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To determine whether behavioral sensitization produced by prolonged D-amphetamine administration affects susceptibility of nigrostriatal dopaminergic neurons to the neurotoxic actions of 6-hydroxydopamine (6-OHDA), rats were treated daily from the 23 rd day after birth for 11 consecutive days with D-amphetamine (1.0 mg/kg s.c.) or saline. On the last day of treatment, one group primed with D-amphetamine and one control group of rats were tested to confirm behavioral sensitization development. The remaining animals were additionally treated on the 34 th day (one day after the last D-amphetamine injection) with 6-OHDA HBr (300 µg in 10 µl i.c.v., salt form, half in each lateral ventricle) or its vehicle. Four weeks later the levels of dopamine (DA) and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), 3-metoxytyramine (3-MT), as well as 5-hydroxytrypatmine (5-HT) and its metabolite 5-hydroxyindoleacteic acid (5-HIAA) were assayed in the striatum, by HPLC/ED. In rats with behavioral sensitization, 6-OHDA reduced endogenous dopamine and its metabolites content to a comparable degree in comparison to controls. This finding indicates that presumed up-regulation of the dopamine transporter in the behaviorially sensitized rats did not increase the neurotoxicity of a high dose of 6-OHDA.
The influence of aminergic pathways on basal and stimulated vasopressin (AVP) release was studied in conscious rats, the stimulus for hormone release being an intracerebroventricular (ICV) injection of 5 µl 0.85M sodium chloride. The animals were treated with either phenoxybenzamine, propranolol or haloperidol prior to administration of the central hypertonic stimulus. Phenoxybenzamine elevated basal plasma vasopressin concentrations, while propranolol and haloperidol had no effect. The secretion of АVР in response to the hypertonic stimulus was potentiated by phenoxybenzamine and haloperidol, but the effect of propranolol was equivocal. The antagonists had no effect on basal arterial pressure at the time of hypertonic saline administration or the pressor response to ICV sodium chloride.
Previous neuroimaging studies have shown that executive processes requiring planning and set-shifting [e.g. Montreal card sorting task (MCST)] may engage the dorsolateral prefrontal cortex (DLPFC) while inducing dopamine (DA) release in the striatum. However, functional imaging studies can only provide neuronal correlates of cognitive performance and cannot establish a causal relation between observed brain activity and task performance. In order to investigate the contribution of the DLPFC during set-shifting and its effect on the striatal DAergic system, we applied continuous theta burst stimulation (cTBS) to left and right DLPFC. Our aim was to transiently disrupt its function and to measure MCST performance and striatal DA release during [11C]raclopride PET. cTBS of the left DLPFC impaired MCST performance and DA release in the ipsilateral caudate–anterior putamen and contralateral caudate, as compared to cTBS of the vertex (control). These effects were limited only to left DLPFC stimulation but not right DLPFC. This is the fi rst study showing that cTBS, by disrupting left DLPFC function, may indirectly affect striatal DA release during performance of executive tasks. This cTBS-induced regional prefrontal effect and modulation of the frontostriatal network may be important for understanding the contribution of hemisphere laterality and its neural bases with regard to executive functions, as well as for revealing the neurochemical substrate underlying cognitive defi cits.
Mesenchymal stem cells (MSCs) constitute an interesting cellular source to promote brain regeneration after Parkinson’s disease. MSCs have significant advantages over other stem cell types, and greater potential for immediate clinical application. The aim of this study was to investigate whether MSCs from the human placenta could be induced to differentiate into dopaminergic cells. MSCs from the human placenta were isolated by digestion and density gradient fractionation, and their cell surface glycoproteins were analyzed by flow cytometry. These MSCs were cultured under conditions promoting differetiation into adipocytes and osteoblasts. Using a cocktail that includes basic fibroblast growth factor (bFGF), all trans retinoic acid (RA), ascorbic acid (AA) and 3-isobutyl-1-methylxanthine (IBMX), the MSCs were induced in vitro to become dopamine (DA) neurons. Then, the expression of the mRNA for the Nestin and tyrosine hydroxylase (TH) genes was assayed via RT-PCR. The expression of the Nestin, dopamine transporter (DAT), neuronal nuclear protein (NeuN) and TH proteins was determined via immunofluorescence. The synthesized and secreted DA was determined via ELISA. We found that MSCs from the human placenta exhibited a fibroblastoid morphology. Flow cytometric analyses showed that the MSCs were positive for CD44 and CD29, and negative for CD34, CD45, CD106 and HLA-DR. Moreover, they could be induced into adipocytes and osteocytes. When the MSCs were induced with bFGF, RA, AA and IBMX, they showed a change in morphology to that of neuronal-like cells. The induced cells expressed Nestin and TH mRNA, and the Nestin, DAT, NeuN and TH proteins, and synthesized and secreted DA. Our results suggest that MSCs from the human placenta have the ability to differentiate into dopaminergic cells.
