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Biomedical subjects

K F Soliman

Publications and source records attributed to K F Soliman.

At least 55 records · Page 3Linked to original sources
PubMed1988

Prenatal effects of acute harmaline exposure on fetal brain biogenic amine metabolism.

Harmaline, a known type A monoamine oxidase (MAO) inhibitor in adult brain of various species was found to elevate whole brain levels of dopamine and serotonin (5-HT) in rat fetuses of mothers injected 2-4 h before Caesarean delivery. Similar stimulatory effects were observed for the norepinephrine metabolite 3-methoxy-4-hydroxy-phenylglycol (MHPG), however, no significant effect was obtained for norepinephrine. The dopamine metabolite, 3,4-dihydroxyphenylacetic acid (DOPAC) and the 5-HT metabolite 5-hydroxyindole acetic acid (5-HIAA) were decreased with the same treatment. These results imply that harmaline or one of its metabolites may cross the placental barrier to affect the fetal brain system not merely as a type A MAO inhibitor (i.e., relatively 5-HT-specific), but possibly also as a stimulatory agent for aldehyde reductase or catechol-O-methyltransferase (COMT) or alternately as an agent inhibiting the conjugation, efflux, or turnover of biogenic amine metabolites such as MHPG.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1987

The role of opioid receptors in diabetes and hyperglycemia-induced changes in pain threshold in the rat.

The role of opioid receptors in diabetes and hyperglycemia-induced analgesia was studied in male Sprague-Dawley rats. Animals maintained under controlled environmental conditions were used in all studies. Pain latency was determined by the hot plate test (55 degrees C) and analgesy-meter force method. The results of these studies indicate that streptozotocin-induced diabetic animals have a significantly higher pain threshold (P less than 0.01) than the control groups. The pain threshold was found to be diurnally controlled with a peak at the beginning of the light phase (1000 hours) and a trough at the end of the dark phase (0800 hours). Diabetes-induced analgesia was found to be reversed by both acute or chronic insulin administration. In another study, glucose-induced hyperglycemic rats were found to have a significantly higher pain threshold (P less than 0.01) than control animals, with a peak occurring at the beginning of the dark phase (2000 hours), and a trough at the beginning of the light phase (0800 hours). The administration of the opioid antagonist naloxone (2 mg/kg) reversed the hyperglycemia and diabetic-induced analgesia. The results of these studies might indicate that analgesia found in diabetic or hyperglycemic animals may be related to the endogenous opioid system.

Analgesia↗
PubMed1987

Brain cholinergic involvement during the rapid development of tolerance to morphine.

In this study, male Sprague-Dawley rats maintained under controlled environmental conditions were used. Choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities were determined in cerebral cortex, bulbus olfactorius, midbrain, hypothalamus, hippocampus, cerebellum, pons and medulla oblongata in control rats and rats treated with morphine (10 mg/kg) for 1 or 2 days. Repeated administration of morphine was associated with a decline in the degree of analgesia produced. Significant increase (p less than 0.01) in AChE activity of the medulla oblongata was observed following morphine administration for 1 or 2 days. A single injection of morphine resulted in a significant decline (p less than 0.01) in ChAT activity of hypothalamus, cerebellum and medulla oblongata. However, no such decline could be observed after 2 consecutive daily injections of morphine. In the cerebral cortex there was a significant decline (p less than 0.01) in ChAT activity after the second administration of morphine. These findings indicate that the changes in the responsiveness of the brain cholinergic enzymes following repeated morphine administration may in part explain the rapid development of tolerance to the analgesic effect of morphine.

Acetylcholinesterase↗
PubMed1987

Effect of ethanol on the rat gastrointestinal cholinergic enzymes.

Male Sprague-Dawley rats weighing between 180 and 220 g and maintained under controlled lighting and temperature conditions were used in this experiment. Animals were given ethanol (3 g/kg, p.o.) 24 h after fasting. One group was given ethanol at 10.00 h (light phase) and the other at 22.00 h (dark phase). One hour later, the treated animals with their proper controls were sacrificed and the mucosa of the stomach, duodenum, ileum and colon were separated and assayed for choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities. Data obtained indicate that the administration of ethanol resulted in significant decline (p less than 0.01) in ChAT activity in the stomach and the colon during the light phase. A significant increase (p less than 0.01) in ChAT activity was also noted in the ileum during the dark phase. There was a significant decrease (p less than 0.01) in AChE activity in the stomach during the dark phase. The administration of ethanol also resulted in a significant decline in AChE activity (p less than 0.05) in the duodenum and the colon (p less than 0.01). The results obtained indicate that the gastrointestinal changes caused by ethanol administration may be related to changes in the cholinergic enzymes of the mucosa of the gastrointestinal tract.

Acetylcholinesterase↗
PubMed1986

The effect of neuroleptic drugs on serum testosterone level in the male rat.

