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PubMed1995

Human diets cooked by microwave or conventionally: comparative sub-chronic (13-wk) toxicity study in rats.

To compare the possible effects of microwave and conventional cooking on a range of common dietary components, mixed human diets containing beef, potatoes and vegetables were fed to groups of 10 male and 10 female Wistar rats for 13 wk. The diet ingredients were cooked by either of the methods in a normal and an abused manner, the latter consisting of the normal treatment followed by two cycles of reheating to approximately 85 degrees C and cooling. The cooked ingredients were freeze-dried, ground and mixed with supplements of vitamins and minerals to meet the rat requirements. An additional control group was fed a cereal-based rodent diet. Criteria to assess toxicity included clinical observations, ophthalmoscopy, growth, food and water intake, haematology, clinical chemistry, urinalysis, organ weights, micronucleated erythrocytes in bone marrow, gross examination at autopsy and microscopic examination of a wide range of organs. The results indicate no adverse effects of the diets cooked by microwave compared with those cooked conventionally.

Analysis of Variance↗

PubMed1991

Iron-induced lipid peroxidation and brain injury responses.

Head trauma with cerebral contusion causes extravasation of red blood cells, followed by hemolysis and deposition of iron-containing blood products within the neuropil. Liberation of heme compounds is associated with deposition of hemosiderin, and with gliosis, neuronal loss and occasionally the development of seizures. In this experiment we injected components of red blood cell contents into rat amygdala, and then measured the rate of appearance of products of lipid peroxidation. Injection of microliter volumes of hemin and hemoglobin, with hematoprotoporphyrin and rodent plasma injection and contralateral uninjected tissue as controls, showed that the presence of the iron moiety within the protoporphyrin ring was required to initiate and propagate peroxidation. Free radical reactions initiated by iron or heme deposited within the neuropil may be a fundamental reaction associated with brain injury responses, and possibly with posttraumatic epileptogenesis.

Amygdala↗

PubMed2006

A new quantitative real-time reverse transcriptase PCR assay and melting curve analysis for detection and genotyping of Ljungan virus strains.

Ljungan virus (LV), a new member of the Picornaviridae, recently isolated from vole species in both Sweden and the USA, is suspected to be pathogenic for humans as an aetiological agent in myocarditis, diabetes, neurological disease and perinatal disease. This study describes for the first time an RT-PCR assay that can identify and quantify LV infection in various tissue sample types using primers and two different minor-groove-binder probes targeting the 5'-untranslated region of the LV genome. The assay, evaluated using control samples derived from various virus cultures and rodent tissues, allows precise quantification of viral load over six orders of magnitude (10(1) to 10(6) viral copies per assay) for all known strains of LV with high sensitivity and specificity. Furthermore, a melting curve analysis (MCA) was developed using two amplicon-specific hybridisation probes that allows rapid genotyping of different LV strains. These new methods provide useful tools to investigate the putative role of LV as a pathogen in both rodents and humans.

Animals↗

PubMed2004

Increased GAD67 mRNA levels are correlated with in vivo GABA synthesis in the MPTP-treated catecholamine-depleted goldfish brain.

The role of catecholamine neuronal input on GABAergic activity in the hypothalamus, telencephalon, optic tectum, and cerebellum was investigated in early recrudescent female goldfish (Carassius auratus). A new quantitative technique was developed and validated, permitting concomitant quantification and correlational analysis of glutamic acid decarboxylase 65 (GAD65), GAD67, and GAD3 mRNA levels and in vivo GABA synthesis. Catecholamine depletion was achieved by the administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; 50 microg/g body weight) and dopamine (DA) depletion verified by HPLC. Endogenous GABA levels were increased by intraperitoneal administration of gamma-vinyl GABA (GVG; 300 microg/g body weight), an inhibitor of the GABA catabolic enzyme GABA transaminase. Treatment with MPTP resulted in a greater than twofold increase in GABA synthesis rate in the optic tectum and telencephalon. The increase in GABA synthesis rate was highly correlated with an increase in GAD67, but not GAD65 or GAD3 mRNA levels. These results suggest that catecholaminergic input exerts inhibitory effects on GABA synthesis rates through the modulation of GAD67 in the optic tectum and telencephalon. Together with previously published observations in rodents and primates, it is suggested that catecholaminergic control of GABA synthesis must have evolved more than 200 million years ago, before the emergence of the teleost fishes.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed2003

Functional characterization of global genomic DNA repair and its implications for cancer.

