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PubMedDate not supplied

Eimeria meleagrimitis in young turkeys: effects on weight, blood, and organ parameters.

Weight and biochemical studies were conducted on 2-week-old turkeys inoculated with 10(4) to 5 X 10(5) sporulated Eimeria meleagrimitis oocysts, on their pair-fed controls (equivalent food intake), and on control turkeys fed ad libitum. Food consumption and rate of weight gain of all inoculated and pair-fed turkeys fell sharply on day 4 postinoculation (PI), but deaths occurred primarily among the birds inoculated with 5 X 10(5) oocysts. Heart weights (expressed as percentage of body weight) were reduced in inoculated and pair-fed birds, but liver, spleen, and pancreas weights did not differ from those of either control group. Feed conversion (feed consumed/gain) was less efficient for inoculated turkeys than for ad libitum or pair-fed controls and was least efficient for turkeys inoculated with 5 X 10(5) oocysts. Plasma glutamic oxaloacetic transaminase (GOT, aspartate and aminotransferase) activity increased, and carotenoid and total protein levels decreased in inoculated turkeys but not in the pair-fed turkeys, indicating that these changes were caused by the infection and not by reduced food intake. Plasma glutamic pyruvic transaminase (GPT, alanine aminotransferase) remained stable in all groups. Plasma glucose levels of inoculated birds did not differ from those of the control groups, but liver glucose and glycogen levels decreased in both the inoculated and pair-fed birds.

Alanine Transaminase↗
PubMedDate not supplied

Consequences of active or passive immunization of turkeys against Escherichia coli O78.

Turkeys were injected at 7 and 14 days of age with live, heat-killed or formalin-killed Escherichia coli O78. Other turkeys were passively immunized at 22 days of age with hyperimmune serum produced against live or heat-killed E. coli O78. All turkeys were challenged at 24 days of age with E. coli O78. Turkeys immunized intramuscularly or intratracheally with live E. coli O78 were protected from death, whereas few turkeys given killed E. coli O78 were protected. Passively immunized turkeys were protected from death regardless of whether live or heat-killed E. coli O78 was used to produce the hyperimmune serum. Most turkeys that survived challenge developed septic polysynovitis 2--4 days after challenge.

Animals↗
PubMedDate not supplied

Effect of avian influenza virus infection on the phagocytic function of systemic phagocytes and pulmonary macrophages of turkeys.

The effects of avian influenza virus (AIV) infection on systemic phagocytes and pulmonary macrophages of turkeys were studied. There was a significant increase (P < 0.0001) in oxidative burst in systemic phagocytes of AIV-inoculated turkeys on 2, 4, 6, and 8 days postinoculation (PI), as measured by chemiluminescence. There was also a significant increase (P < 0.02) in oxidative burst in pulmonary macrophages on day 4 PI. The chemiluminescence response was depressed on 6, 8, and 10 days PI in AIV-inoculated turkeys compared with controls. The increase in oxidative response in both systemic phagocytes and pulmonary macrophages correlated with the peak virus titer in the lungs and trachea of AIV-inoculated inoculated turkeys. Bacterial killing by pulmonary macrophages from AIV-inoculated turkeys was reduced on days 6 and 10 PI compared with uninoculated controls. Histopathological changes in trachea were more pronounced on day 6 PI in AIV-inoculated turkeys; no significant changes were detected in the lungs. These data indicate that compromised functional capacity of pulmonary macrophages predisposes turkeys to secondary bacterial infections.

Animals↗
PubMedDate not supplied

IgA, IgG, and anti-Pasteurella multocida antibody levels in bursectomized and/or cyclophosphamide-treated turkeys after CU vaccination.

In bursectomized, cyclophosphamide-treated, and bursectomized/cyclophosphamide-treated turkeys, IgA, IgG, and anti-Pasteurella multocida were determined before and after vaccination with the Clemson University (CU) strain of P. multocida. Before vaccination, the average total serum level of IgA was significantly (P < 0.05) lower in bursectomized and bursectomized/cyclophosphamide-treated turkeys than in untreated controls, and the average serum levels of anti-P. multocida were significantly (P < 0.05) lower in bursectomized, cyclophosphamide-treated, and bursectomized/cyclophosphamide-treated turkeys than in untreated controls. After vaccination, average serum IgA levels were still significantly (P < 0.05) lower in all treated groups of turkeys than in the untreated controls. Also after vaccination, total IgG increased significantly (P < 0.05) only in the bursectomized turkeys, and serum anti-P. multocida antibody levels increased significantly (P < 0.05) in cyclophosphamide-treated, bursectomized/cyclophosphamide-treated, and untreated turkeys. After challenge with virulent P. multocida, survivability was significantly (P < 0.05) lower in the three treated groups of turkeys than in the untreated groups.

