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G D Riegle

Publications and source records attributed to G D Riegle.

At least 19 recordsLinked to original sources

Responsiveness of tuberoinfundibular dopamine neurons in the aged female rat to the stimulatory actions of prolactin.

The autoregulatory feedback control of prolactin, which is mediated by tuberoinfundibular dopamine (DA) neurons, is altered in the aged rat; this is evidenced by increased circulating concentrations of prolactin and decreased activity of these neurons. In the present study the action of prolactin on tuberoinfundibular DA neurons in young and aged female rats was estimated by measuring the rate of DA synthesis (dopa accumulation following the administration of a decarboxylase inhibitor) in the median eminence. The rate of dopa accumulation in the median eminence of the aged (26 months) rat was reduced to 50-60% of that in the young (3 months) rat. The acute systemic administration of haloperidol, a DA antagonist which increases serum concentrations of prolactin or intracerebroventricular infusions of prolactin increased the rate of dopa accumulation in the median eminence of both young and aged rats by the same relative amount. The administration of haloperidol and prolactin increased the rate of DA synthesis to a greater extent in young than in aged rats. The administration of bromocriptine, a DA agonist which reduces serum concentrations of prolactin, decreased the rate of dopa accumulation in the median eminence of both young and aged rats. In young animals the intracerebroventricular administration of prolactin reversed the bromocriptine-induced decrease in DA synthesis in the median eminence after 4 h and caused a further increase after 12 h. Qualitatively similar effects were seen in the aged rats; however, prolactin-treated young rats had much higher levels of DA synthesis than aged rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging

Restraint stress decreases the neurosecretory activity of tuberoinfundibular dopaminergic neurons in young but not in aged female rats.

The regulation of prolactin secretion by tuberoinfundibular dopamine (DA) neurons appears to be altered in the aged rat: the concentration of prolactin in the serum increases and the activity of the tuberoinfundibular DA neurons decreases. In the young female rat a brief period of stress reduces the tuberoinfundibular DA neurosecretory activity and increases the secretion of prolactin. The purpose of the present study was to determine if the responsiveness of tuberoinfundibular DA neurons to restraint stress is altered in the aged female rat. The activity of these neurons was estimated from the rate of DA synthesis in their terminals in the median eminence, as measured by the rate of accumulation of dihydroxyphenylalanine (DOPA) after the administration of a decarboxylase inhibitor. Thirty minutes of restraint stress increased serum prolactin concentrations in both young (3 months) and aged (26 months) constant estrous rats, but reduced the rate of DOPA accumulation in the median eminence of only the young rats. Restraint also decreased the rate of DOPA accumulation in the median eminence of intermediate-aged rats (14 months) independently of whether the rats were exhibiting normal ovarian cycles (measured on the day of estrus) or were in a constant estrus. This suggests that the loss of ovarian cyclicity per se is not associated with the age-related change in the response of tuberoinfundibular DA neurons to restraint stress.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging

The rapid 'tonic' and the delayed 'induction' components of the prolactin-induced activation of tuberoinfundibular dopaminergic neurons following the systemic administration of prolactin.