The most versatile cellular pathway for dealing with a large variety of structurally-unrelated DNA alterations is nucleotide excision repair (NER). Most genomic damage, if not repaired, may contribute to mutagenesis and carcinogenesis, as well as to cellular lethality. There are two subpathways of NER, termed global genomic repair (GGR) and transcription-coupled repair (TCR); While GGR deals with all repairable lesions throughout the genome, TCR is selective for the transcribed DNA strand in expressed genes. Proteins involved in the initial recognition of lesions for GGR as well as for TCR (i.e. RNA polymerase) may sometimes initiate gratuitous repair events in undamaged DNA. However, the damage recognition enzymes for GGR are normally maintained at very low levels unless the cells are genomically stressed. Following UV irradiation in human fibroblasts the efficiency of GGR is upregulated through activation of the p53 tumor suppressor gene. The transactivation role of p53 includes control of expression of the genes, XPC and XPE, which are implicated in GGR but not TCR. These inducible responses are essential for the efficient repair of the most prominent lesion produced by UV, the cyclobutane pyrimidine dimer (CPD). They are also clinically relevant, as we have shown them to operate upon chemical carcinogen DNA damage at levels to which humans are environmentally exposed (e.g. through smoking). Thus, for benzo(a)pyrene (at 10-50 adducts per 10(8) nucleotides) repair was essentially complete within 1 day in p53(+/+) human fibroblasts while no repair was detected within 3 days in p53(-/-) cells. The levels of all four DNA adducts formed by benzo(g)chrysene, also exhibited p53-dependent control in human fibroblasts. However, unlike humans most rodent tissues are deficient in the p53-dependent GGR pathway. Since rodents are used as surrogates for humans in environmental cancer risk assessment it is very important that we determine how they differ from humans with respect to DNA repair and oncogenic responses to environmental genotoxins.

DNA Repair↗

PubMed2002

A transmission disequilibrium test of the Ser9/Gly dopamine D3 receptor gene polymorphism in adult attention-deficit hyperactivity disorder.

Convincing data support the hypothesis that genetic factors are involved in the etiology of attention-deficit hyperactivity disorder (ADHD). Various lines of evidence have shown that the dopamine system plays a crucial role in the pathophysiology of ADHD. The dopamine D3 receptor gene (DRD3) represents a promising candidate to examine in ADHD. Animal studies have shown that DRD3 mRNA is highly expressed in the ventral striatum suggesting an involvement of this receptor in the control of motor behaviour. Manipulation of DRD3 in rodents has led to a mouse model with nonfunctional D3 receptors that displays hyperactive behaviour in various environmental conditions. Furthermore, administration of 7-OH-DPAT, a dopaminergic agonist that binds preferentially to D3 receptors exerts an inhibitory effect on locomotor activity while D3 antagonists induce hyperactivity. Among various polymorphisms described for DRD3, the BalI polymorphism is most interesting because it codes for an aminoacid substitution in the N-terminus of the receptor. The receptor products of the two alleles (Ser/Gly) exhibit differential affinity for dopamine. To determine if DRD3 Ser9/Gly is involved in the susceptibility to ADHD we genotyped 39 adults with ADHD and their respective parents (trios). Adult ADHD represents a promising phenotype for studying the genetic component of the disorder. In fact, a recent family study has shown that relatives of adult ADHD patients have a higher rate of ADHD compared to relatives of children with ADHD suggesting a stronger genetic component for the adult version. The results of genotyping in the 39 trios analyzed with the transmission disequilibrium test showed no excess of transmission for DRD3 MscI/BalI alleles (chi(2) = 0.360; df = 1; P = 0.54). This result, although from a relatively small sample, indicates that it is unlikely that DRD3 is playing a major role in the etiology of ADHD in our sample.

Adult↗

PubMed1998

Lipocortin 1 and chemokine modulation of granulocyte and monocyte accumulation in experimental inflammation.

