The role of monoamines in female puberty

The estradiol positive feedback mechanism appears to become mature between days 10 and 20 after birth. Rising serum prolactin levels between day 20 after birth and puberty are correlated with high hypothalamic norepinephrine turnover. High prolactin levels stimulate hypothalamic dopamine (DA) turnover, which may actively inhibit hypothalamic luteinizing hormone-releasing hormone (LHRH) release. Hypothalamic DNA receptor sensitivity is high in 10- to 20-day-old rats and gradually decreases between day 20 after birth and puberty. The reason for this desensitization may be the high hypothalamic DA turnover. This may result in a less strong inhibition of LHRH release allowing the positive feedback action of estradiol to elicit the first preovulatory luteinizing hormone (LH) surge initiating puberty.     

Platelet‐activating factor: role in long‐term potentiation and in brain damage

Brain platelet‐activating factor (PAF) is a lipid mediator involved in neurotransmission and in LTP. It has been reported that the induction of LTP by high frequency stimulation increases the activity of the enzymes responsible for its synthesis by a still unknown mechanism ( 1 ). One of the two biosynthetic pathways is Ca²⁺‐dependent and transforms a membrane ether phospholipid into PAF by a sequence of two reactions being the first one, catalyzed by a phospholipase A₂ (PLA₂), rate limiting. Overproduction of PAF, taking place in pathological conditions, contributes to brain damage. Various PLA₂s are present in brain tissue and, particularly, sPLA₂‐IIA is very likely involved in the production of PAF as its expression increases in pathological conditions. Recently, we have found the release of sPLA₂‐IIA from rat brain cortex mitochondria and its association with nuclear membranes, which might be an intracellular target for the enzyme.     

Role of 5-hydroxytryptamine in Moringa oleifera induced potentiation of pentobarbitone hypnosis in albino rats

The role of 5-hydroxytryptamine (5-HT) in pentobarbitone (PB) sleeping time, gross behaviour, electrical activity of the brain and serum 5-HT level was studied in Holtzman strain adult albino rats following treatment with M. oleifera (MO). MO (350mg/kg) caused inhibition of awareness, touch response, motor activity, righting reflex, and grip strength. It significantly increased the PB sleeping time, serum 5-HT level (P<0.001) and alpha-wave activity. These observations indicate that the aqueous extract of MO potentiated PB induced sleeping time and increased the alpha-wave activity through 5-HT.     

Brain monoamines and peptides: role in the control of eating behavior

Studies of brain monoamines and neuropeptides have provided extensive evidence in support of their role in the control of normal eating behavior. In this process, the medial and lateral portions of the hypothalamus, working in conjunction with forebrain and hindbrain sites and with peripheral autonomic-endocrine systems, have a critical responsibility in balancing signals for hunger and satiety. Via its rich and biologically active neurotransmitter substances, the hypothalamus monitors and integrates the complex sensory and metabolic input concerning the nutritional status of the organism and transduces this information into appropriate quantitative and qualitative adjustments in food intake. The specific neurotransmitters for which there is the most extensive evidence for a physiological function include the eating-stimulatory substances norepinephrine (alpha 2), opioid peptides, pancreatic polypeptides, growth hormone-releasing factor, and gamma-aminobutyric acid; the eating-inhibitory substances dopamine, epinephrine, serotonin, cholecystokinin, neurotensin, calcitonin, glucagon, and corticotropin-releasing factor; and possibly other gut-brain peptides. From biochemical, pharmacological, and anatomical studies, hypotheses have been generated to explain the role of these various monoamines and neuropeptides in controlling total energy intake, in determining the amount and pattern of macronutrient selection, and in maintaining normal energy and nutrient stores under fluctuating conditions within the external environment.     

Isolation of brain monoamines using high-performance reversed-phase chromatography

The content of monoamines, their precursors and metabolites was measured in brain specimens weighing several milligram by ion-pair high performance liquid chromatography on reversed phase microcolumns together with electrochemical detection. The properties of different sorbents are compared and the choice of a mobile phase is discussed. The technique of column packing and preparation of brain samples are described.     

Long-term effects of 5,7-dihydroxytryptamine on brain monoamines

5,7-dihydroxytryptamine (75 and 150 μg) was injected intraventricularly to adult male rats; animals were killed at various times after the injection and brains were examined for changes in the concentration of tryptophan, serotonin, 5-hydroxyindole acetic acid, norepinephrine and dopamine. Brain 5-hydroxyindoleamines were markedly depleted at all time periods examined, even after the administration of a tryptophan load (50 mg/kg). A small but significant decline in brain norepinephrine but not dopamine was also noted after the administration of the dihydroxytryptamine.     

