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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of Cadmium (Cd) on embryo transport through the oviduct and on ovarian progesterone (P) secretion were studied in the rat. Animals were given 2.5, 5, 10 mg/kg CdCl2 or 1.0 mL/kg NaCl sc on day 1 of pregnancy. On days 1, 2, 3, 4, and 5, they were anesthetized with pentobarbital, cannulae were inserted in one of the utero-ovarian veins, and 5-minute blood samples were taken from the ovary. Ovarian venous outflow was recorded, P was determined from the blood fractions, and secretion rates were calculated. P levels were determined in peripheral blood. Body weights and the wet weight of adrenals, ovaries, and oviducts were checked; oviducts and uterine horns were flushed; and number, location, and developmental stage of embryos were observed. Cd content of the oviducts was measured. Cd accumulated dose and time dependently in oviducts and induced a dose-dependent depression and delay in the rise of ovarian P secretion during days 1 through 5 of pregnancy. In the peripheral blood, P levels also failed to rise until day 4 of pregnancy in Cd-treated rats. In embryo transfer, however, no alteration could be observed. It is hypothesized that lack of vascular contact in the oviduct makes it possible for the preimplantation embryos to escape toxic effects of Cd.
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PMID:Altered ovarian progesterone secretion induced by cadmium fails to interfere with embryo transport in the oviduct of the rat. 156 2

Cutaneous pectoris muscles of frogs were isolated, mounted in a chamber and superfused with Ringer's solution. With a macro-patch-clamp electrode placed on a section of a motor nerve terminal, quantal synaptic currents were elicited by depolarizing pulses and recorded. The electrode tip and the section of the terminal recorded from were perfused rapidly by Ringer's solution alone or containing 20-500 microM Cd2+ to block Ca2+ inflow. Separate superfusion of the muscle and the rest of the terminal with normal or elevated Ca2+ Ringer's solution provided a sufficiently high resting Ca2+ concentration in the terminal even when Ca2+ was blocked by Cd2+. The depolarization level of maximal Ca2+ inflow into the terminal was found by measuring maximal test pulse facilitation, Fc. In control solution as well as in the case of Cd2+ block, the rate of phasic release after depolarizing pulses rose further when depolarization was increased past the level of Fc, and reached a saturation level which was maintained at estimated depolarizations up to +200 mV. Block of Ca2+ inflow by Cd2+ decreased release substantially, but did not suppress it. The depression of release was greater in the range of large Ca2+ inflow (around Fc) than for very large depolarizations. The time course of phasic release was unaltered by blockage of Ca2+ inflow. It is concluded that Ca2+ inflow contributes to the promotion of evoked release only in the depolarization range in which Ca2+ inward current is large.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evoked phasic release in frog nerve terminals obtained after block of Ca2+ entry by Cd2+. 166 Jan 29

1. The effects of brief exposures to hypoxia on the membrane currents of isolated hippocampal CA1 neurons were studied with the use of the whole-cell variation of the patch-clamp technique. Neurons were acutely dissociated from immature (day 2-7) and mature (day 21-43) rats. 2. In the current-clamp mode, Na-cyanide (CN) hyperpolarized both mature and immature neurons. In the voltage-clamp mode, CN decreased the magnitude of the hyperpolarizing holding current in both age groups. 3. CN did not have a consistent effect on the voltage-dependent calcium and potassium currents of immature and mature CA1 neurons but decreased the voltage-dependent inward current of neurons at both ages. This effect was age dependent: the inward current of immature neurons decreased by only 10%, but that of mature neurons decreased by approximately 40%. 4. The decrease in the magnitude of the hyperpolarizing holding current and the depression of the voltage-dependent inward current of mature neurons were observed during brief exposure to N2 (PO2 = 0), indicating that the electroresponses observed with CN were the result of blocking oxidative respiration. 5. The hypoxia-sensitive inward current was blocked by tetrodotoxin (TTX) but was not blocked by cadmium or cesium + tetraethylammonium (TEA). Therefore this current was identified as the voltage-dependent, fast-inactivating sodium current (INa). 6. The isolated sodium current was studied with the use of cadmium to block calcium and TEA + cesium to block potassium currents. In mature neurons, CN left-shifted the steady-state inactivation curve for INa and slowed the deactivation kinetics of INa. CN caused little or no change in INa activation, fast inactivation, recovery from inactivation, or current-voltage (I-V) relationship. 7. We conclude that brief exposures to CN and hypoxia alter the intrinsic excitability of CA1 neurons by at least two mechanisms: 1) alterations in leakage currents and 2) alterations in the fast Na+ conductance that are maturationally dependent. We propose that the alterations in the Na+ conductance may play an adaptive role by reducing O2 demands and thus possibly delaying neuronal injury.
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PMID:Effect of metabolic inhibition on the excitability of isolated hippocampal CA1 neurons: developmental aspects. 166 12