1. Migration of blood-derived leukocytes to tissue sites of inflammation is a hallmark of the response that the host organizes to counteract an insult or a trauma or an infection. A cascade of events is then activated to allow interaction between the leukocyte and the endothelium of postcapillary venule, and this cascade is finely regulated such that mechanisms of negative control are operating side by side with pathways that promote and sustain the extravasation process. Examples of both these positive and negative regulatory systems are discussed here. 2. In vivo accumulation of specific subtypes of leukocytes in response to application of selective chemokines operates through an indirect mechanism that includes the perivenular mast cell and, in particular, the mast cell-derived amines, such as histamine and serotonin. In fact, treatments of animals with (1) histamine H1 or serotonin antagonists or with (2) the mast cell stabilizer cromolyn or with (3) prior depletion of intact mast cells are maneuvers that successfully reduce eosinophil, neutrophil and monocyte extravasation in response to eotaxin, interleukin-8 or monocyte chemoattractant protein-1, respectively. A model in which histamine provides a P-selectin-dependent rolling phenomenon is then postulated. 3. The discovery that neutrophil-derived lipocortin 1 acts as an autocrine mediator with an inhibitory action on the emigration (diapedesis) process confirms the growing body of experimental data that showed that exogenously administered lipocortin 1 and lipocortin 1 mimetics (peptide Ac2-26) potently inhibit neutrophil extravasation in response to different stimuli. Externalization of lipocortin 1 on the plasma membrane of adherent neutrophils reduces their rate of passage through the endothelial gaps. Because cell-associated lipocortin 1 levels are under the partial control of corticosterone (endogenous circulating glucocorticoid hormone in rodents) and dexamethasone (a synthetic glucocorticoid hormone with a potent anti-inflammatory profile), a model is proposed in which a balance between anti-inflammatory (lipocortin 1, etc.) and pro-inflammatory (adhesion molecules, cytokines and chemokines) mediators explains the difference in the rate of leukocyte accumulation during the different stages of the host inflammatory response. 4. In conclusion, this review emphasizes the importance of in vivo experimental systems as a valid way of obtaining pertinent observations and reiterates the importance of negative regulatory mechanisms on the leukocyte extravasation process operating within the host.

Animals↗

PubMed2002

Provisional mapping of quantitative trait loci modulating the acoustic startle response and prepulse inhibition of acoustic startle.

Prepulse inhibition (PPI) of the acoustic startle response (ASR) is a form of sensorimotor gating, defined as an inhibition of the startle response when a low intensity stimulus, the prepulse, precedes the startling stimulus. Deficits in PPI have been reported in schizophrenia and other psychiatric/neurological disorders, and correlate with symptom severity in schizophrenia, suggesting that deficient PPI per se or abnormalities in neural circuits regulating PPI may cause some symptoms of schizophrenia. If so, then genes conferring reduced PPI may contribute toward genetic vulnerability to schizophrenia. Studies with selectively bred rodent strains indicate that PPI is under genetic control; however, the identity of the relevant genes is unknown. The current study used recombinant congenic mouse strains derived from C57BL/6J and A/J parents to assess genetic variability in PPI and in ASR and to identify provisional quantitative trait loci (QTLs) modulating these phenotypes. Significant between-strain differences in ASR and in PPI at each of several prepulse intensities (75, 80, 85, 90, 95 dB) were found. Correlations between PPI at the various prepulse intensities were highly significant, suggesting appreciable overlap in genetic regulation of PPI across prepulse intensities. Five QTLs (chromosomes 3, 5, 7, 16) associated with PPI across all prepulse intensities, but not with ASR, were identified. Two additional QTLs (chromosomes 2, 11) associated with both PPI and ASR were found. Fifteen QTLs were associated with ASR alone. Data on genotypes of informative congenic strains were used to support probable involvement of loci modulating PPI and to narrow the probable chromosomal location of QTLs. If confirmed, these QTLs may suggest candidate genes directing novel mechanisms for regulation of PPI

Acoustic Stimulation↗

PubMed1985

Cortical cholinergic impairment and behavioral deficits produced by kainic acid lesions of rat magnocellular basal forebrain.

The magnocellular basal forebrain (MNBF) provides extensive cholinergic innervation to frontoparietal cortex. In the rat, the MNBF is homologous to the human nucleus basalis of Meynert, a structure implicated in the cholinergic hypothesis of cognitive impairment in Alzheimer's disease (AD). Kainic acid (KA) was used to make lesions in the MNBF of rats which were compared with unoperated controls, sham-operated controls, and control rats injected with KA in the cortical area directly above the MNBF. The MNBF lesions depleted choline acetyltransferase in cortex but not in striatum or hippocampus. Cortical dopamine levels were unchanged; serotonin levels were unchanged in hippocampus and parietal cortex but decreased in frontal cortex. The metabolite levels of these neurotransmitters were unchanged in all brain regions examined. Compared with controls, rats with MNBF lesions were impaired in 24-hr retention, but not acquisition, of a passive avoidance task with escapable footshock. There were no differences between groups in mean number of daily avoidances on a bar-press active avoidance task, although the data suggested a slower rate of learning in MNBF rats. In a serial spatial discrimination reversal test with a snout-poke response, the MNBF rats performed significantly worse than controls, although all groups learned the task. This rodent model is useful for studying the role of the cholinergic system in memory and possibly for developing treatment strategies to alleviate the cognitive dysfunction of AD.

