Effects of a new sulfonamide combination on experimental pyelonephritis.
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Animals↗
Biomedical subjects
L Eroğlu
Publications and source records attributed to L Eroğlu.
The long-term clonidine treatment induced behavioral depression in rats.
Effects of acute and long term clonidine treatment on motor and exploratory activities in rats were investigated in the presence and absence of imipramine. Rats received saline (control), clonidine HCl (0.8 mg/kg), imipramine HCl (30 mg/kg) and clonidine in combination with imipramine for 15 days. Clonidine caused hypoactivity and loss of interest and investment in the environment both acutely (on day 1) and chronically (on day 15). These effects of clonidine were reversed by acute and chronic imipramine pretreatments. Chronic clonidine treatment seemed more suitable in producing a model for depression in rats.
Animals↗
Antidepressant action of lithium in behavioral despair test.
The effects of long term (30 days) lithium treatment of various doses on behavioral despair test and on serotonin metabolism in the hypothalamus, midbrain and striatum of rats were examined. Lithium at doses of 0.5, 2 and 5 mEq/kg significantly decreased the duration of immobility. In other words, lithium behaved as an antidepressant drug. Serotonin turnover increased only in the hypothalamus in response to 0.5 and 2 mEq/kg doses of lithium.
Animals↗
Naloxone and lithium interaction on the levels of homovanillic acid in the rat brain.
The effects of long term (10 days) treatment of lithium and naloxone on HVA levels of striatum, hypothalamus and frontal cortex in rats were investigated. Lithium (400 mg/l in drinking water) itself had no effect on HVA levels of any region. Naloxone (2 mg/kg) treatment caused significant increases in the levels of HVA in hypothalamus and striatum and lithium cotreatment prevented the effect of naloxone. Neither of those were observed in the frontal cortical region.
Animals↗
The effect of aspartic acid on the intensity of physical dependence in morphine dependent mice.
The mice (Balb/C strain) given 2% aspartic acid in 5% saccharose solution or only saccharose solution (p. os) starting 12 hr before the sc morphine pellet implantation until the removal of pellet were rendered physically morphine dependent. During the development of morphine dependence and after the removal of pellets (on 3-d day) spontaneous motor activity and analgesic threshold were measured as reliable abrupt withdrawal signs. Aspartic acid prevented to some extent the appearance of symptoms of physical morphine dependence.
Analgesia↗
Effect of naloxone on apomorphine-induced changes in locomotor activity of stress-exposed rats.
Acute and subacute effects of naloxone (10 mg/kg), apomorphine (0.125 mg/kg; 5 mg/kg) and stressful stimuli (immobilization, cold and sound) on locomotor activity were examined. In both acute and subacute (8 days) treatments, the lower dose of apomorphine decreased locomotor activity and the higher dose of apomorphine increased it. In the acute treatment, naloxone enhanced significantly the depressant effect of the lower dose of apomorphine on locomotor activity. Stress seemed to have no effect on apomorphine induced changes in locomotor activity of rats either in acute or in subacute treatment.
Acoustic Stimulation↗