Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Long-Evans male adult rats were exposed for sixteen weeks to 2450-MHz CW microwaves at an average power density of mW/cm2. The resulting dose rate was 1.23 (+/- 0.25SEM) mW/g. The animals were exposed eight hours a day, five days a week, for a total of 640 h in a monopole-above-ground radiation chamber while housed in Plexiglas holding cages. Daily measures of body mass and of food and water intakes indicated no statistically significant effects of microwave irradiation. Biweekly stabilimetric tests immediately after exposure revealed a significant depression of behavioral activity by 15 microwave-exposed rats as compared with 15 sham-exposed animals. Measures of locomotor activity based on revolutions of a running wheel, which were obtained during 12-h periods between each 8-h exposure, showed no significant effect of irradiation. Blood sampled after 2, 6, 10, and 14 weeks of exposure indicated slight alterations of sulfhydryl groups, and of red and white blood-cell counts. Measures of levels of 17-ketosteroids in urine at weeks 1, 5, 9, and 12 of exposure, and mass of adrenals, heart, and liver at the end of the sixteen-week period of exposure, revealed no indications of stress.
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PMID:Physiological and behavioral effects of chronic exposure to 2450-MHz microwaves. 26 97

The behavioral effects of orally administered clonidine were investigated in Long--Evans (LE), Sprague--Dawley (SD) or Kyoto Wistar (KW) rats assumed to be normotensive and in NIH spontaneously hypertensive (SH) rats. Although clonidine (0.05-1 mg/kg) resulted in the same qualitative effect, i.e., depression of motor activity, the dose of clonidine required to depress motor activity to 50% of control levels (ED50) tended to vary according to strain. An analysis of variance of the dose response curves for the four strains of rats indicated a significant strain effect. When the effects of clonidine on food-reinforced operant responding were investigated it was observed that SD and SH rats differed with regard to rate and temporal pattering of IRT greater than 20 sec responding. Although oral administration of clonidine (0.006-0.1 mg/kg) produced similar percentage decreases from control in SH and SD rats, and analysis of the temporal patterning of responding indicated differences in responsiveness to the behavioral effects of clonidine. These studies demonstrate strain-related differences in responsiveness to the behavioral suppressant effects of clonidine. Marked differences between genetically hypertensive rats and rats assumed to be normotensive were not evident.
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PMID:Behavioral suppressant effects of clonidine in strains of normotensive and hypertensive rats. 87 75

High-frequency stimulation of the granule cell layer of the olfactory bulb (OB) has previously been shown to result in a selective long-term potentiation (LTP) of late components of potentials evoked in the OB and piriform cortex (PC). The functional impact of this potentiation was explored in male Long-Evans rats with chronically implanted electrodes by comparing the effects of paired-pulse stimulation of the OB in potentiated and control animals. Effects were examined on two components of the potential evoked in the PC: A1, which represents the population EPSP produced by OB mitral cells in PC pyramidal cells via the lateral olfactory tract (LOT), and B1, which represents the subsequent population EPSP produced by PC pyramidal cells in other pyramidal cells. Two separate functional correlates of selective LTP were found. First, there was enhanced paired-pulse depression of B1, indicating increased inhibition of PC pyramidal cells. Second, there was a shift from paired-pulse facilitation to depression of A1, which was accompanied by a decrease in amplitude of the LOT volley, indicating that fewer mitral cells were activated by the stimulation. This shift was most prominent in animals with stimulating electrodes closest to the mitral cell layer, suggesting that it is dependent upon direct stimulation of mitral cell somata. These observations, together with other results reported in the manuscript, support the conclusion that there is an enhanced inhibition of mitral cells following selective LTP. Thus a primary consequence of selective LTP appears to be enhanced inhibition of principal neurons in both the PC and OB. These findings are consistent with our previous proposal that selective LTP represents potentiation at excitatory synapses made by PC pyramidal cells on inhibitory interneurons in the PC and OB.
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PMID:Functional correlates of selective long-term potentiation in the olfactory cortex and olfactory bulb. 151 5