Animals↗

PubMed1993

Cope's rule, the island rule and the scaling of mammalian population density.

Cope's rule--the generalization that animal taxa tend to evolve toward larger body size--suggests that there are widespread net selective advantages to being large. Size-abundance relationships within bird and desert rodent guilds show that larger species usually do control more energy locally, and thus maintain larger populations than expected for their body size, implying that larger individuals are relatively better at obtaining and using local resources. But we report here results that show that this is not generally the case among mammal species. Within dietary groups containing only small species, larger species usually do better, but within those that contain the largest mammals, small species tend to control more energy. This suggests that in mammals there is an optimum body size for energy acquisition at about 1 kg. Thus, net adaptive advantages of large individuals for resource control cannot be used as a general explanation for evolutionary size increase in mammals, although other proposed explanations for Cope's rule are unaffected. Instead, these results suggest a partial explanation for another widespread ecotypic pattern, the 'island rule': that on islands, small mammal species evolve to larger size and large species to smaller size. If on an island a species' usual competitors and predators are absent, it should often tend to evolve toward the optimum body size, and the adaptive advantages of doing so would be greatest for populations starting at body-size extremes.

Animals↗

PubMed2004

Identification of a novel PDX-1 binding site in the human insulin gene enhancer.

Islet beta cell type-specific transcription of the insulin gene is regulated by a number of cis-acting elements found within the proximal 5'-flanking region. The control sequences conserved between mammalian insulin genes are acted upon by transcription factors, like PDX-1 and BETA-2, that are also involved in islet beta cell function and formation. In the current study, we investigated the contribution to human insulin expression of the GG2 motif found between nucleotides -145 and -140 relative to the transcription start site. Site-specific mutants were generated within GG2 that displayed a parallel increase (i.e. -144 base pair) or decrease (i.e. -141 base pair) in insulin enhancer-driven reporter and gel shift binding activity in beta cells consistent with human GG2 being under positive regulatory control. In contrast, the corresponding site in the rodent insulin gene, which only differs from the human at nucleotides -144 and -141, is negatively regulated by the Nkx2.2 transcription factor (Cissell, M. A., Zhao, L., Sussel, L., Henderson, E., and Stein, R. (2003) J. Biol. Chem. 278, 751-756). Human GG2 activator binding activity was present in nuclear extracts prepared from human islets and enriched in those from rodent beta cell lines. The human GG2 activator binding factor(s) was shown to be approximately 38-40 kDa and distinct from other size-matched islet-enriched transcription factors, including Nkx2.2, Pax-4, Cdx2/3, and Isl-1. Combined DNA chromatographic purification and mass spectrometry analysis revealed that the GG2 activator was PDX-1. These results demonstrate that the GG2 element, despite its divergence from the core homeodomain consensus binding motif, is a site for PDX-1 activation in the human insulin gene.

Amino Acid Motifs↗

PubMedDate not supplied

A tobacco smoke inhalation exposure device for rodents.

A system which utilizes a piston pump to generate cigarette smoke under standard conditions, and expose rodents to the inhalation of diluted smoke for controlled periods of time is described. Variations of the basic system have been employed to exposure groups of ten to twenty hamsters or rats, and should allow exposures of up to forty mice. The system has been in use for approximately 24 months in routine chronic exposures of rats. Data are presented to define the operating characteristics and typical dosimetry. Animal containment peculiar to this apparatus is described.

Animals↗

PubMedDate not supplied

The north american control animal database: a resource based on standardized nomenclature and diagnostic criteria.

