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Featured researches published by J. W. Simpkins.


Neuroendocrinology | 1976

Selective Actions of Prolactin on Catecholamine Turnover in the Hypothalamus and on Serum LH and FSH

G.A. Gudelsky; J. W. Simpkins; G.P. Mueller; Joseph Meites; Kenneth E. Moore

The effects of prolactin (PRL) administration on catecholamine turnover in various brain regions of ovariectomized rats were determined by observing the decline of dopamine and norepinephrine concentrations after alpha-methyltyrosine (alphaMT) administration. PRL had no effect on the steady state concentration of dopamine in the median eminence, anterior hypothalamus and corpus striatum or on the norepinephrine concentration in the anterior hypothalamus. However, PRL selectively enhanced dopamine turnover in the median eminence and anterior hypothalamus after a latent period of 10-26 h. In addition, PRL administration significantly decreased serum concentrations of LH and FSH. These results suggest that the PRL-induced increase in activity of dopaminergic neurons in the median eminence or anterior hypothalamus may be responsible for the reduction of the post-castration rise in serum concentrations of LH and FSH.


Neuroendocrinology | 1976

Differential Effects of Dopamine Agonists and Haloperidol on Release of Prolactin, Thyroid Stimulating Hormone, Growth Hormone and Luteinizing Hormone in Rats

G.P. Mueller; J. W. Simpkins; Joseph Meites; Kenneth E. Moore

The dose-response effects of apomorphine and ET-495 (piribedil), 2 specific dopamine (DA) receptor stimulators, and haloperidol, a DA receptor blocker, were tested on the secretion of prolactin (PRL), thyroid stimulating hormone (TSH), growth hormone (GH) and luteinizing hormone (LH) in male rats. Both apomorphine and piribedil reduced serum PRL and TSH levels, stimulated GH release at low but not at high doses and either had no effect or tended to reduce serum LH levels. The minimal effective dose of apomorphine for reducing PRL by 30 min was 0.01 mg/kg; TSH inhibition was observed with a dose of 0.1-0.3 mg/kg. The inhibitory effects of apomorphine (1.0 mg/kg) on PRL and TSH levels were maximal by 15 min and diminished by 120 min; plasma GH was highest 120 min after injection. Thyroidectomy (10 days) markedLH elevated serum TSH, had no effect on serum PRL and inhibited the ability of apomorphine (0.1 or 0.3 mg/kg) to reduce TSH but not PRL levels. These observations may indicate that separate dopaminergic control mechanisms exist for TSH and PRL secretion. Administration of haloperidol elevated serum PRL, tended to lower TSH, dramatically reduced GH and had no effect on LH levels. Haloperidol pre-treatment blocked the effects of apomorphine on PRL, TSH, and GH secretion. The overall results of this study indicate that DA agonists inhibit PRL and TSH, stimulate GH but do not stimulate LH release in male rats.


Neuroendocrinology | 1977

Inhibition by prolactin of post-castration rise in LH.

L. Grandison; C.A. Hodson; H.T. Chen; J. P. Advis; J. W. Simpkins; Joseph Meites

Castration of male and female rats resulted in a marked rise in serum LH. The rise in serum LH was partially or completely prevented by injection of prolactin (Prl), by implantation of a small amount of Prl in the median eminence (ME), by grafting 2 anterior pituitaries (APs) underneath the kidney capsule, or by transplantation of a Prl-secreting pituitary tumor underneath the skin. The larger pituitary tumor transplants secreted more Prl and were more effective in reducing LH release than the smaller tumors which secreted less Prl. Suppression of LH release generally was greater during the earlier than in the later phases of the different treatments. The pituitary LH response to synthetic LH-RH was the same in ovariectomized rats with or without pituitary grafts, and the decrease in hypothalamic LH-RH after orchidectomy was prevented by pituitary grafts. These results indicate that Prl can depress LH release after castration and that these effects are mediated via the hypothalamus.