Animals↗
PubMedDate not supplied

Use of virulent hemorrhagic enteritis virus for the induction of colibacillosis in turkeys.

Three hundred fifty 1-day-old large white turkeys were reared in brooding batteries to 10 days of age, after which they were moved to floor pens on litter. At 7 weeks of age, poults were allotted into four treatment groups as follows: 1) virulent hemorrhagic enteritis virus (HEV) alone (100 turkeys), 2) Escherichia coli alone (100 turkeys), 3) HEV + E. coli (100 turkeys), and 4) negative controls (50 turkeys). HEV was given orally at 7 weeks of age, followed by E. coli challenge in the drinking water 2 days later for 10 consecutive days. All groups were observed daily for mortality, both during and after challenge. Turkeys that died or were moribund were necropsied, and cultures were taken from the liver and bone marrow for bacterial isolation. Total mortality rates were 23% in the HEV + E. coli group, 10% in the HEV-only group, 3% in the E. coli-only group, and 0% in the negative control group. Cumulative mortality values were significantly different from those of the negative controls (P < or = 0.05) for HEV only and the HEV + E. coli group. E. coli was isolated from the liver and bone marrow of almost all turkeys that died.

Adenoviridae Infections↗
PubMedDate not supplied

Skeletal myopathy produced with experimental dosing of turkeys with monensin.

Monensin was given via gavage to 5- and 6-week-old broad-breasted white turkeys. The birds were allotted into four groups--three groups given monensin and one group of controls--in two experimental trials. Treated turkeys in Trial 1 received one dose of monensin per day for 4 days at 4.7 mg monensin/kg body weight, 8.8 mg/kg, or 17.6 mg/kg. Treated turkeys in Trial 2 received one dose of monensin per day for 5 days at 1.93 mg/kg, 4.7 mg/kg, or 8.8 mg/kg. Turkeys receiving the lowest dose showed no clinical signs of myopathy. Birds receiving 4.7 mg monensin/kg developed ataxia after the third dose and rear limb paresis and paralysis after the fifth dose. Turkeys receiving 8.8 mg/kg were ataxic after the second dose and paretic or paralyzed after the fourth dose. Turkeys receiving 17.6 mg/kg were ataxic 3 hours after the first dose and paretic or paralyzed 8 hours after the first dose. Histologically, a necrotizing skeletal myopathy was present in the muscles of the rear limbs. A dose-related response was observed in the percentage of myofibers damaged in birds that survived until the end of the trials. Intrafiber edema and vacuolation were observed in histologic sections from myocardium of turkeys from the two highest dose groups.

Animals↗
PubMed1996

[Avian Chlamydia psittaci phyla and their pathogenic significance for turkeys].

The present study demonstrates that Chlamydia psittaci is an important cause of respiratory disease in turkeys in Europe. The serotyping of isolates revealed that European turkeys frequently become infected with Chlamydia psittaci serovar D strains, but also can become infected with serovar A and B strains. In turkeys, differences in pathogenicity were observed not only between strains belonging to the serovars A (strain 84/55), serovar B (strain 89/1326) and serovar D (Texas Turkey strain and strain 92/1293), but also between two strains belonging to the same serovar D (Texas Turkey strain and strain 92/1293). In order to find an explanation for these differences in pathogenicity, the pathogenesis of the infection was studied in specific pathogen free turkeys. However, for all three serovars examined a similar pathogenetic sequence of events was deduced. In order to try and elucidate the observed differences in pathogenicity between different Chlamydia psittaci strains, the bacterium-host cell interaction was studied in BGM cell culture using transmission electron microscopy and immuno electron microscopy. Strains most pathogenic for turkeys, namely the serovar A strain and strain 92/1293 (serovar D) produced significantly larger inclusions with more numerous infectious organisms, produced the most severe degenerative changes in the host cell an also replicated freely in the cytoplasm of the host cell.

Animals↗
PubMedDate not supplied

Intravascular cartilaginous emboli in the spinal cord of turkeys.