Historical control data have been shown to be valuable in the interpretation and evaluation of results from rodent carcinogenicity studies. Standardization of terminology and histopathology procedures is a prerequisite for meaningful comparison of control data across studies and analysis of potential carcinogenic effects. Standardization is particularly critical for the construction of a database that includes incidence data from different studies evaluated by pathologists in different laboratories. Standardized nomenclature and diagnostic criteria have been established for neoplasms and proliferative lesions. Efforts of the National Toxicology Program, the Society of Toxicologic Pathology (STP), and the Registry of Industrial Toxicology Animal-data (RITA) have led to a harmonized pathology nomenclature for the rat and the mouse. This nomenclature with detailed descriptions of lesions is available in publications by the STP and International Agency for Research on Cancer (IARC). A listing of these terms is available on the World Wide Web. Utilizing the model established by RITA and working with the International Life Sciences Institute (ILSI), companies with laboratories in North America formed a working group in 1994 to establish and maintain a database of neoplastic and proliferative lesions from control animals in carcinogenicity studies. The rationale for development of the North American Control Animal Database (NACAD), the factors that influence tumor incidence, operation of the database, and the benefits to be realized by using a standardized approach are discussed.

Animals↗

PubMedDate not supplied

Angiostrongylus (Parastrongylus) eosinophilic meningitis.

Angiostrongylus (Parastrongylus) cantonensis is the commonest cause of eosinophilic meningitis in the world. Infective third-stage larvae develop in slugs and snails. Humans are infected primarily in the central nervous system after ingesting an infected intermediate host. Damage by motile worms, inflammatory responses to foreign bodies, and possible toxicity of worm substances work in concert to produce the pathologic and clinical picture of neurologic angiostrongyliasis. This disease manifests itself by headache, paresthesias, generalized weakness, and occasionally visual disturbances and extraocular muscular paralysis. Eosinophilic pleocytosis is the major laboratory finding. Although the diagnosis of neurologic angiostrongyliasis is usually made clinically, serologic methods such as ELISA (enzyme-linked immunosorbent assay) can be helpful. Occasionally, living larvae can be identified histologically in the CSF, eye, or other tissue. There is no specific treatment for this disease. Corticosteroids may be useful to relieve increased intracranial pressure. The role of anthelmintic drugs, such as thiabendazole and ivermectin, is not yet known. The prognosis of neurologic angiostrongyliasis is usually good; however, fatal and chronic cases do occur. Appropriate preparation of food, control of mollusks and planarians, and elimination of rodents are important measures in limiting the further spread of eosinophilic meningitis caused by A. cantonensis.

Adolescent↗

PubMed2001

Glutamine in animal science and production.

With its many proposed metabolic roles, glutamine would seem to have major potential in normal animal production systems as well as during situations involving adverse challenges. In practice, however, responses to glutamine supplementation have been inconsistent. Thus, during lactation and growth studies in ruminants, both positive and null effects on production responses have been reported. Similarly, therapeutic responses to glutamine supplementation during various digestive tract disorders have been inconsistent in both pigs and ruminants. This is despite a proven involvement in the nucleic acid biosynthesis necessary to support cell proliferation. In sheep, at least, glutamine may exert a protective effect against hepatic amino acid (AA) oxidation, particularly for methionine. This may offer anabolic potential because methionine is the first limiting AA in a number of animal feedstuffs. Glutamine is also important in control of metabolic acidosis, but, in contrast to rodents, the main site of production seems to be extra-hepatic. In the immune system, while lymphocyte proliferation is glutamine-dependent, intracellular concentrations are low (in contrast to other tissues, such as muscle and liver). Instead, glutamate is accumulated, but the majority of this (approximately 65%) is derived in vivo from plasma glutamine. In sheep, endotoxin challenge elevates the plasma flux of glutamine, with a corresponding decrease in plasma concentration. At the same time, both the glutamate accumulation and fractional rate of protein synthesis within lymphocytes are enhanced. These lymphocyte responses, however, are not altered by an AA supplement that contains glutamine. Overall, although glutamine obviously plays important metabolic roles within the body, supplementation does not appear to provide consistent beneficial or therapeutic effects, except during certain catabolic situations. Glutamine availability, therefore, does not seem to be a limitation in many challenge situations. Rather, glutamine may signal alterations in nutrient demands among organs and a better understanding of this role may increase understanding of where modulation of glutamine status would be beneficial.

Acid-Base Equilibrium↗

PubMed2001

DNA sequence variation in the mitochondrial control region of red-backed voles (Clethrionomys).