This study examined the relationship between inhibition of cholinesterase activity (CA) and thermoregulatory response in the rat following exposure to the organophosphate (OP), diisopropyl fluorophosphate (DFP). Male Long-Evans rats were injected with DFP dissolved in peanut oil in doses ranging from 0 to 1.5 mg/kg (s.c.). Colonic (Tcol) and tail skin temperature (Ttail) were recorded at 0, 1, 2 and 3 h post-injection. At 3 h post-injection the rat was sacrificed and a blood sample was taken by cardiac puncture and analyzed for CA. There was a biphasic dose effect of DFP on Tcol with slight but significant elevation in Tcol in the dose range of 0.01-0.5 mg/kg and a significant depression in Tcol at doses of 1.0 and 1.5 mg/kg. There was a dose-dependent fall in CA with DFP administration in the erythrocyte, plasma, and whole blood fractions. Hypothermia was associated with 80-87% inhibition in CA, whereas the elevation in Tcol was associated with 20-70% inhibition in CA. DFP also elicited significant elevations in Ttail. Overall, the data fail to demonstrate any clear relationship between inhibition of blood CA and thermoregulatory response following exposure to DFP. However, the elevation in Tcol following relatively low doses of DFP may be of relevance to the frequently reported symptom of fever in humans exposed to OP agents.
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PMID:Relationship between cholinesterase inhibition and thermoregulation following exposure to diisopropyl fluorophosphate in the rat. 175 22

The rat's (Long-Evans) acoustic startle reflex to a high-frequency tone burst (10.5 kHz) was depressed by intense high-frequency band-pass noise (8-16 kHz) but enhanced by low frequency noise (1-2 kHz). However, contrary to the hypothesis that the depression of startle in intense background noise is produced by sensory masking, the reflex to a low-frequency tone burst (at 1 kHz) was depressed by both high- and low-frequency band-pass noise. Two additional hypotheses are offered to supplement sensory masking in order to explain the asymmetry in these data. The first is that the intratympanic reflex, which acts as a high pass filter on acoustic input, is elicited in intense backgrounds. The second is that acoustic startle reflexes elicited by intense low-frequency tones are in part elicited by their high-frequency distortion products and that these distortion products are then masked by high-frequency background noise.
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PMID:Spectral frequency and the modulation of the acoustic startle reflex by background noise. 230 89

To evaluate the effect of various anesthetic agents on hyperosmolar blood-brain barrier disruption (BBBD), Sprague-Dawley rats were given pentobarbital (PB), ketamine-xylazine (KX), isoflurane (IF), methoxyflurane (MF), or fentanyl-droperidol (FD) before intracarotid infusion of mannitol or saline. Physiological monitoring showed that the effects of mannitol infusion differed significantly from those of saline infusion and were associated with transient bradycardia, hypotension, metabolic acidosis, and electroencephalographic depression. With PB, KX, or IF anesthesia, we obtained excellent BBBD as evidence by 3+ Evans blue staining of the mannitol-infused cerebral hemisphere. FD anesthesia was associated with tachycardia and MF anesthesia resulted in hypotension; both showed poor Evans blue staining. Radioisotope delivery to the disrupted hemisphere averaged 0.80% of the administered 125I-albumin compared to 0.03% in the contralateral and 0.06% in control (saline-infused) hemispheres. 99mTc-glucoheptonate delivery measured 0.49% of the administered dose after BBBD, 0.03% contralaterally, and 0.05% in control hemispheres. Pharmacological manipulation to normalize the cardiac index in the FD and MF groups resulted in 3+ Evans blue staining and significantly increased delivery of albumin and glucoheptonate. This study suggests that the cardiovascular changes of these specific anesthetic agents are important in obtaining optimal hyperosmolar BBBD.
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PMID:The effects of anesthesia on osmotic blood-brain barrier disruption. 230 75

The neurotoxic effects of long-term, low-level exposure to the commercially available insecticide, Fenthion, were examined in the present study. Young (2 month) adult, male Long-Evans rats were dermally exposed to Fenthion (25 mg/kg, 3X week) and sampled after 2 and 10 months exposure to assess neurotoxic damage in the hippocampus using morphological and biochemical endpoints. Histopathology, consisting of gliosis, swollen and necrotic neurons, and cell dropout, occurred in the dentate gyrus (DG), CA4 (hilus), and CA3 sectors as early as 2 months postexposure. Acetylcholinesterase (AChE) staining of brain tissues taken at this time was severely reduced in the septal nuclei, the DG molecular layer, the CA4, and the hippocampus proper. After 10 months exposure to Fenthion, cellular necrosis and gliosis intensified in the CA4 and CA3 regions and occasionally involved the CA2. Radiometric assays of AChE activity in the hippocampus indicated a 65 and 85% depression after 2 and 10 months exposure, respectively. Quinuclidinyl benzilate binding for the hippocampal muscarinic receptor was reduced by 6 and 15%, after 2 and 10 months exposure, respectively. A separate group of older (12 month) rats was exposed to the same dosing regimen of Fenthion and examined for neuropathological damage after 2 and 10 months exposure. Aged animals exposed for only 2 months expressed severe hippocampal degeneration in a pattern similar to that seen in the young adult after 10 months exposure (viz., DG, CA4, CA3). Aged animals exposed for 10 months showed more extensive histopathology of the CA4-2 and occasionally CA1. These observations indicate that in both young adult and aged animals, subchronic, low-level exposure to anticholinesterase compounds can result in serious neurotoxic consequences to the mammalian hippocampus.
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PMID:The neurotoxicity of subchronic acetylcholinesterase (AChE) inhibition in rat hippocampus. 238 36