The present study was designed to characterize the time and dose relationships of the response of tuberoinfundibular dopaminergic (TIDA) neurons in the rat to systemically administered prolactin (PRL). The activity of TIDA neurons was estimated by measuring the rate of dopamine (DA) synthesis in the median eminence (DOPA accumulation following the administration of a decarboxylase inhibitor). Rats were pretreated with bromocriptine, a dopaminergic agonist, so as to inhibit the release of endogenous PRL from the anterior pituitary, and thereby reduce the activity of TIDA neurons to a 'basal' level from which it could be increased subsequently by exogenously administered PRL. In control animals an intraperitoneal injection of ovine PRL (oPRL) increased DOPA accumulation at 16 h, but not before, whereas in bromocriptine-pretreated animals an intraperitoneal injection of oPRL increased DOPA accumulation after 4 h ('tonic' component) and caused a further increase after 16 h ('induction' component). Continuous intravenous infusions of oPRL into bromocriptine-pretreated rats increased DOPA accumulation in the median eminence by 4 h, and when infused into control rats oPRL reduced serum concentrations of endogenous rat PRL (rPRL) by 2 and 4 h. Continuous intravenous infusions of rPRL increased DOPA accumulation in the median eminence after 2 h; this effect exhibited a very steep dose-response relationship (possibly an 'all-or-none' response). TIDA neurons were very sensitive to changes in circulating concentrations of PRL; their activity was increased if serum PRL concentrations were merely doubled by infusing a low concentration of rPRL for 4 h. Three daily injections of haloperidol elevated circulating rPRL concentrations and increased the rate of DOPA accumulation in the median eminence.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Progesterone and luteinizing hormone secretion following stress-induced interruption of constant estrus in aged rats.

Concentrations of progesterone and luteinizing hormone (LH) were measured during the first diestrus and subsequent proestrus after constant estrous was interrupted by restraint stress. Stress stimulated an acute increase in serum progesterone. Although stress resulted in changes in vaginal cytology characteristic of normal estrous cycles, stress-treated constant estrous (CE) rats had no midcycle (diestrous day 1) elevation of progesterone and markedly lower LH and progesterone during the afternoon of proestrous than age-matched normally cycling controls. The majority of the treated rats resumed CE without completing a cycle. In a separate experiment, progesterone injection during proestrous resulted in increased LH secretion in aging rats with normal estrous cycles. These data indicate that decreased proestrous progesterone secretion may contribute to the decrease in neuro-endocrine stimulation of proestrous gonadotropin secretion in the aged rat and may be associated with the initiation of CE.

Aging

Hypoprolactinemia induced by hypophysectomy and long-term bromocriptine treatment decreases tuberoinfundibular dopaminergic neuronal activity and the responsiveness of these neurons to prolactin.

The effect of long-term decreases in circulating concentrations of prolactin was determined on the responsiveness of tuberoinfundibular dopamine (DA) neurons to this hormone. The activity of these neurons in ovariectomized rats was estimated by measuring the rate of DA synthesis (DOPA accumulation after the administration of a decarboxylase inhibitor) in the median eminence at various times after serum concentrations of prolactin had been reduced by hypophysectomy or the chronic administration of a DA agonist (bromocriptine, 3 mg/kg/day). The concentration of DA in the median eminence, but not in striatum, declined progressively up to 12 days after hypophysectomy, but did not change at any time during bromocriptine treatment. On the other hand, norepinephrine concentrations in the median eminence were increased 12 days after both treatments. Within 24 h after hypophysectomy or the first injection of bromocriptine the rate of DA synthesis in the median eminence was decreased; this decrease was maintained for at least 12 days suggesting that tuberoinfundibular DA neuronal activity is normally maintained by endogenous prolactin. Intracerebroventricular (ICV) injections of prolactin (10 micrograms, 12 h prior to sacrifice) increased the rate of DA synthesis in the median eminence of control, 24-hour hypophysectomized and 24-hour bromocriptine-treated rats. After longer periods (6-12 days) of bromocriptine treatment or after hypophysectomy the responsiveness of tuberoinfundibular DA neurons to prolactin was reduced. Dose-response studies revealed that the sensitivity and magnitude of response to ICV prolactin was markedly reduced in 12-day hypophysectomized rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Acute restraint stress decreases dopamine synthesis and turnover in the median eminence: a model for the study of the inhibitory neuronal influences on tuberoinfundibular dopaminergic neurons.