The effects of systemically administered haloperidol (haldol) and N-ethoxycarbonyl-2-ethoxy-1,2, dihydroquinoline (EEDQ) on serum testosterone level were studied in Sprague-Dawley adult male rats. Animals were injected intraperitoneally with either 0.1, 5 and 10 mg/kg of haldol or 0.5 and 5 mg/kg of EEDQ. Animals were sacrificed at 15, 60 min, 12, 24 or 48 hr after drug treatment and blood was collected for subsequent testosterone analysis. Results obtained indicate that 10 mg/kg of haldol significantly (P less than 0.01) suppressed serum testosterone levels both at 1 and 24 hr post drug treatment. EEDQ treatment significantly (P less than 0.01) suppressed serum testosterone levels only when administered at the higher dose of 5 mg/kg. This effect was observed as long as 12 hr after drug treatment. These results suggest that high doses of haldol and EEDQ can suppress serum testosterone levels in the male rat. The sexual dysfunction associated with neuroleptic drugs may be partially due to the effects of the drugs on serum testosterone levels.

Adrenergic alpha-Antagonists↗
PubMed1986

Role of 5-hydroxytryptamine in the regulation of brain neuropeptides in normal and diabetic rat.

The effect of 5-hydroxytryptamine (5-HT) alteration on brain dopamine (DA), norepinephrine (NE), beta-endorphin (beta E) and immunoreactive insulin (IRI) was studied in Sprague-Dawley diabetic and control rats. Diabetes was induced using alloxan (45 mg/kg), 15 days prior to sacrificing. Both control and diabetic animals were treated with either p-chlorophenylalanine (PCPA, 300 mg/kg) 3 days prior to sacrificing or fluoxetine (10 mg/kg) twice daily for 3 days. PCPA treatment significantly decreased brain content of 5-HT and 5-hydroxyindole acetic acid (5-HIAA) while it caused significant increase and decrease in brain beta E and insulin levels, respectively, in both normal and diabetic rat. Meanwhile, the administration of fluoxetine resulted in significant increase in brain content of 5-HT, DA, NE and insulin but significant decline of beta E in diabetic and saline control rats. The results of this experiment indicate that 5-HT may be regulating both beta E and insulin regardless of the availability of pancreatic insulin.

Animals↗
PubMed1986

The effect of altered 5-hydroxytryptamine levels on beta-endorphin content in rat brain.

The purpose of the present study was to examine the effect of altering the concentration of 5-hydroxytryptamine (5-HT) on beta-endorphin (beta-Ep) content in the hypothalamus, thalamus, and periaqueductal gray (PAG)-rostral pons regions of the rat brain. The selective 5-HT reuptake inhibitor, fluoxetine (10 mg/kg), significantly lowered beta-Ep content in the hypothalamus and the PAG. Parachlorophenylalanine, which inhibits 5-HT synthesis, significantly elevated beta-Ep in all brain parts studied. Intracisternal injections of the neurotoxin, 5',7'-dihydroxytryptamine, with desmethylimipramine pretreatment, significantly increased beta-Ep content in the hypothalamus and the PAG. In adrenalectomized rats, fluoxetine significantly decreased beta-Ep levels in the hypothalamus and increased the levels in the PAG. The results indicate that 5-HT may modulate the levels of brain beta-Ep.

5,7-Dihydroxytryptamine↗
PubMed1986

Effect of stress and glucocorticoids on the gastrointestinal cholinergic enzymes.

Male Sprague-Dawley rats maintained under controlled lighting and temperature conditions were used in this experiment. Animals were exposed to acute cold (4 degrees C) and immobilization stress for one hour, exposed to cold stress for 7 days (chronic stress) or treated with corticosterone (2 mg/kg) 1 hr prior to sacrificing. Animals with their proper controls were sacrificed and the stomach, duodenum, ileum and colon were separated and assayed for choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities. The data obtained indicated that exposure to acute stress resulted in significant decline in ChAT activity in all tissues studied. The administration of corticosterone resulted in significant decline in ChAT activity in all tissues studied except for the duodenum. Meanwhile, the exposure to chronic stress did not have any significant effect on ChAT activity. On the other hand, acute stress caused significant increase in AChE activity in all tissues studied except for the ileum and stomach. The duodenal AChE activity of stressed animals increased thirty-fold when compared to control. The administration of glucocorticoids significantly reduced AChE in all tissues studied, except for the duodenum and stomach where there was thirty-two-fold increase as compared to the control levels. The exposure to chronic stress also caused significant increase in AChE of all tissues studied, except for the colon. The results of this experiments indicate that the duodenal AChE is extremely sensitive to stress or glucocorticoids and that stress induced changes in the cholinergic enzymes of the gastrointestinal tract may be mediated by adrenal steroids.

Acetylcholinesterase↗
PubMed1985

Brain cholinergic involvement in the rapid development of tolerance to the hypothermic action of ethanol.

