine (CA) or norepinephrine (NE) synthesis, respectively. When given intraperitoneally 16 h after α MT, the precursors did not alter LH levels; however, plasma FSH was significantly increased by either L DOPA or DOPS. When α MT was given 8 h after castration and precursors were injected 30 min later, L DOPA increased both LH and FSH levels significantly 10 h after injections. When α MT was injected 18 h after castration and precursors were injected 30 min later, DOPS prevented the fall in plasma LH, but L DOPA was ineffective. The selective blockade of NE synthesis with diethyl dithiocarbamate (DDC) injected intraperitoneally 18 h after castration at two doses, 500 or 250 mg/kg, markedly decreased LH levels but did not alter plasma FSH. L DOPA or DOPS, injected 30 min later, did not reverse the effect of the higher dose of DDC; however, when DOPS was injected 15 min after the lower dose of DDC, it partially prevented the decrease in plasma LH. Even at a dose of 200 mg/kg L DOPA was ineffective. The selective blockade of DA receptors with Pimozide did not alter the rise in LH that follows orchidectomy, but partially blocked the rise of plasma FSH. The α blocker, phenoxybenzamine, administered intraperitoneally 18 h after castration, markedly decreased the high plasma FSH and LH levels observed at that time. Pronethalol, a β blocker, was ineffective. The selective blockade of 5 hydroxytryptamine (5 HT) synthesis with p clorophenylalanine (p CPA) did not modify the increase in plasma gonadotropins after castration. It is suggested that the rise in gonadotropins that follows castration is caused by increased transmission across adrenergic and probably largely NE synapses via α receptors.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 295-315 |
| Number of pages | 21 |
| Journal | Neuroendocrinology |
| Volume | 12 |
| Issue number | 4-5 |
| State | Published - 1973 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Endocrinology
- Neuroscience(all)
Cite this
Evidence for participation of a catecholaminergic mechanism in the post castration rise in plasma gonadotropins. / Ojeda, Sergio; McCann, S. M.
In: Neuroendocrinology, Vol. 12, No. 4-5, 1973, p. 295-315.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Evidence for participation of a catecholaminergic mechanism in the post castration rise in plasma gonadotropins
AU - Ojeda, Sergio
AU - McCann, S. M.
PY - 1973
Y1 - 1973
N2 - Orchidectomy produced a rise in plasma gonadotropin levels after 16 h, which was completely prevented by an intraperitoneal injection of DL α methyltyrosine (α MT). When α MT was injected 18 h after castration, a sharp fall in plasma LH, but not of FSH, followed. L dihydroxyphenylalanine (L DOPA) and dihydroxyphenylserine (DOPS) were given to restore catecholamine (CA) or norepinephrine (NE) synthesis, respectively. When given intraperitoneally 16 h after α MT, the precursors did not alter LH levels; however, plasma FSH was significantly increased by either L DOPA or DOPS. When α MT was given 8 h after castration and precursors were injected 30 min later, L DOPA increased both LH and FSH levels significantly 10 h after injections. When α MT was injected 18 h after castration and precursors were injected 30 min later, DOPS prevented the fall in plasma LH, but L DOPA was ineffective. The selective blockade of NE synthesis with diethyl dithiocarbamate (DDC) injected intraperitoneally 18 h after castration at two doses, 500 or 250 mg/kg, markedly decreased LH levels but did not alter plasma FSH. L DOPA or DOPS, injected 30 min later, did not reverse the effect of the higher dose of DDC; however, when DOPS was injected 15 min after the lower dose of DDC, it partially prevented the decrease in plasma LH. Even at a dose of 200 mg/kg L DOPA was ineffective. The selective blockade of DA receptors with Pimozide did not alter the rise in LH that follows orchidectomy, but partially blocked the rise of plasma FSH. The α blocker, phenoxybenzamine, administered intraperitoneally 18 h after castration, markedly decreased the high plasma FSH and LH levels observed at that time. Pronethalol, a β blocker, was ineffective. The selective blockade of 5 hydroxytryptamine (5 HT) synthesis with p clorophenylalanine (p CPA) did not modify the increase in plasma gonadotropins after castration. It is suggested that the rise in gonadotropins that follows castration is caused by increased transmission across adrenergic and probably largely NE synapses via α receptors.
AB - Orchidectomy produced a rise in plasma gonadotropin levels after 16 h, which was completely prevented by an intraperitoneal injection of DL α methyltyrosine (α MT). When α MT was injected 18 h after castration, a sharp fall in plasma LH, but not of FSH, followed. L dihydroxyphenylalanine (L DOPA) and dihydroxyphenylserine (DOPS) were given to restore catecholamine (CA) or norepinephrine (NE) synthesis, respectively. When given intraperitoneally 16 h after α MT, the precursors did not alter LH levels; however, plasma FSH was significantly increased by either L DOPA or DOPS. When α MT was given 8 h after castration and precursors were injected 30 min later, L DOPA increased both LH and FSH levels significantly 10 h after injections. When α MT was injected 18 h after castration and precursors were injected 30 min later, DOPS prevented the fall in plasma LH, but L DOPA was ineffective. The selective blockade of NE synthesis with diethyl dithiocarbamate (DDC) injected intraperitoneally 18 h after castration at two doses, 500 or 250 mg/kg, markedly decreased LH levels but did not alter plasma FSH. L DOPA or DOPS, injected 30 min later, did not reverse the effect of the higher dose of DDC; however, when DOPS was injected 15 min after the lower dose of DDC, it partially prevented the decrease in plasma LH. Even at a dose of 200 mg/kg L DOPA was ineffective. The selective blockade of DA receptors with Pimozide did not alter the rise in LH that follows orchidectomy, but partially blocked the rise of plasma FSH. The α blocker, phenoxybenzamine, administered intraperitoneally 18 h after castration, markedly decreased the high plasma FSH and LH levels observed at that time. Pronethalol, a β blocker, was ineffective. The selective blockade of 5 hydroxytryptamine (5 HT) synthesis with p clorophenylalanine (p CPA) did not modify the increase in plasma gonadotropins after castration. It is suggested that the rise in gonadotropins that follows castration is caused by increased transmission across adrenergic and probably largely NE synapses via α receptors.
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UR - http://www.scopus.com/inward/citedby.url?scp=0015840975&partnerID=8YFLogxK
M3 - Article
C2 - 4147209
AN - SCOPUS:0015840975
VL - 12
SP - 295
EP - 315
JO - Neuroendocrinology
JF - Neuroendocrinology
SN - 0028-3835
IS - 4-5
ER -