A flock of 15-wk-old tom turkeys experienced an acute onset of paresis and ataxia in 75% of the birds after handling. Cartilaginous emboli were found in the spinal cord vasculature from one of five turkeys at this initial presentation. Most of the flock recovered within 6 days, but 3% remained paretic. Myelomalacia was present in three turkeys that failed to recover. Two of these turkeys had cartilaginous and osseous emboli within the medullary spaces of the vertebral bodies, internal vertebral venous sinuses, and spinal cord. The third turkey had vascular and spinal cord necrosis consistent with thrombosis and resultant ischemia. These changes suggest that turkeys may be susceptible to a syndrome analogous to fibrocartilaginous embolism of the spinal cord in mammals. The articular cartilage of the vertebral body endplate may be the source of the emboli. The turkeys with emboli had articular cartilage defects consisting of matrix eosinophilia, chondrocyte loss, multicellular cluster formation, cartilage detachment, and cartilage clefts. Cartilaginous emboli in the spinal cord should be considered as a potential cause for acute paresis and ataxia, especially in flocks with preexisting abnormalities of the vertebral articular cartilage surfaces.

Animals↗
PubMed1976

Hypercholeresis in turkeys following the ingestion of Crotalaria spectabilis seeds.

Young female turkeys received diets containing Crotalaria spectabilis seeds for 18 weeks. Mean values for total bile flow, biliary bile acid excretion, bile acid-dependent flow and bile acid-independent flow were significantly higher in crotalaria-fed turkeys than in controls. The hypercholeresis observed in crotalaria-fed birds involved both bile acid-dependent and bile acid-independent components of bile. Crotalaria-fed turkeys developed biliary hyperplasia. Liver weights were similar in the two groups. Since increases in 14C-erythritol clearances paralleled increases in total bile flow in crotalaria-fed turkeys (14C-erythritol bile to plasma ratios were similar in both groups), it was evident that the hypercholeresis in crotalaria-fed turkeys did not involve the ductal/ductular component of bile. Little or no ductal/ductular bile flow occurred in either group since total bile flow was equal to erythritol clearance and extrapolation to zero erythritol clearance yielded zero bile flow rates in both groups. Crotalaria-fed turkeys exhibited significantly higher biliary concentrations of chlorides (associated with lower sodium , potassium and bicarbonate concentrations) than did control birds. Validation of the use of 14C-erythritol clearance for the estimation of canalicular bile flow in turkeys was provided both by substantial decreases in bile to plasma 14C-erythritol concentration ratios following the injection of avian vaso-active intestinal peptide and the failure to demonstrate chromatographically the presence of radioactive metabolites of 14C-erythritol in plasma.

Animals↗
PubMed1998

Functional responses of neonatal chicken and turkey heterophils following stimulation by inflammatory agonists.

OBJECTIVE: To determine functional responses of neonatal chicken and turkey heterophils to various inflammatory agonists. ANIMALS: 100 one-day-old chickens and turkeys. PROCEDURE: Blood heterophils were isolated and stimulated for 30 minutes at 39 C with ionomycin, phorbol myristate acetate (PMA), opsonized zymosan (OZ), or formyl-methionyl-leucyl-phenylalanine (FMLP). Functional responses (shape change, adherence, phagocytosis, influx of intracellular calcium, and oxidative burst) of stimulated heterophils were measured and compared with responses of unstimulated (control) heterophils. RESULTS: Turkey and chicken heterophils did not respond to FMLP stimulation. Stimulation of chicken and turkey heterophils with ionomycin resulted in significant increases in adherence, percentage of cells with a shape change, phagocytosis, intracellular calcium concentration, and oxidative burst. Turkey heterophils did not respond to PMA stimulation, whereas stimulation of chicken heterophils with PMA resulted in significant increases in adherence, percentage of cells with a shape change, phagocytosis, and oxidative burst but not intracellular calcium concentration. Stimulation of chicken and turkey heterophils with OZ resulted in significant increases in oxidative burst. CONCLUSIONS: Mechanisms regulating initiation of heterophil activation in neonatal chicken and turkey heterophils are consistent with those described for heterophils isolated from mature birds. The biochemical and cytoskeletal systems of neonatal avian heterophils undergo functional alterations following stimulation with inflammatory agonists. CLINICAL RELEVANCE: Understanding heterophil activation and regulation should eventually lead to methods for controlling bacterial diseases in poultry.

Animals↗
PubMed1995

Hemorrhagic enteritis virus induced changes in the lymphocyte subpopulations in turkeys and the effect of experimental immunodeficiency on viral pathogenesis.