Na+ and Ca2+ currents were monitored using a suction electrode in unclamped presynaptic axons of rat olfactory cortex pretreated with 0.1 mM 3,4-diaminopyridine and 5 mM tetraethylammonium. The effects of anaesthetics on these currents were compared with tetrodotoxin or cadmium. Ketamine (0.1-1 mM), ether (20-200 mM), diisopropylphenol (0.01-0.5 mM) and lignocaine (0.01-0.2 mmol/l) all depressed both the initial Na+ component and the Ca(2+)-mediated tail of the response. Urethane (5-100 mM), halothane (1-5 mM) and pentobarbitone (0.1-2 mM) showed slight selectivity for the axonal Ca2+ tail. Diisopropylphenol apparently enhanced the Ca2+ tail at low concentrations. The alphaxalone (1-50 microM) depression was very weak. In a few cases the depression may contribute to anaesthesia but with others, high concentrations may contribute to the toxicity of the substances in vivo.
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PMID:Action of general anaesthetics on unclamped Ca(2+)-mediated currents in unmyelinated axons of rat olfactory cortex. 166 92

In vivo assessment of toxicant action on Leydig cell function is subject to homeostatic mechanisms which make it difficult to determine whether any changes seen in serum testosterone (T) concentration are due to extragonadal endocrine alterations or to a direct effect on the Leydig cell. For example, metal cations administered in vivo have been shown to depress serum T concentration and alter serum concentrations of pituitary hormones in laboratory animals. The studies reported here use a testicular cell culture technique to evaluate Leydig cell testosterone biosynthesis in the presence of several metal cations. To determine the site of toxic action, the Leydig cells were stimulated to produce testosterone by using human chorionic gonadotrophin (hCG), dibutyl cyclic adenosine monophosphate (db-cAMP), or several substrates required for the biosynthesis of testosterone. hCG was chosen because resultant T production requires an intact membrane receptor and db-cAMP was used to test for post LH receptor defects caused by the metals. The other substrates were chosen to isolate the effect of metals on enzymatic pathways. Collagenase dispersed testicular cells (15% Leydig cells) were incubated with metal cations (1 to 5000 microM) for 3 hr in the absence and presence of maximally stimulating concentrations of hCG, db-cAMP, 20 alpha-hydroxycholesterol (HCHOL), or pregnenolone (PREG), and T concentration was determined by radioimmunoassay. In one separate experiment we also tested the effect of the substrates progesterone, 17 alpha-hydroxy-progesterone, and androstenedione on Cd2(+)-treated Leydig cells. The results show no change in Leydig cell viability with any metal cation treatment during the 3-hr incubation. Ca2+, Cr3+, Fe3+, Mg2+, Na+, or Pb2+ had no effect on stimulated testosterone. Dose-response depression in both hCG- and db-cAMP-stimulated T production were seen with Cd2+, Co2+, Cu2+, Hg2+, Ni2+, and Zn2+ treatment. Surprisingly, Cd2+, Co2+, Ni2+, and Zn2+, which caused a depression in hCG- and db-cAMP-stimulated T production, caused significant increases in HCHOL- and PREG-stimulated T production over untreated and similarly stimulated cultures. This indicates that these cations may act at multiple sites within the Leydig cell.
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PMID:Effect of cadmium and other metal cations on in vitro Leydig cell testosterone production. 185 Jan 71

