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Journal Article 2006; 27(1-2): 21-33 PubMed PMID: 16648819 Citation  Keywords:  Diet, Eating:psychology, Food, Humans, Motivation, Receptors, Opioid, mu:physiology, Reward, Satiety Response:physiology,.   

: Over the last decades, the importance of food in the development of chronic diseases has been examined, as well as the medical value of eating healthy. The contribution of the eating process itself to health and well-being, however, has not been questioned until most recently. Biology has linked eating to appetitive motivational processes with their underlying neurophysiology, including CNS reward circuitries: Eating uses the pleasure-reward physiology to motivate us to eat. Endogenous opiates, such as morphine, insure our survival by helping us to make eating motivational via pleasure induction. After taking in enough food, we become satisfied, i.e., tolerant to food. Our appetite, and so is our appetence, are then low and need a certain time span to reach their former levels for then inducing food-seeking behaviors, food intake, etc. again. When tolerance passes, we once more engage in this pleasurable process related to positive behavioral motivation. Opioid receptor agonists, however, may induce energy intake even beyond an actual need. This interesting potential of opioidergic signaling may have its roots in biological mechanisms that insured the intake and storage of high energy foods, hence preparing for future famines. In our world of today, however, such neurobiological pathways may pose a threat on our health. Thus, feedback mechanisms, such as tolerance, aversion and satiety, have to be finely tuned. Therefore central autoregulation that involves, for example, limbic mu receptor signaling and other endogenous signaling compounds comes into the focus of modern science. The time where research recognizes the importance of neurobiological pathways such as endogenous opiate autoregulation or CNS reward circuitries for examining the physiology of food intake has yet begun. Many questions remain open and have to be answered through future scientific inquiry....

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Journal Article 2006; 27(1-2): 236-240 PubMed PMID: 16648784 Citation  Keywords:  Adolescent, Alleles, Attention Deficit Disorder with Hyperactivity:epidemiology, Child, Czech Republic:epidemiology, DNA:genetics, Gene Frequency, Humans, Male, Polymorphism, Genetic, Psychiatric Status Rating Scales, Receptors, Dopamine D2:genetics, Reve.   

OBJECTIVES: Attention deficit hyperactivity disorder (ADHD) is a prevalent childhood disorder. Evidence from the family and twin studies suggest that ADHD is familiar and highly heritable. Association studies are frequently used for the searching of markers responsible for genetic basis of ADHD. We investigated TaqI polymorphism of the dopamine receptor D2 (DRD2) in relationship with ADHD. The association between TaqI A polymorphism of DRD2 gene and ADHD has previously been published.

DESIGN: We used the association study to test the relationship between TaqI A polymorphism of DRD2 gene and ADHD on groups of ADHD boys and control boys.

SETTING: For DNA isolation, buccal tissue was used. PCR with restriction analysis of PCR products was used for genotyping.

RESULTS: We found statistically different genotypic and allelic frequencies (p < 0.008, p < 0.002, respectively) of DRD2 polymorphism between two studied groups of boys.

MAIN FINDINGS: According to our results we suppose that polymorphism TaqI A of DRD2 gene is involved in the pathogenesis of childhood ADHD in male subjects. Allele A1 and genotype A1A1 in male subjects is associated with ADHD.

CONCLUSIONS: Our study confirmed the relationship between TaqI A polymorphism of DRD2 gene and ADHD published previously....

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Journal Article 2005; 26(5): 541-547 PubMed PMID: 16264403 Citation  Keywords:  Aging:metabolism, Animals, Brain Chemistry:physiology, Digoxigenin, In Situ Hybridization, Liver:metabolism, Male, Mice, Mice, Inbred C57BL, RNA Probes, RNA, Complementary:biosynthesis, RNA, Messenger:analysis, Receptors, Cytoplasmic and Nuclear:biosynthe.   

OBJECTIVES: The distribution of Liver receptor homolog 1 (LRH-1) mRNA was studied in mice brain with the aim to establish whether this nuclear hormone receptor is expressed also in the brain in addition to liver and classical steroidogenic tissues.

METHODS: Expression of LRH-1 mRNA in juvenile (30 days old) and adult (60 days old) mouse brain was examined using non-radioactive in situ hybridization with digoxigenin labeled cRNA probes and with RT PCR using specific primers.

RESULTS: LRH-1 was strongly expressed throughout the brain. Semiquantitative RT PCR revealed very strong expression of LRH-1 mRNA in cerebrum in comparison to liver and testis, and in situ hybridization revealed that LRH-1 mRNA is uniformly expressed in most brain areas.