Potentiation of pentobarbital hypnosis by Rosa damascena in mice

Rosa damascena has been found to act on central nervous system including brain. It inhibits the reactivity of the hypothalamous and pituitary systems in rat. In traditional medicine hypnotic effect of Rose is also suggested. In the present study hypnotic effect of ethanolic, aqueous and chloroformic extracts of R. damascena was investigated in mice. Hypnotic method was based on potentiation of pentobarbital induced sleeping time by extracts. Three doses of extracts (100, 500 and 1000 mg/kg) were injected i.p. in comparison with diazepam (3mg/kg) as positive control and saline as negative control. After 30 min of injection of extracts, pentobarbital (30mg/kg) was injected and increase in sleeping time by extracts was recorded. The results showed that the ethanolic and aqueous extracts in 500 and 1000 mg/kg doses significantly increased pentobarbital induced sleeping time which was comparable to diazepam. The chloroformic extract had no hypnotic effect.     

Effect of guanidinoethanesulfonic acid on brain monoamines in the mouse

Guanidinoethanesulfonic acid (GES) is known to induce convulsive seizures when administered intracisternally to rabbits and cats. The effects of GES on behavior, electroencephalographic recording and brain monoamine levels were examined in mice. When GES (900 nmol) was intraventricularly injected into mice, focal clonic movements of the face, vibrissae and ears together with twitching of the limbs were observed 0.5–1 min after the injection. Hypersensitivity was observed up to 7 min after the injection, after which the mice behaved normally. GES also induced sporadic spike discharges on electrocorticogram. The levels of 5-hydroxytryptamine (5-HT) of the GES-injected mice were lower than those of the saline-injected mice in the hippocampus, diencephalon, pons-medulla oblongata and cerebellum 5 min after the injection. No changes in the norepinephrine or dopamine levels were found after the GES injection. The level of 5-hydroxyindoleacetic acid increased in the striatum and cerebellum 5 min after the GES injection. These results suggest that GES-induced convulsive activities enhance the serotonergic neuroactivity in order to suppress the convulsions.     

Biogenic monoamines in ovum cells and preimplantation embryos of mice

Histofluorescence technique using glyoxylic acid revealed a specific fluorescence suggesting the presence of biogenic monoamines in early developmental stages of CBA x C57 Black mice. A yellow fluorescence observed in the blastomere surface from the stage of zygote up to that of four blastomere points to the presence of indole derivates. As development proceeds, the fluorescence increases and its colour becomes more and more green, which is characteristic of catecholamines. From the stage of eight blastomeres up to stage of blastocyst specific fluorescence is revealed in the cytoplasm. The inhibitors of monoamine oxidase, introduced into pregnant mice, markedly increased the specific fluorescence. An assumption is made of functional activity of biogenic monoamines in early mouse embryos.     

Long term potentiation is impaired in membrane glycoprotein CD200-deficient mice: a role for Toll-like receptor activation

The membrane glycoprotein CD200 is expressed on several cell types, including neurons, whereas expression of its receptor, CD200R, is restricted principally to cells of the myeloid lineage, including microglia. The interaction between CD200 and CD200R maintains microglia and macrophages in a quiescent state; therefore, CD200-deficient mice express an inflammatory phenotype exhibiting increased macrophage or microglial activation in models of arthritis, encephalitis, and uveoretinitis. Here, we report that lipopolysaccharide (LPS) and Pam(3)CysSerLys(4) exerted more profound effects on release of the proinflammatory cytokines, interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNFα), in glia prepared from CD200(-/-) mice compared with wild type mice. This effect is explained by the loss of CD200 on astrocytes, which modulates microglial activation. Expression of Toll-like receptors 4 and 2 (TLR4 and -2) was increased in glia prepared from CD200(-/-) mice, and the evidence indicates that microglial activation, assessed by the increased numbers of CD11b(+) cells that stained positively for both MHCII and CD40, was enhanced in CD200(-/-) mice compared with wild type mice. These neuroinflammatory changes were associated with impaired long term potentiation (LTP) in CA1 of hippocampal slices prepared from CD200(-/-) mice. One possible explanation for this is the increase in TNFα in hippocampal tissue prepared from CD200(-/-) mice because TNFα application inhibited LTP in CA1. Significantly, LPS and Pam(3)CysSerLys(4), at concentrations that did not affect LTP in wild type mice, inhibited LTP in slices prepared from CD200(-/-) mice, probably due to the accompanying increase in TLR2 and TLR4. Thus, the neuroinflammatory changes that result from CD200 deficiency have a negative impact on synaptic plasticity.