The action of group IIb cations [Cadmium (Cd2+), Zinc (Zn2+), Mercury (Hg2+)] on the cardiac fast sodium current (INa) was investigated in calf Purkinje fibres and in ventricular cells isolated from guinea-pig hearts. In calf Purkinje fibres, INa was depressed by submillimolar concentrations of Zn2+ and Hg2+. With both cations, the current reduction occurred at all voltages in the range of current activation and the voltage dependence of peak current was unchanged. The degree of peak current inhibition depended on the cation concentration but not on voltage. The position of the inactivation curve on the voltage axis was unaltered at cation concentrations giving substantial current inhibition, and moved to the right only with concentration exceeding 1-1.5 mM. These effects can be interpreted as due to INa channel blockade. The action of Zn2+ and Hg2+ was similar to that described earlier of Cd2+ on Purkinje fibres (DiFrancesco et al. 1985b). INa was also inhibited by group IIb cations in isolated guinea-pig ventricular cells. Depression of INa by Cd2+, Zn2+ and Hg2+ was essentially voltage-independent, in agreement with its being caused by channel block. The dependence of INa block by Cd2+ upon external Na concentration [Na+0] was investigated in ventricular myocytes. The fraction of INa block by 0.1 mM CdCl2 was 0.50 at 140 mM, 0.81 at 70 mM and 0.83 at 35 mM [Na+]0. A similar increase of block efficiency at low [Na+0] was observed with 0.05 mM CdCl2. In both the Purkinje fibre and the ventricular cell, the order of potency of INa block by group IIb cations was Hg2+ greater than Zn2+ greater than Cd2+. Manganese (Mn2+, 2-5 mM), an ion of group VIIa, also depressed the INa in Purkinje fibres and ventricular myocytes. This effect was however due mainly to a positive shift on the voltage dependence of current kinetics rather than to a reduction of the conductance of the channel (GNa), and can be accounted for by an ion-screening action of Mn2+ on the external membrane surface. The block by group IIb cations is a typical property of cardiac Na+ channels and characterizes the cardiac as opposed to other types of Na+ channel.
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PMID:Sodium current block caused by group IIb cations in calf Purkinje fibres and in guinea-pig ventricular myocytes. 196 24

The effects of dopamine (DA) on voltage-dependent Ca2+ currents were investigated in cultured rat lactotroph cells using the patch clamp recording technique. Each recorded cell was identified by the reverse hemolytic plaque assay. In the whole-cell configuration, two types of Ca2+ currents, L and T, were characterized on the basis of their kinetics, voltage sensitivity, and pharmacology. The L component had a threshold of -25 mV, showed little inactivation during a 150-msec voltage step, and was maximal at +10 mV. Cadmium ions (100 microM) significantly reduced its amplitude (75%). The T component was activated at a membrane potential close to -50 mV, was maximal at -10 mV, and showed a voltage-dependent inactivation between -90 and -30 mV. It was quickly inactivated during a maintained depolarization (time constant, 27 ms at -30 mV) and was strongly reduced (80%) by nickel ions (100 microM). Bath application of DA (10 nM) caused a markedly general depression of inward Ca2+ currents, acting differently on the T- and L-type currents. DA application shifted the voltage-dependence of the L-type current activation toward depolarization values (8 mV) without modifying its time- and voltage-dependent inactivation. In contrast, DA enhanced the inactivation of the T-type current by accelerating its time-dependent inactivation (25% decrease in the time constant of inactivation) and by shifting the voltage-dependence of the T-type current inactivation toward hyperpolarizing values (-63 mV in control vs. -77 mV in the presence of DA). These effects of DA were dose-dependent and involved the activation of a D2 receptor type. They were mimicked by bromocriptine application (10 nM), whereas sulpiride (100 nM) blocked the DA-evoked response. The D1 antagonist SCH 23390 was ineffective up to 100 microM. All of these DA-induced modifications in Ca2+ currents were abolished using a GTP-free pipette solution or after pretreatment of cells with pertussis toxin, suggesting that DA can regulate the function of Ca2+ channels through GTP-binding proteins (G-proteins). Our results show that DA acts simultaneously by reducing both voltage-dependent Ca2+ currents on lactotroph cells. Thus, DA reduces the entry of Ca2+ ions across the surface membrane and thereby influences electrical activity and the cytosolic free Ca2+ concentration involved in both basal and evoked PRL release.
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PMID:Dopamine inhibits two characterized voltage-dependent calcium currents in identified rat lactotroph cells. 216 20