CONCLUSIONS: LRH-1 is strongly expressed throughout the mouse brain suggesting important roles for this transcription factor, although its precise roles in the CNS remain to be elucidated....

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Journal Article 2005; 26(4): 367-372 PubMed PMID: 16136007 Citation  Keywords:  Animals, Hypothalamo-Hypophyseal System:metabolism, In Vitro Techniques, Male, Neurokinin A:analogs & derivatives, Neurokinin-1 Receptor Antagonists, Neurotransmitter Agents:pharmacology, Peptide Fragments:pharmacology, Rats, Rats, Wistar, Receptors, Neur.   

OBJECTIVES: Present experiments were undertaken to study the influence of peptide NK-1 and NK-2 receptor agonists and antagonists as well as substance P and neurokinin A (the natural ligands for these tachykinin receptors) on vasopressin (AVP) secretion from the rat hypothalamo-neurohypophysial (HN) system in vitro.

RESULTS: The results showed that both substance P and highly selective tachykinin NK-1 receptor agonist, i.e., [Sar9,Met(O2)11]-Substance P, enhanced significantly AVP secretion, while the NK-1 receptor antagonist (Tyr6,D-Phe7,D-His9)-Substance P (6-11)--sendide--was found to antagonize the substance P-induced hormone release from isolated rat HN system (all peptides at the concentration of 10(-7) M/L). The NK-2 receptor selective agonist (beta-Ala8)-Neurokinin A (4-10) was essentially inactive in modifying AVP release from the rat HN system in vitro, while neurokinin A (the natural ligand for this tachykinin receptor) was found to stimulate the AVP release; this effect of neurokinin A has been diminished by the NK-2 receptor antagonist (Tyr5,D-Trp(6,8,9),Lys-NH2(10))-Neurokinin A (4-10).

CONCLUSION: The present data indicate a role for tachykinin NK-1 (and possibly for NK-2) receptors in tachykinin-mediated stimulation of AVP secretion from the rat HN system in vitro....

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Comparative Study 2005; 26(2): 125-130 PubMed PMID: 15855883 Citation  Keywords:  Action Potentials:physiology, Animals, DNA-Binding Proteins:metabolism, Electrophysiology, Hypothalamus:cytology, In Vitro Techniques, Male, Milk Proteins:metabolism, Neurons:metabolism, Prolactin:physiology, Rats, Rats, Wistar, Receptors, Prolactin:metab.   

OBJECTIVES: The study investigated the role of prolactin (PRL) in modulating STAT5 and electrical activity of magnocellular neurones in the supraoptic (SO) nucleus of male rats.

METHODS: Evidence of expression of STAT5 in the SO nucleus was investigated by immunocytochemical methods. Effect of blocking prolactin receptors on STAT 5 expression was investigated by Western blotting following transfection of SO neurones with a dominant negative mutant form of the PRL receptor. Prolactin-induced changes in electrical activity were investigated by extracellular recording in hypothalamic slices.

RESULTS: A high proportion of SO neurones in male rats expressed immunoreactive STAT5. Levels of activated STAT5 within the SO nucleus of PRL-treated rats was reduced following transfection with a dominant negative mutant form of the PRL receptor, as compared to rats transfected with wild type PRL receptor. Electrophysiological recordings from the SO nucleus in horizontal brain slices showed that approximately 25% of neurones were responsive to PRL, with both inhibitory and excitatory effects being observed. Cells displaying PRL responses included pharmacologically-identified oxytocinergic neurones.

CONCLUSIONS: Collectively, the results suggest that central PRL targets neurones of the SO nucleus, influencing both activation of the JAK-STAT signalling pathway and neuronal excitability. Whilst the functional significance of this interaction remains to be established, it might be important in co-ordinating oxytocin secretion with physiological events associated with changes in plasma PRL, or in mediating a feedback loop in the oxytocinergic regulation of lactotrophs....

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Journal Article 2003; 24(3-4): 141-147 PubMed PMID: 14523347 Citation  Keywords:  Animals, Brain Chemistry:genetics, Estrogens:physiology, Female, Humans, Male, Neurodegenerative Diseases:physiopathology, Receptors, Estrogen:genetics,.   