We examined the changes in the lymphocyte subpopulations in the spleen and peripheral blood of turkeys and the effects of experimental immunodeficiency in the B and T cell compartments on the pathogenesis of hemorrhagic enteritis (HE) in turkeys. Inoculation of turkeys with hemorrhagic enteritis virus (HEV) induced a drop in the relative proportions of IgM bearing cells on Day 2, 3, and 9 post-infection and an elevation in the relative proportions of CD4+ cells on Day 4 and 6 post-infection. Elevated levels of CD8+ cells were observed in the infected turkeys only on Day 16 after infection. Marked depletion of IgM+ cells may play a role in immunodepression caused by HEV. Cyclophosphamide (CY) treatment induced B cell deficiency in turkeys severely impaired HEV replication in the spleen suggesting that B lymphocytes are important for viral replication. Cyclosporin A (CsA) selectively impaired T cell mitogenesis and protected the turkeys against HEV-induced intestinal hemorrhages. CsA did not prevent viral replication in the spleen or the associated splenomegaly. This result suggested that T cell immunity may be important for intestinal hemorrhaging induced by HEV.

Animals↗
PubMedDate not supplied

Propagation of virulent and avirulent turkey hemorrhagic enteritis virus in cell culture.

Virulent and apathogenic isolates of turkey hemorrhagic enteritis virus (HEV) were successfully propagated in lymphoblastoid cell lines of turkey origin, whereas spleen and kidney cell cultures from HEV-infected turkeys failed to replicate the virus. The lymphoblastoid cell lines used were MDTC-RP16 and MDTC-RP19, which were previously established from tumors induced by Marek's disease virus in turkeys. Virus replication followed co-cultivation of lymphoblastoid cells with spleen cells from HEV-infected turkeys. Virus replication was demonstrated by immunofluorescence, by agar-gel-precipitin tests, and by electron microscopy. Supernatant fluid of cultures infected with virulent HEV caused death and specific lesions in turkey poults. Poults vaccinated with apathogenic HEV were protected against death and lesions after challenge with pathogenic HEV, which was recovered from infected cultures. The MDTC-RP19 cell line appeared far more susceptible than the MDTC-RP16 cell line to infection with HEV.

Animals↗
PubMed1996

Changes in pituitary somatotroph and lactotroph distribution in laying and incubating turkey hens.

Turkey hens can rapidly shift from a laying condition to one characterized by ovarian regression, incubation behavior, and hyperprolactinemia. Although remarkable changes occur in hormonal profiles as turkey hens pass from a laying to an incubating state, studies have not been undertaken to examine histochemical alterations of functionally relevant pituicytes in the adenohypophysis. The objective of this study was to compare the immunocytochemical changes in pituitary lactotrophs and somatotrophs in incubating turkey hens with those of egg laying hens. Based upon nest visiting and egg production records, laying and incubating hens were selected for sampling blood, pituitaries, and ovaries. Plasma prolactin (PRL) and growth hormone (GH) concentrations were determined. Sagittal pituitary sections of laying and incubating hens were immunostained using antibodies against turkey growth hormone or synthetic chicken PRL peptide. Somatotrophs were found predominantly in the caudal lobe while lactotrophs occurred only in the cephalic lobe of adenohypophysis in laying hens. In incubating hens, somatotrophs in the ventral half of the caudal lobe were replaced by lactotrophs. The sagittal area which immunostained for PRL was significantly greater while the area that immunostained for GH was less in the adenohypophysis of incubating turkey hens. Some of the lactotrophs were hypertrophied in incubating hens. The lactotrophic recruitment and hypertrophy provide a cellular basis for the hyperprolactinemia in incubating turkey hens.

Animals↗
PubMed1998

Dietary protein restriction stress in the domestic turkey (Meleagris gallopavo) induces hypofunction and remodeling of adrenal steroidogenic tissue.

