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Photostimulation (PS) of turkeys increases the number of hypothalamic vasoactive intestinal peptide (VIP)-immunoreactive neurons, the number of anterior pituitary VIP binding sites, and prolactin (PRL) secretion. Serotonin (5-HT) was recently shown to stimulate PRL secretion through VIP. This study tested the hypothesis that 5-HT's ability to induce PRL secretion is mediated by reproductive status and/or photoperiod in normally cycling turkey hens. Initially, saline or 5-HT was infused into the third ventricle of nest-deprived, previously incubating (ND) hens for 60 min at rates of 0.1, 1.0, or 10 nmol/min. The results led to use of the 10 nmol/min infusion rate for the remaining 5-HT infusions. Next, 5-HT was infused into short-day (SD;6), laying (6), ND (5), and photorefractory (P/R;6) hens. Plasma PRL was elevated in all groups except for the SD hens (P < 0.05). In Experiment 3, VIP was infused into the median eminence of SD (6), laying (5), and P/R (5) hens, increasing circulating PRL levels in all three groups (P < 0.05). Finally, SD hens were photostimulated for 0, 3, or 10 days and then infused with 5-HT. Only the birds which were photostimulated for 10 days exhibited elevated plasma PRL (P < 0.05). In conclusion, PS regulates PRL secretion at the hypothalamic level and more than 3 days of PS are required for 5-HT-ergic stimulation of PRL secretion.

The stimulatory and inhibitory effects of dopamine (DA) upon avian prolactin (PRL) secretion suggest that, in birds, these actions are mediated by multiple DA receptors. To test this hypothesis, combined intracranial infusions of DA and selective D1 or D2 DA receptor blockers, plus electrical stimulation (ES) of the brain and vasoactive intestinal peptide (VIP) immunoneutralization, were used to characterize the actions of DA on PRL secretion in the turkey. Blockade of D1 DA receptors prevented the increase in circulating PRL observed in response to infusion of stimulatory concentrations of DA or to ES. Stimulatory infusions of DA also failed to increase circulating PRL in birds immunized against VIP. Results from infusion of the D2 DA receptor antagonist were unclear. Low concentrations had no effect, while the highest concentration (100 nmol/min) produced an increase in plasma PRL. At the high concentration the drug may be affecting PRL secretion by (1) acting nonspecifically, (2) acting as a partial DA agonist on D1 DA receptors, or (3) diffusion to the pituitary and blockade of D2 receptors there. These data suggest that avian PRL secretion is mediated by D1 DA receptors within the brain and that the stimulatory effect of DA upon PRL secretion requires an intact VIPergic system.

Photostimulation initiates and maintains the rise in circulating prolactin (PRL) observed during the reproductive cycle of the female turkey. Vasoactive intestinal peptide (VIP) is the principal PRL-releasing factor. This study tested the hypothesis that gonadal stimulatory photoperiods stimulate PRL secretion by releasing hypothalamic VIP. Therefore, an experiment was designed to determine if VIP immunoneutralization altered photo-induced PRL secretion. Reproductively quiescent female turkeys were divided into two groups comprising turkeys actively immunized with synthetic VIP conjugated to keyhole limpet hemocyanin (VIP-KLH; immunized; n = 48) or KLH alone (control; n = 48). The first immunization was administered 6 weeks before photostimulation. Blood samples were collected at frequent intervals prior to and following photostimulation, and plasma PRL concentrations were determined. Vasoactive intestinal peptide antibody titer was estimated from the percentage of 125I-labeled VIP bound to plasma diluted 1:1000. At the onset of photostimulation (Day 0), plasma PRL levels were similar for immunized and control turkeys (9.1 +/- 0.3 versus 8.9 +/- 0.3 ng/ml, respectively). Plasma PRL of control birds increased (P < 0.05) by Day 16 of photostimulation, reaching a peak value of 724.9 +/- 90.1 ng/ml on Day 84. In contrast, plasma PRL remained essentially unchanged in immunized birds. Titer of anti-VIP antibodies expressed as 125I-VIP bound by plasma in immunized birds was 10.9 +/- 1.5% on the day of photostimulation. Incubation behavior was blocked in immunized birds, whereas 75% of controls exhibited incubation behavior. The control group laid 1.83 eggs/ week/hen compared to 3.40 eggs/week/hen in immunized hens. These findings suggest that photoperiodic modulation of PRL secretion in the turkey is influenced by hypothalamic VIP neuronal system.

Dopamine (DA) was infused into the third ventricle of anesthetized laying turkey hens at various concentrations to determine its effect on both basal prolactin (PRL) levels and ongoing electrically induced PRL secretion. The infusion of DA at rates of 1.0 or 10.0 nmol/min resulted in dose dependent increases in plasma PRL. These infusions had no inhibitory effect on electrically stimulated PRL release. The infusion of DA at 100.0 or 500.0 nmol/min caused no stimulation of PRL secretion and totally inhibited the PRL response elicited by electrical stimulation of the medial preoptic nucleus. These results show that dopaminergic influences are involved in both stimulating and inhibiting avian PRL secretion and suggest possible biphasic actions of DA within the brain.

The neuronal mechanisms that govern prolactin (PRL) secretion in the turkey appear to involve monoaminergic systems. Considerable evidence indicates that serotonin (5-HT), acting centrally, is a potent stimulator of PRL secretion. This study, using birds actively immunized against VIP, tests the hypothesis that 5-HT stimulates PRL secretion by releasing vasoactive intestinal peptide (VIP). Nonimmunized turkeys were injected ip with saline, quipazine (5-HT agonist; 5 mg/kg), methysergide (5-HT antagonist; 8 mg/kg), or methysergide plus quipazine, and VIP-immunized birds were injected with saline or quipazine. Quipazine increased plasma PRL levels from 26.8 ± 7.1 ng/ml at Time 0 to a peak value of 148.1 ± 31.4 ng/ml 2 hr after injection. Pretreatment with methysergide or VIP-immunoneutralization abolished the PRL response to quipazine. Intraventricular infusion of 5-HT (1 nmol/min) caused plasma PRL to rise from a baseline of 16.3 ± 2.6 ng/ml to 85.2 ± 14.3 ng/ml after 30 min in nonimmunized control birds. Serotonin infusion did not induce PRL secretion in the VIP immunized birds. These findings suggest that serotonergic stimulation of PRL secretion in the female turkey requires a functional VIPergic system.