: In trying to rectify the differences in the risk, onset, and progression of neurodegenerative diseases between men and women, the gonadal hormone estrogen has been the primary focus of investigation for many years. Although this gender difference may encompass disparate and overlapping reasons, estrogen and signaling events mediated by its receptor have been shown to be neuroprotective in a number of neurodegenerative disease models such as Alzheimer's, Parkinson's, and Schizophrenia. Although data from human studies remains highly controversial, a large body of research findings suggests that this hormone plays a pivotal role in retarding and preventing the formation of neurodegenerative diseases through its receptor. By activating common intracellular signaling pathways and initiating "cross talk" with neurotrophins, estrogen plays an influential role in neuronal survival from injuries induced by ischemia or other environmental insults. Gaining a better understanding of these estrogen receptor mediated neuroprotective mechanisms may lead to new therapeutic strategies for the treatment or prevention of neurodegenerative diseases....

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Journal Article 2003; 24(1-2): 68-72 PubMed PMID: 12743536 Citation  Keywords:  Animals, Bivalvia:metabolism, Cold Temperature:adverse effects, Down-Regulation, Ganglia, Invertebrate:metabolism, Nitric Oxide:biosynthesis, RNA:analysis, Receptors, Opioid, mu:biosynthesis, Reverse Transcriptase Polymerase Chain Reaction, Stress, Physio.   

OBJECTIVES: Subjecting the marine bivalve Mytilus edulis to an immediate temperature change has been shown to rapidly alter the animals' ganglionic monoamine levels, as well as its ciliary activity. Recently, we extended this observation to include the organism's ganglionic mu opiate receptor and morphine levels. In the past, we demonstrated that M. edulis ganglionic mu receptors exposed to morphine was coupled to the immediate release nitric oxide (NO). In this study, we measured morphine-induced NO release in M. edulis subjected to acute cold stress.

METHODS: NO release was monitored with an NO-selective microprobe. Temporal changes in mu opiate receptor expression were also examined over 24 hours.

RESULTS: In this study, we demonstrate that after 12h cold exposure (4 degrees C from 24 degrees C), the estimated relative mu opiate receptor (MOR) gene expression in M. edulis pedal ganglia, measured by real-time PCR, did not differ significantly from the control group (1.23+/-0.25, p>0.05). However, the measured M. edulis pedal ganglia MOR expression demonstrated that ganglia significantly (0.77+/-0.05, p<0.001) down regulated their mu opiate receptor mRNA expression after 24h exposure to the cold water. The mean value for control animal (24 degrees C, n=14) morphine-stimulated NO release was 36.7 +/- 9.8 nM. Morphine additions to cold-treated tissues (4 degrees C, n=7) produced an average of 6.7 +/- 4.9 nM NO, which was a statistically significant difference between 25 degrees C and 4 degrees C animals (p=0.025).

CONCLUSION: The study further demonstrates that mu opiate receptor expression is coupled to NO release....

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Journal Article 2003; 24(1-2): 46-49 PubMed PMID: 12743531 Citation  Keywords:  Animals, Baclofen:pharmacology, Catecholamines:metabolism, Dopamine:metabolism, Female, GABA Agonists:pharmacology, Hypothalamus:growth & development, Muscimol:pharmacology, Norepinephrine:metabolism, Rats, Rats, Wistar, Receptors, GABA-A:drug effects, Re.   

OBJECTIVES: The aim of the present investigation was to determine whether the catecholaminergic system is involved in gabaergic and serotoninergic effects on gonadotrophin secretion during sexual development. To this end, we studied the effect of GABAergic and serotoninergic systems on hypothalamic catecholamine content at different stages of sexual development.

METHODS: The effect of GABA A and GABA B agonists and 5-hydroxy-L-tryptophan on hypothalamic noradrenaline and dopamine content were determined in prepubertal (16 days old) and peripubertal (30 days old) rats.

RESULTS: At 16 days of age GABA agonists did not modify hypothalamic noradrenaline content, whereas a significant decrease in catecholamine concentration was observed in peripubertal rats at 30 days of age. Similar changes were observed with GABA agonists administration on dopamine hypothalamic levels, i.e no effects at 15 days of age and a significant decrease at 30 days. The administration of 5-hydroxy-l-tryptophan (5-HTP) induced a decrease of hypothalamic concentration of noradrenaline and dopamine at both ages.

CONCLUSION: Results indicate that the GABAergic system modifies the hypothalamic catecholamine content in peripubertal but not in prepubertal rats while serotonin has an inhibitory effect at both stages of sexual maturation. Even though both systems induce similar ontogenic modifications on the gonadotrophin axis (stimulatory effect in prepubertal and inhibitory action in peripubertal and adult rats) the present results appear to indicate that GABAergic and serotoninergic systems regulate gonadotrophin secretion by different hypothalamic mechanisms....

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