The effects of acute stress on serum prolactin concentrations and tuberoinfundibular dopaminergic (TIDA) neuronal activity were studied in female rats. TIDA neuronal activity was estimated by measuring the rate of dihydroxyphenylalanine (DOPA) accumulation after the administration of a decarboxylase inhibitor (NSD 1015) and the rate of decline of dopamine (DA) after the administration of a tyrosine hydroxylase inhibitor (alpha-methyltyrosine) in the median eminence. Serum prolactin concentrations were increased following 30 min of supine immobilization (restraint stress), but returned to control levels by 2, 8, and 16 h after the onset of this stress. The rate of DOPA accumulation was decreased during the 30 min of restraint; it was still further reduced 2 h later but had returned to control levels 8 and 16 h later. No change in the rate of DOPA accumulation was observed in the striatum or neurointermediate lobe of the pituitary at any time after the start of restraint. Restraint stress also decreased the rate of DA turnover in the median eminence, but was without effect on the rates of DA turnover in the striatum or neurointermediate lobe. These results suggest that restraint stress activates an inhibitory neuronal pathway which decreases the activity of TIDA neurons and may be responsible, at least in part, for the increase in serum prolactin concentrations. The responsiveness of TIDA neurons to the stress-induced decrease in activity was not influenced by the time of day or the stage of the estrous cycle. Not all stressful manipulations decreased TIDA neuronal activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine

Acute restraint stress decreases tuberoinfundibular dopaminergic neuronal activity: evidence for a differential response in male versus female rats.

The basal activity o f tuberoinfundibular dopaminergic (TIDA) neurons is higher and the response of these neurons to the stimulatory actions of prolactin is greater in the female than in the male rat. In the female rat, the restraint-stress-induced increase in serum prolactin concentrations is accompanied by a concurrent decrease in the activity of TIDA neurons. The purpose of the present study was to compare these effects of restraint in male and female rats. TIDA neuronal activity was estimated by measuring the rate of dopamine (DA) synthesis (DOPA accumulation after the administration of a decarboxylase inhibitor, NSD 1015) and the rate of DA turnover (decline of DA after administration of a tyrosine hydroxylase inhibitor; alpha-methyltyrosine) in the median eminence. Thirty minutes of restraint increased serum prolactin concentrations in both male and female rats, but a greater response was observed in the females. Restraint also decreased the rates of synthesis and turnover of DA in the median eminence of the female but not the male rat. The difference in the response of TIDA neurons in male and female rats to restraint is not the consequence of neuronal differentiation resulting from neonatal androgen exposure, because restraint aso decreased the activity of TIDA neurons in androgen-sterilized female rats. The inability of restraint stress to reduce TIDA neuronal activity in the male rat appears to be the consequence of testosterone, since TIDA neurons were responsive to restraint following castration of the males.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid

Adenohypophysial dopamine content and prolactin secretion in the aged male and female rat.

In male rats the concentrations of dopamine (DA) in the adenohypophysis and of PRL in serum increase progressively with age. The increase in the DA content is not a consequence of reduced metabolism of DA, since the activities of the enzymes that deaminate (monoamine oxidase) and O-methylate (catechol-O-methyltransferase) this amine are not reduced in the anterior pituitary of aged male rats; indeed, both type A and B monoamine oxidase activities are increased in the pituitaries of aged rats. The increased DA present in the aged adenohypophysis is not in a static pool but, as in young rats, is rapidly decreased by pharmacological treatments that reduce the activity of tuberoinfundibular DA neurons (gamma-butyrolactone), reduce the synthesis of DA in these neurons (alpha-methyltyrosine), or block DA receptors (haloperidol) in the adenohypophysis. All of these treatments increased serum PRL levels and reduced DA concentrations in the adenohypophysis of both young and aged rats. Similarly, in female rats, where age-related differences in BW and body composition are minimized, serum PRL concentrations and DA concentrations in the adenohypophysis of both young and aged rats changed in the same way after the administration of a DA agonist (apomorphine) or a DA antagonist (haloperidol). Apomorphine reversed the alpha-methyltyrosine-induced increase in serum PRL concentrations and the decrease in anterior pituitary DA content in both young and aged rats, although the latter animals appear to be more responsive to this drug. Similarly, aged rats were more sensitive to the increase in serum PRL concentrations and the decrease in anterior pituitary DA content caused by haloperidol. The actions of acute and chronically administered haloperidol are reversible, with the reduced DA content of the adenohypophysis and the elevated serum concentrations of PRL returning to respective pretreatment levels in both young and aged rats once treatment stops. The time course for recovery of serum PRL levels and anterior pituitary DA contents after both the acute and chronic haloperidol treatment is of longer duration in the aged rat, which is consistent with a decreased rate of clearance of haloperidol in these animals. Twelve daily injections of bromocriptine, a DA agonist, reduced serum PRL and anterior pituitary DA concentrations in both young and aged rats, and these effects persisted for up to 7 days after the injections were stopped.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging

The effect of age on reproduction in repeatedly mated female rats.

The effects of age and repeated pregnancies on reproduction were studied in Long-Evans rats. Indices of reproduction measured included estrous cycles, successful mating, numbers of rats producing litters, average litter size, average pup weight and serum LH-from a 4 pm proestrous blood sample. There were no differences in these reproductive parameters between rats with serial pregnancies initiated at 2 or 9 mo of age. The percentage of rats producing normal litters was reduced much faster than the percentage of successfully mated rats with normal ovarian cycles. Although 60% of the rats still had normal ovarian cycles and were mated at 17 mo of age, only one rat (4%) produced a litter. Increasing age and multiple pregnancies did not significantly affect the LH concentration of the proestrous blood sample or the average litter size or pup weight of the rats with successful pregnancies. These data suggest post-ovulatory loss of reproduction in the aging rat.

Animals

Hypothalamic LH-releasing activity in young and aged intact and gonadectomized rats.

Hypothalamic LH-releasing activity content was measured in young (3-5 mo) and aged (22-26 mo) intact and gonadectomized male and female rats. Hypothalamic extracts (0.25, 0.5 and 1.0 hypothalamus equivalents) from young and aged rats were incubated with untreated hemisectioned rat pituitaries in medium 199. All hypothalamic extract treatments stimulated LH release from the incubated pituitaries. Increased amounts of hypothalamic extracts added to to the incubation medium proportionally increased LH release. There were no differences in LH release stimulated by young or aged hypothalamic extracts from either the intact or gonadectomized groups. In addition serum testosterone concentrations were reduced in the aged male rats and serum LH was lower in aged male and female rats than in the young groups. Although serum LH was increased after gonadectomy in all groups, the increase was of smaller magnitude in the aged rats. These data indicate significant alterations in the responsiveness of the hypothalamus to steroid feedback in the aged rat. Although the hypothalamus contains sufficient LH-releasing activity to stimulate higher levels of pituitary and gonadal endocrine function, aging effects on the neuroendocrine control mechanisms inhibit hypothalamic hormone function.

Aging

Serum testosterone and testicular response to HCG in young and aged male rats.

Serum testosterone and testicular response to HCG was measured in young (3 - 6 mo) and aged (20 - 30 mo) male Long-Evans rats. Serum testosterone was measured by radioimmunoassays on serial blood samples taken before and after injections of HCG. Control group serum testosterone concentrations were lower in aged compared to young groups. Intravenous injection of 1, 5, and 20 IU of HCG increased serum testosterone in both age groups and testosterone remained elevated throughout the 150-min sampling interval. The increase in serum testosterone concentrations following acute HCG stimulation was greater in young than in aged rats. Serum testosterone concentrations and testicular response to intravenous HCG injections were increased to similar levels in young and aged male rats following 7 days of daily subcutaneous injections of 5 IU of HCG/100 gm bw. These data suggest that while testicular secretion and responsiveness is reduced with age, the aged male rat retains the capacity to secrete more testosterone than it normally maintains.

Aging

Thermorespiratory responses of shorn and unshorn sheep to mild heat stress.