In the present study, we investigated the influence of dietary protein restriction stress on adrenal steroidogenic function of the domestic turkey. Immature male turkeys (2 weeks old) were fed isocaloric synthetic diets containing either 28% (control) or 8% (restriction) soy protein for 4 weeks. Trunk plasma was processed for the determination of adrenocorticotropin (ACTH), corticosterone, aldosterone, and total 3, 5, 3'-triiodothyronine (T3). In addition, adrenal glands were processed for the isolation of defined, density-separable, adrenal steroidogenic cell subpopulations: three low-density adrenal steroidogenic cell subpopulations [LDAC-1 (rho = 1.0350-1.0490 g/ml). LDAC-2 (rho = 1.0490-1.0570 g/ml), and LDAC 3 (rho = 1.0370-1.0585 g/ml)] and a high-density subpopulation [HDAC (rho = 1.0590-1.0720 g/ml)], and the steroidogenic function of these cell subpopulations was evaluated. Protein restriction did not influence plasma ACTH However, it increased relative adrenal weight (mg/100 g body wt) (+37.8%) and plasma corticosterone (+317%). By contrast, it depressed plasma aldosterone (-51.2%). In addition, it caused a modest depression in plasma T3 (-25.9%). At the cellular level, protein restriction induced panhypofunction. Basal corticosteroid (aldosterone and corticosterone) production values of LDAC-1, -2, and -3 and HDAC from protein-restricted birds were, respectively, 42.9, 47.9, 30.8, and 57.5% less than those of corresponding cell subpopulations from control birds. In addition, maximal corticosteroid production values of LDAC-1, -2, and -3 and HDAC from protein-restricted birds, in response to ACTH, angiotensin II (AngII), and 25-hydroxycholesterol support, were depressed by 56.8, 55.1, 22.7, and 42.9%, respectively. Interestingly, LDAC-3 was relatively refractory to the influence of this stressor. By contrast, there was the lack of a concentration-dependent aldosterone response of LDAC-1 and -2 to AngII with protein restriction. This was not due to a failure in cell function since aldosterone responses of these cell subpopulations to ACTH and to 25-hydroxycholesterol support were apparent. In addition, the concentration of AngII receptors of cell subpopulations from protein-restricted turkeys, if anything, was greater than that of cell subpopulations from control turkeys. Protein restriction also altered the cell subpopulation composition of the adrenal gland: compared to control, it decreased the proportion of LDAC-2 by 42.3% and increased the proportion of LDAC-3 and HDAC by 68.7 and 302%, respectively. Thus, dietary protein restriction induces adrenal steroidogenic hypofunction in turkeys. In addition, the present study suggests that this nutritional stressor induces marked remodeling of the steroidogenic tissue in the turkey adrenal gland.

Adrenal Glands↗
PubMed1998

Effect of exogenous progesterone on luteinizing hormone secretion in domestic turkey hens at different reproductive states.

To determine effects of progesterone (P4) treatment on luteinizing hormone (LH) secretion in turkey hens, two trials were conducted. Trial 1 was to determine changes in LH, P4, and testosterone (T) during photostimulation. Photosensitive turkey hens were maintained under short days (SD) of 6 h light and 18 h dark. At the beginning of Trial 1, blood samples were taken daily for 4 days, then one-half of the hens were switched to long days (LD) of 14 h light and 10 h dark, and daily blood samples were continued until 5 days after eggs were laid by all the hens switched to LD. Concentrations of LH, P4, and T increased significantly 1 day after switching hens from SD to LD, but the increase in P4 was initially low with a further increase occurring by 3 days prior to first eggs. In Trial 2, turkey hens were injected with exogenous P4 to determine if P4 is an initiator of the preovulatory surge of LH. P4 or vehicle were injected im in hens at three different reproductive states: (1) while hens were maintained under SD, (2) on the 5th day after hens were switched from SD to LD, and (3) after hens were laying for 1 week. The hens were serially bled at 10-min intervals for 8 h to monitor changes in LH and P4. After 2 h of serial bleeding, P4 or vehicle was injected and bleeding was continued for an additional 6 h. After P4 injection, its concentration increased rapidly from a base level of 0.25-1.20 ng/ml to a postinjection high level of 4.42-6.10 ng/ml within 20 min. The high level of P4 was then maintained throughout the remaining 6 h. No increases of LH secretion were observed after P4 or vehicle injection in hens at either State 1 or State 2. Small increases of LH secretion were detected about 2 h after P4 injection in hens at State 3, but these increases were not significantly above vehicle-injected controls. Thus, there was no positive feedback effect of P4 injection on LH secretion in this trial. These results suggest that P4 might not induce LH secretion in immature or mature turkey hens and might not be the factor which induces the preovulatory surge of LH in laying turkey hens. Nonsteroidal factors of ovarian origin might be involved in regulating the preovulatory surge of LH in turkey hens.

Animals↗
PubMed2000

Biochemical basis for the extreme sensitivity of turkeys to aflatoxin B(1).