The complete mitochondrial DNA (mtDNA) control region was sequenced for 71 individuals from five species of the rodent genus Clethrionomys both to understand patterns of variation and to explore the existence of previously described domains and other elements. Among species, the control region ranged from 942 to 971 bp in length. Our data were compatible with the proposal of three domains (extended terminal associated sequences [ETAS], central, conserved sequence blocks [CSB]) within the control region. The most conserved region in the control region was the central domain (12% of nucleotide positions variable), whereas in the ETAS and CSB domains, 22% and 40% of nucleotide positions were variable, respectively. Tandem repeats were encountered only in the ETAS domain of Clethrionomys rufocanus. This tandem repeat found in C. rufocanus was 24 bp in length and was located at the 5' end of the control region. Only two of the proposed CSB and ETAS elements appeared to be supported by our data; however, a "CSB1-like" element was also documented in the ETAS domain.

Animals↗

PubMed2002

Differential regulation of the expression of matrix metalloproteinases and tissue inhibitors of metalloproteinases by cytokines and growth factors in bovine endometrial stromal cells and trophoblast cell line BT-1 in vitro.

Degradation and reconstitution of extracellular matrix in uterine endometrium is a crucial event for embryonic implantation and is regulated by matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs). In the present study, we investigated the regulation of MMP and TIMP expression in cultured bovine endometrial stromal cells (BESCs) and a bovine trophoblast cell line BT-1 (BT-1 cells). The production of proMMP-9 was induced by transforming growth factor beta (TGFbeta) and 12-O-tetradecanoylphorbol 13-acetate in the stromal cells. The treatment of BESCs with TGFbeta, insulin-like growth factor-I, and hepatocyte growth factor (HGF) resulted in a significant increase in the level of TIMP-1 in the culture medium. In addition, a significant increase of TIMP-2 production was observed in interleukin (IL)-1alpha and HGF-treated BESCs. However, the expression of TIMP-1 and TIMP-2 mRNA was not augmented by these factors. The treatment of BESCs with 12-O-tetradecanoylphorbol 13-acetate resulted in a significant increase in the level of TIMP-1 but a significant decrease in the level of TIMP-2 in the stromal cells. Membrane type-1 MMP mRNA expression in the stromal cells was augmented by tumor necrosis factor alpha (TNFalpha), IL-6, HGF, and 12-O-tetradecanoylphorbol 13-acetate. On the other hand, BT-1 cells constitutively produced proMMP-9 and proMMP-2, and the treatment of BT-1 cells with TNFalpha, HGF, and 12-O-tetradecanoylphorbol 13-acetate resulted in a significant increase in the level of proMMP-9 but not in the level of proMMP-2. The production of TIMP-1 in BT-1 cells was also augmented by IL-1alpha, TNFalpha, and HGF at the level of translation and was transcriptionally increased by 12-O-tetradecanoylphorbol 13-acetate. However, the level of TIMP-2 mRNA in BT-1 cells was not affected by any of the treatments. These results suggest that the expression of MMPs and TIMPs is differentially regulated by cytokines and growth factors and that the production of TIMP-1 and TIMP-2 may not be accompanied by changes in their mRNA expression in bovine endometrium and trophoblasts. Furthermore, as in humans and rodents, MMPs and TIMPs may contribute to the control of degradation and reconstitution of extracellular matrix in bovine endometrium during embryonic implantation and early placentation.

Animals↗

PubMed1977

Positive feedback of oestrogen on LH secretion in women in neuroleptic drugs.

The effect of a-adrenergic and dopaminergic blockade on the ability of pituitary-hypothalamic axis to produce an LH surge in response to oestrogen, was studied in eleven women treated with the neuroleptic agents haloperidol, fluphenazine or chlorpromazine. Seven women on no medication were controls. 6.6 mg of oestradiol benzoate (OB) was injected i.m. after control serum was obtained and daily serum samples were obtained for four additional days. Sera were assayed for total oestrogens, LH, FSH and prolactin. Six of seven women in the control group and eight of eleven women treated with neuroleptic agents had LH surges to OB challenge. The mean prolactin of the treated women was 33.1 +/- 3.6(SEM) ng/ml and the mean prolactin of the controls was 14.9 +/- 1.5(SEM) ng/ml, P less than 0.005). Elevated levels of circulating prolactin did not prevent an LH surge to OB challenge. These results indicate that even in subjects with catecholamine blockade, an LH surge can be induced. This contrasts to results obtained in rats and suggests that the control mechanism of LH surge production differs in rodents and humans.

Adolescent↗