Three 3-year-old ewes with surgically exteriorized carotid loops were twice exposed to ambient temperatures (Ta) of 25, 30, 35 and 40 C (at constant 40% relative humidity) for 120 min in the presence (6.6 cm) and absence (less than 0.3 cm) of fleece. Thermoregulatory responses were evaluated during the last 30 min of each exposure by measurements of rectal (Tre), 6 skin surface temperatures (Ts), respiratory frequency (f), oxygen consumption (Vo2) and respiratory evaporative heat (Er); arterial blood samples were analyzed for pH, Pco2 and HCO-3 concentration. Both shorn and unshorn sheep exhibited a progressive increase in f, Er and Ts as Ta was elevated, with the unshorn group showing a higher Er than the shorn sheep at each Ta without a significant change in heat production. Er was found to be the principal avenue of heat loss, accounting for as much as 59% of the total in the shorn sheep compared to65% for the unshorn sheep. Increases in Er were accompanied by a decline in the arterial Pco2 which was linearly related to the Ta in both shorn and unshorn sheep. These data suggest that in defending against hyperthermia, sheep appear unable to increase Er without a concurrent elevation in Va at nearly allstages of acute heat stress.

Animals

Effect of aging on hypothalamic LH-releasing and prolactin inhibiting activities and pituitary responsiveness to LHRH in the male laboratory rat.

Hypothalamic content of LH releasing and prolactin inhibiting activities and pituitary responsiveness to LH releasing hormone was measured in young (4 mo.) and aged (26 mo.) Long-Evans rats by in vitro methods. Hypothalamic extracts (0.5 and 1.0 hypothalamic equivalents) from young and aged male rats were incubated with untreated hemisected rat pituitaries in medium 199. Doses of 0.5 and 1.0 hypothalamic equivalents (HE) from both age group stimulated LH secretion. The increase in pituitary LH release stimulated by 0.5 HE from aged male rats was about half that stimulated by 0.5 HE from the young male group (p less than .20). The increase in LH secretion stimulated by hypothalamic extracts of either age group was not associated with a change in pituitary LH content. Although 0.5 and 1.0 HE from young male rats and 1.0 HE from the aged group reduced incubated pituitary prolactin release, 0.5 HE from the aged males did not affect prolactin release. Treatment with hypothalamic extracts also resulted in increased pituitary prolactin concentrations. Pituitaries from young and aged male rats were incubated in medium 199 containing 0, 25, or 100 ng of LH releasing hormone. Although LH releasing hormone stimulated LH secretion in all groups, the increase in release of LH was less in the aged groups than from pituitaries from the young male rats. Pituitary LH content of the aged male group was only about 1/4 that of the young group.

Aging

Effects of electroanesthesia and a phenothiazine tranquilizer on thermoregulation in the sheep.

The effects of giving propiopromazine alone and of electroanesthesia-propiopromazine treatment on thermoregulation (body temperature regulation) were studied in 3 sheep at ambient temperatures of 5, 25, and 35 C. Measures of thermoregulation during a 120-minute treatment and 120-treatment recovery period included rectal temperature, respiratory frequency, respiratory evaporative heat loss, metabolic heat production, multiple skin temperatures, and shivering. During cold exposure (5 C), both the propiopromazine administration and the electroanesthesia-propiopromazine treatment resulted in hypothermia which was attributed to increased peripheral and respiratory heat losses, a transient inhibition of shivering thermogenesis, and a reduction in metabolic heat production. At 35 C ambient temperature, both resulted in hyperthermia caused principally by a reduction in respiratory evaporative heat loss. The effects of electroanesthesia-propiopromazine treatment on thermoregulation appeared to be additive at both the cold (5 C) and the hot (35 C) environments, in that simultaneous administration resulted in a more profound thermoregulatory impairment. Nevertheless, shifts in body temperature during electroanesthesia are partly attributable to phenothiazine premedication.

Animals