The induction of hepatic metallothionein (MT) by the parenteral administration of iron was studied. Iron administered to chicks by intravenous or subcutaneous injection caused a 1.9-fold increase in hepatic MT. In marked contrast, intraperitoneal (ip) Fe resulted in a 10-fold increase, thus demonstrating the importance of the route of metal administration. This route-dependent effect was found to be dose-dependent, with ip injections between 1 and 10 mg Fe/kg resulting in a linear increase in MT and a concomitant reduction in serum zinc concentration and feed intake. High ip doses of Fe resulted in a persistent depression in serum Zn and elevated MT and MTmRNA. Equimolar ip injections of either Zn or Fe showed similar patterns of MTmRNA accumulation. In both cases MTmRNA levels were elevated by 3 h, with a peak at 6 h postinjection (Fe 8-fold, Zn 12-fold above 0 h). Plasma Zn was maximally reduced by Fe at 9 h (60%). The MT induction by Fe, as well as related depression in plasma Zn, was completely inhibited by actinomycin D. Zn depletion eliminated the accumulation of hepatic Zn and MT protein following ip injection of Fe or endotoxin, but not of cadmium, despite marked elevation of hepatic MTmRNA. Our results demonstrate Fe injected into the body cavity of chicks results in a rapid induction of hepatic MT that, like endotoxin induction, is independent of dietary Zn status.
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PMID:Iron-induced metallothionein in chick liver: a rapid, route-dependent effect independent of zinc status. 221 49

The effects of sodium N-benzyl-D-glucamine dithiocarbamate (BGD), sodium N-p-hydroxymethylbenzyl-D-glucamine dithiocarbamate (HBGD), and sodium N-p-carboxybenzyl-D-glucamine dithiocarbamate (CBGD), which were newly synthesized, on the distribution and excretion of cadmium were compared in mice exposed to cadmium. Mice were injected with 109CdCl2 (1 mg Cd/kg and 74 KBq of 109Cd/one animal) and 30 min or 24 h later, they were injected with the dithiocarbamates (400 mumols/kg). At 30 min after treatment with cadmium, these chelating agents significantly enhanced the biliary excretion of cadmium, and HBGD and CBGD significantly increased the urinary excretion of the metal. At 24 h after cadmium injection, BGD and HBGD significantly increased the biliary excretion of cadmium and HBGD was the most effective on the biliary excretion of the metal. These chelating agents were effective in mobilizing cadmium from the liver and kidney at 30 min after cadmium treatment. HBGD showed the largest effectiveness on the depression of cadmium contents in the liver and kidney. At 24 h after cadmium treatment, only HBGD among these chelating agents significantly reduced the cadmium contents in the liver and kidney. These results show that the injection of HBGD at both 30 min and 24 h after cadmium treatment can much more effectively mobilize cadmium from the body mainly through the bile without redistribution of cadmium to other tissues, such as brain, testes, and heart, than injection of BGD and CBGD.
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PMID:Comparative effects of three dithiocarbamates on tissue distribution and excretion of cadmium in mice. 221 70

Growing male rats were exposed to cadmium (Cd, 100 micrograms/kg, ip) for 51 days and the effect on the different components of locomotor behaviour was assessed on days 38, 46 and 51 of Cd exposure. Significant decrease in distance travelled, stereotypic time and movements, ambulatory time and vertical movements were observed in Cd-exposed rats, whereas the time of rest was increased. The number of entries into the inner as well as the outer squares and the total time spent in the inner squares of the floor area were significantly reduced. Results indicate that Cd exposure results in a general depression in all aspects of motor behaviour leading to decrease in gross locomotor activity. The involvement of an exaggerated emotional reactivity in the behavioural expression of the Cd-treated animals is also emphasized.
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PMID:Effect of chronic cadmium exposure on locomotor behaviour of rats. 227 52


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