The aim of the experiment was to identify the possibilities of stimulating pikeperch spawning with human chorionic gonadotropin (hCG) and Ovopel, a mammalian GnRH analogue (D-Ala⁶ Pro⁹ NEt-mGnRH) with a dopamine inhibitor (metoclopramide). Pikeperch spawners were caught with trap gear (fyke-nets) during the pre-spawning season from the Tałty and Tałtowisko lakes (Masurian Lakeland, northern Poland). After transport that lasted an hour, the fish were placed in tanks in a recirculating system and then segregated by sex. The females were divided into five experimental groups, each containing six specimens. The fish were injected twice at 24 hour intervals with hCG (group I - 200 and 200IU kg⁻¹ body weight (BW); group II - 200 and 500IU kg⁻¹ BW), Ovopel (group III - 0.25 and 0.50 pellets kg⁻¹ BW; group IV - 0.25 and 1.0 pellets kg⁻¹ BW) or 0.7% NaCl solution (group V, control - 0.2 and 0.5 cm³ kg⁻¹ BW). The effects of the hormonal stimulation expressed as the percentage of ovulating females, the degree of spawning synchronicity, and survival of the embryos to the eyed-egg stage were highly differentiated. The highest percentages of spent fish were obtained in the group stimulated with hCG - 83.3% (group I) and 100% (group II) of the females ovulated. The development of the oocytes in this group was rapid and synchronous, which was reflected in the shortened and relatively similar latency period (47 - 57 hours following the first injection; mean ≈ 51 hours) in individual females. No impact was noted with regard to hCG dose (400 vs. 700 IU kg⁻¹ BW) on the latency time or on egg quality. Ovopel did not positively affect either oocyte maturation or pikeperch ovulation. None of the fish from group III ovulated, and in group IV, as in the control group, eggs were obtained only from three (50%) females. In contrast to group V, the eggs of females stimulated with Ovopel were of low biological quality and survival to the eyed-egg stage ranged from 0 to 8%. Higher mortality among the females was also noted, especially in group III. The experiment indicated that hormonal stimulation with hCG is effective, while that with Ovopel was surprisingly ineffective.
We investigated the effect of injections of four biogenic amines (serotonin, dopamine, octopamine and tyramine) on behavior patterns displayed by workers of the red wood ant Formica polyctena during dyadic confrontations with four types of opponents: a nestmate, an alien conspecific, an allospecific ant (Formica fusca), and a potential prey, a nymph of the house cricket (Acheta domesticus). Significant effects of biogenic amine administration were observed almost exclusively in the case of confrontations with allospecific opponents. Serotonin treatment exerted stimulatory effects on behavior patterns involving physical aggression (biting accompanied by gaster flexing, dragging and formic acid spraying), but these effects were relatively weak and/or documented by indirect evidence. Dopamine administration exerted a stimulatory effect on open-mandible threats directed by F. polyctena to F. fusca and to cricket nymphs, and on biting behavior directed to cricket nymphs. Surprisingly, octopamine treatment did not exert significant effects on aggressive behavior of the tested ants. Tyramine administration exerted a suppressing effect on threatening behavior directed to F. fusca, but led to shortening of the latencies to the first open-mandible threat during the tests with cricket nymphs. Biogenic amine administration also influenced non-aggressive behavior of the tested ants. Our findings confirmed the role of serotonin and dopamine in the mediation of ant aggressive behavior and documented for the first time significant effects of tyramine treatment on ant aggressive behavior. We also demonstrated that not only specific patterns of ant aggressive behavior, but also behavioral effects of biogenic amine treatments are as a rule strongly context-dependent.
The present study indicates that activation of dopamine D1-like receptors by administration of SKF 38393 leads to dose-dependent (doses: 5, 10 and 20 mg/kg) increases in the expression of cFos proteins in the rat paraventricular nucleus of the hypothalamus (PVN). This effect was abolished by administration of SCH 23390, a dopamine D1-like receptor antagonist (0.5 and 1 mg/kg, given 30 min before SKF 38393 - 10 mg/kg), suggesting that the apparent effect is specific for activation of dopamine D1-like receptors. Expression of cFos after SKF 38393 (10 mg/kg) was observed in some, but not all, CRF-immunoreactive neurons, as well as in small portion of oxytocin- but not vasopressin-immunoreactive neurons (double-immunofluorescence experiments). There were also certain populations of nuclei that showed expression of cFos but did not co-localize with the above markers. We also found that both acute and repeated (once daily for 5 consecutive days) exposure to cocaine (25 mg/kg) attenuated the induction of cFos expression triggered by SKF 38393 when administered 24 hours after single or the last dose of cocaine (25 mg/kg). Attenuation was observed at the same level after single and chronic exposure to cocaine, indicating a rapid functional down-regulation of dopamine D1-like receptors that are resistant to subsequent doses of cocaine. These data provide evidence for the functional role of dopamine D1-like receptors in the PVN and indicate a functional adaptation of dopamine D1-like receptors following a single dose of cocaine without further progression of adaptation or resistance of D1-like receptor-mediated genomic function in the course of repeated cocaine intake.
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