The enzymes of the cholinergic system have been investigated in discrete brain regions in mice treated with repeated injection of ethanol. Male mice kept under controlled environmental conditions were treated with ethanol (3 g/kg/day) for 3 days. Animals were sacrificed 1 hr after ethanol injections. Brain regions studied were cerebral cortex, cerebellum, midbrain, hypothalamus, medulla oblongata, amygdala, and hippocampus. The administration of a single dose of ethanol resulted in significant increase (P less than 0.05) in choline acetyltransferase (ChAT) activity in all different brain regions. Repeated injections of ethanol at the 2nd and 3rd day did not result in any further rise in ChAT activity of the brain regions studied except for the midbrain. The results also show that acetylcholinesterase (AChE) activities increased significantly (P less than 0.05) in the pons and hippocampus in acutely ethanol intoxicated animals. The repeated injection of ethanol resulted in significant increase in AChE activities of the cortex and the amygdala. Meanwhile, animals developed tolerance to the hypothermic action of ethanol after ethanol third injection. The results of the present investigation indicate that the rapid development of the hypothermic tolerance to ethanol might be mediated by the brain cholinergic system.

Acetylcholinesterase↗
PubMed1984

The role of the adrenal gland in ethanol-induced triglyceride mobilization.

The effect of a large ethanol (ETOH) dose (4.8 g/kg) on triglyceride (TG) levels of plasma, brain and liver was studied in the rat. TG levels were measured in fasted male rats treated with ETOH or after ETOH and tetraethylammonium treatment in intact rats. The levels of TG were also measured after treatment with ETOH and dexamethasone (DXM) in adrenalectomized rats. Plasma TG levels significantly increased in the nonadrenalectomized and adrenalectomized rats by one- and twofold respectively. Brain TG levels increased significantly when intact animals were placed under either stress or when they were treated with ETOH and stress simultaneously. The adrenalectomized rats showed a similar response when they were treated with ETOH and DXM simultaneously. The liver TG levels were significantly different from control in all treated animals. The ETOH-treated adrenalectomized rats' TG levels were significantly less than control. This study suggests that stress and the adrenal gland play important roles in ETOH-induced TG levels in the rat.

Adrenal Glands↗
PubMed1983

Effect of biogenic amines reuptake inhibition on ethanol induced hypothermia.

The mechanism of ethanol induced hypothermia (EIH) was examined by the use of chemically related compounds which inhibit 5-hydroxytryptamine (5-HT) or norepinephrine (NE) reuptake. Desipramine, a tricyclic antidepressant drug (TCA) and NE reuptake inhibitor partially antagonizes EIH. However, Nisoxetine (NE reuptake inhibitor but not TCA) did not abolish EIH. Chlorimipramine, a TCA compound and 5-HT reuptake inhibitor abolishes EIH. Meanwhile, fluoxetine (5-HT reuptake inhibitor, but not TCA) potentiated ethanol induced hypothermia. It was concluded that the antagonism of EIH is probably related to the antidepressant effect of TCA compounds.

Animals↗
PubMed1983

Effect of prenatal exposure to phenobarbital on the development of monoamine oxidase and glucocorticoids.

1. Fetal exposure to phenobarbital (PB, 30 mg/kg) 2-5 days prior to parturition was conducted in Sprague-Dawley rats. The fetal exposure to PB resulted in: (a) Significant increase (P less than 0.01) in body wt at 23 and 42 days of age; (b) Significant increase (P less than 0.01) in brain wt at all ages studied; (c) Significant decline (P less than 0.05) in liver monoamine oxidase at day 13 of age; (d) Significant (P less than 0.05) increase in plasma corticosterone levels at days 23 and 42.

Adrenal Cortex↗
PubMed1983

Effect of stress on the acetylcholinesterase activity of the hypothalamus-pituitary-adrenal axis in the rat.

Acetylcholinesterase (AchE, EC 3.1.1.7) activity was determined in cerebral cortex, hypothalamus, adenohypophysis and adrenal gland in response to acute and chronic stress. Chronic exposure of animals to cold stress (at 4 degrees C for 7 days) resulted in significant decline of AchE activity in all tissues studied. Similar results were obtained when animals were exposed to acute immobilization and cold stress (at 4 degrees C) simultaneously. In another experiment, animals were treated with 2 mg/kg of corticosterone prior to AchE determination. Corticosterone administration resulted in a significant decline in AchE activity of the cortex, the hypothalamus and the adrenal but failed to affect the adenohypophysis AchE level. Exposing adrenalectomized animals to acute stress resulted in no significant changes in the cortex and the hypothalamus but caused a significant decline in AchE of the adenohypophysis. It was concluded from this study that corticosterone might mediate the stress effect on AchE activity.

Acetylcholinesterase↗
PubMed1982

Diurnal variation in ornithine decarboxylase activity of different brain regions of the rat.

The activity of ornithine decarboxylase (ODC) was studied in the brain of Sprague-Dawley male rats weighing 200-250 g. In this study, animals were maintained at a temperature of 21 +/- 1 degree C and a 12:12 h light--dark cycle for a minimum of 3 weeks prior to any experimentation. Animals were sacrificed at 06.00 h and 18.00 h and the brain cerebral cortex, hypothalamus, amygdala, hippocampus, midbrain, pons, medulla oblongata and cerebellum were isolated and assayed for ODC activity. The data show significant diurnal variations (P less than 0.05) in hypothalamus, midbrain, medulla oblongata and cerebellum, with peak values during the active phase of the animal. Other brain parts studied did not show any significant diurnal variations.

Amygdala↗