Poultry are the most susceptible food animal species to the toxic effects of the mycotoxin aflatoxin B(1) (AFB(1)). Feed contaminated with even small amounts of AFB(1) results in significant adverse health effects in poultry. The purpose of this study was to explain the biochemical mechanism(s) for this extreme sensitivity. We measured microsomal activation of AFB(1) to the AFB(1)-8,9-epoxide (AFBO), the putative toxic intermediate, as well as cytosolic glutathione S-transferase (GST)-mediated detoxification of AFBO, in addition to other hepatic phase I and phase II enzyme activities, in 3-week-old male Oorlop strain turkeys. Liver microsomes prepared from these turkeys activated AFB(1) in vitro with an apparent K(m) of 109 microM and a V(max) of 1.25 nmol/mg/min. Preliminary evidence for the involvement of cytochromes P450 (CYP) 1A2 and, to a lesser extent, 3A4 for AFB(1) activation was assessed by the use of specific mammalian CYP inhibitors. The possible presence of avian orthologues of these CYPs was supported by activity toward ethoxyresorufin and nifedipine, as well as by Western immunoblotting using antibodies to human CYPs. Cytosol prepared from turkey livers exhibited GST-mediated conjugation of 1-chloro-2,4-dinitrobenzene (CDNB) and 3,4-dichloronitrobenzene (DCNB), but at a much lower rate than that observed in other species. Western immunoblotting indicated the presence of alpha and sigma class GSTs and another AFB(1)-detoxifying enzyme, AFB(1)-aldehyde reductase (AFAR). Turkey liver cytosol also had quinone oxidoreductase (QOR) activity. Importantly, cytosol exhibited no measurable GST-mediated detoxification of microsomally activated AFB(1), indicating that turkeys are deficient in the most crucial AFB(1)-detoxification pathway. In total, our data indicate that the extreme sensitivity of turkeys to AFB(1) may be attributed to a combination of efficient AFB(1) activation and deficient detoxification by phase II enzymes, such as GSTs.

Aflatoxin B1↗
PubMed1985

The regulation of adenylate cyclase activity in turkey erythrocyte membranes by forskolin.

The mechanisms by which forskolin stimulates adenylate cyclase activity in turkey erythrocyte membranes and is influenced by manganese and Gpp(NH)p were studied. Forskolin-dependent adenylate cyclase activity in particulate turkey erythrocyte membranes is enhanced following preincubation of membranes with isoproterenol and GMP (cleared membranes). In contrast, solubilization of turkey erythrocyte membranes, previously cleared, renders them relatively refractory to forskolin but not to Gpp(NH)p. Whereas adenylate cyclase activity due to the simultaneous presence of forskolin and Mn2+ in particulate turkey erythrocyte membranes is additive, their copresence becomes synergistic after solubilization. The apparent Kact for forskolin activation of adenylate cyclase is not influenced by clearance or by the presence of Mn2+ in particulate turkey erythrocyte membranes. Following solubilization, the Vmax for forskolin-dependent adenylate cyclase activation determined in the presence of Mn2+ is also independent of clearance. Forskolin activation of turkey erythrocyte adenylate cyclase appears to be influenced at sites in addition to the catalytic unit.

Adenylyl Cyclases↗
PubMed1987

Prolactin release following electrical stimulation of the brain in female turkeys (Meleagris gallopavo).

Different regions of the hypothalamus were electrically stimulated in anesthetized adult female turkeys. Plasma levels of prolactin (Prl) were measured before (-20, 0 min), during (5, 10, 20, 30 min), and after (5, 15, 30, 60, 90 min) a 30-min period of electrical stimulation. In turkeys with electrode placements in the regions of the preoptic-anterior hypothalamus, ventromedial hypothalamus, inferior hypothalamus, and the median eminence, the onset of stimulation increased plasma Prl within 5 min (P less than 0.05) and the maximum level was reached by the end of the 30-min stimulation period. The termination of hypothalamic stimulation was followed by decreased plasma Prl to prestimulation levels. In a subsequent study plasma Prl was measured in hens at different stages of the reproductive cycle, following electrical stimulation in the ventromedial hypothalamus. Ventromedial stimulation induced increases in plasma Prl in laying, photorefractory, and incubating turkeys; however, the relative change in the maximal Prl level was greater in incubating (21-fold) than in either laying (3.5-fold) or photorefractory (5-fold) turkeys. We conclude that Prl release in the female turkey can be affected by electrical stimulation of selected hypothalamic areas and that stimulation-induced Prl release in the ventromedial hypothalamus is enhanced in incubating turkeys.

Animals↗