Neuroendocrinology | 1980

Effects of a Prolactin-Secreting Pituitary Tumor on Hypothalamic, Gonadotropic and Testicular Function in Male Rats

C.A. Hodson; J. W. Simpkins; K.A. Pass; Charles F. Aylsworth; R. W. Steger; Joseph Meites

The presence of a transplanted prolactin- and GH-secreting pituitary tumor (Furth MtT.215) in inbred male rats resulted in increased hypothalamic LHRH and pituitary LH content, decreased serum LH and testosterone concentrations, and very high serum prolactin values. The pituitary tumor also inhibited LH release by the in situ pituitary in response to orchidectomy, or orchidectomy, or adrenalectomy, and reduced the LH response to LHRH administration. Testes weight was significantly reduced and adrenal weight was significantly increased in the rats carrying pituitary tumors. These results that inhibitory effects of the transplanted pituitary tumor on LH and testosterone secretion were affected both a reduction in hypothalamic LHRH release and a reduced responsiveness of the pituitary to LHRH.


Life Sciences | 1977

Effects of pargyline on hypothalamic biogenic amines and serum prolactin. LH and TSH in male rats.

H.T. Chen; J. W. Simpkins; G. P. Mueller; Joseph Meites

Abstract The time course effects of pargyline on hypothalamic biogenic amines and serum prolactin (PRL), LH and TSH were studied in adult male rats. The rats were killed at intervals of 1–6 hrs after pargyline injection. Hypothalamic dopamine (DA) rose 79% by 1 hr and was 41% above “0” time by 6 hrs. Norepinephrine (NE) increased 31% by 1 hr and remained at about this level through 6 hrs, whereas serotonin (5HT) increased from 42% by 1 hr and to 95% by 6 hrs. Serum PRL LH and TSH fell significantly during the first 2 hrs, but all had returned to pretreatment values by 4 hrs. Serum PRL was about 4-fold above pretreatment values by 6 hrs, but LH and TSH remained at pretreatment levels. Stimulation by pargyline of PRL release was potentiated by Lilly compound 110140, a serotonin reuptake inhibitor, and blocked by parachlorophenylalanine, a serotonin synthesis inhibitor. These results suggest that the inhibitory effects of pargyline on PRL, LH, and TSH release during the first 2 hrs were associated mainly with a rapid increase in DA, and subsequent elevation of PRL release was related to the increase in 5HT. Return of serum LH and TSH to pretreatment levels at 4 and 6 hrs appeared to be associated mainly with the decrease in DA and perhaps to elevated NE levels. These results suggest that changes in relative concentrations of hypothalamic amines are related to differential release of PRL, LH and TSH.


Experimental Biology and Medicine | 1978

Differential Effects of Stress on Release of Thyroid-Stimulating Hormone in Young and Old Male Rats

J. W. Simpkins; C. A. Hodson; Joseph Meites

Summary In response to the stress of serial bleeding, ether exposure, or physical restraint, serum TSH was depressed more quickly and to a greater extent in young than in old male rats. These results suggest that the hypothalamo-hypophy-seal mechanisms which mediate inhibition of TSH release are less sensitive in old than in young male rats.


Endocrinology | 1977

Evidence for Depressed Catecholamine and Enhanced Serotonin Metabolism in Aging Male Rats: Possible Relation to Gondotropin Secretion2

J. W. Simpkins; G.P. Mueller; H. H. Huang; Joseph Meites


Life Sciences | 1979

Serotonergic control of prolactin release in male rats.

J. P. Advis; J. W. Simpkins; J. Bennett; Joseph Meites


Endocrinology | 1978

Relation of biogenic amines to onset of puberty in the female rat.

J. P. Advis; J. W. Simpkins; H.T. Chen; Joseph Meites


Endocrinology | 1979

Blockade of Steroid-Induced Luteinizing Hormone Release by Selective Depletion of Anterior Hypothalamic Norepinephrine Activity

J. W. Simpkins; J. P. Advis; C. A. Hodson; Joseph Meites

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Joseph Meites

Michigan State University

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J. P. Advis

Michigan State University

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C.A. Hodson

Michigan State University

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G.P. Mueller

Michigan State University

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H.T. Chen

Michigan State University

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C. A. Hodson

Michigan State University

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G. P. Mueller

Michigan State University

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G.A. Gudelsky

Michigan State University

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