Treatment of pregnant Long Evans rats with a low dose of diazepam (1.25 mg/kg per day s.c.) from gestational day (GD) 14 to 20 resulted in severe and long lasting depression of cellular immune responses in male and female offspring. T lymphocyte proliferation, induced by allogeneic stimulation in mixed lymphocyte culture (MLC) or geneic stimulation in mixed lymphocyte culture (MLC) or mitogenic stimulation (concanavalin A), decreased by 50 % or more over a postnatal period of about 2 months. Treatment of the pregnant dam during the early fetal period, from GD 12 to GD 16, did not significantly affect these immune parameters, whereas treatment during later gestation, from GD 16 to 20, significantly affected T lymphocyte function. Clonazepam, a benzodiazepine with high affinity for the central type benzodiazepine site, also affected cellular immune response in offspring. Our data indicate that benzodiazepine treatment during the fetal period may result in persistent postnatal deficiency of cellular immune responses. The relative role of central and peripheral type benzodiazepine receptor and possible interactions with maternal and fetal pituitary - adrenocortical systems are discussed.
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PMID:Prenatal diazepam induced persisting depression of cellular immune responses. 253 99

Treatment of time-pregnant Long Evans rats with 1.25 mg/kg s.c. diazepam (2.5 mg/kg in Sprague Dawley rats) from gestational day 14 to 20 produced transient depression of an olfactory guided behavior (nest odor behavior) in suckling offspring. Enhanced drug sensitivity to diazepam was seen in adult male and female off-spring as indicated by increased temperature depression. In addition, increased sensitivity to an opiate (morphine) was noted for the female offspring in the tail flick test. Treatment of the pregnant dam with diazepam or clonazepam, a benzodiazepine with selective affinity for the central benzodiazepine receptor, resulted in a marked depression of cellular immune responses in the offspring of both sexes up to 2 months of age. Drug treatment during early fetal period (GD 12-16), at a time central benzodiazepine receptors are not present in all brain regions of the fetal brain, did not affect the quality of cellular immune responses, whereas treatment from GD 16 to 20 was effective. Prenatal diazepam effects are discussed in view of presence and functionality of both central and peripheral benzodiazepine binding sites in the fetus.
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PMID:Diazepam effects on the fetus. 256 May 34

The role of brain catalase in the mediation of ethanol's effects on motor activity was investigated. Male Long-Evans rats were pretreated with i.p. injections of the catalase inhibitor, 3-amino-1,2,4-triazole (AT) (1 g/kg) or saline (S). Four hours later, animals in each group received i.p. injections of one of two doses of ethanol (ETOH) [1.0 g/kg (E1) or 2.0 g/kg (E2)] or one of two volumes of distilled water (W1 or W2). Ten minutes after the administration of these agents, animals were placed in open-field chambers and motor activity was recorded during a 10-min testing period. Results indicated that the motor depression produced by 2.0 g/kg of ETOH was significantly attenuated in AT pretreated rats (group AT-E2). AT pretreatment, however, had no effect on motor activity for subjects injected with 1.0 g/kg ethanol or water. Total brain catalase activity in AT-pretreated animals was 15% of control animals. No differences in blood ethanol levels were observed between AT- and S-pretreated animals. An interaction between ethanol and AT at the level of the central nervous system is suggested. The results of the present study suggest that brain catalase activity may be involved in ethanol's effects. They also provide further support for the notion that acetaldehyde may be produced directly in the brain via catalase and that it may be a factor mediating some of ethanol's central effects.
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PMID:Effects of 3-amino-1,2,4-triazole on ethanol-induced open-field activity: evidence for brain catalase mediation of ethanol's effects. 264 62


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