Enhanced brain regional lipid peroxidation in developing rats exposed to low level lead acetate

Neurotoxicity associated with lead exposure may be the result of a series of small perturbations in brain metabolism, and, in particular, of oxidative stress. Some studies have suggested a lead-induced enhancement on lipid peroxidation as a possible mechanism for some toxic effects of lead. However, there are no reports about the association between lipid peroxidation enhancement and brain lead content. In this study, we determined the concentration of lead and the formation of lipid fluorescence products in the blood, as well as in the parietal cortex, striatum, hippocampus, thalamus, and cerebellum of rats exposed prenatally and postnatally to variable concentrations of lead acetate through drinking water. Pregnant Wistar rats were intoxicated throughout gestation with solutions containing either 320 or 160 ppm of lead. The pups were treated after birth in the same way until 45 days of age. Control animals received deionized water for the same period of time. The developing rats were sacrificed at postnatal day 45 and lead level was assessed biochemically in the blood and different brain regions. Results showed that blood lead levels were increased in a dose-dependent manner. In the brain, lead accumulated preferentially in the parietal cortex, striatum, and thalamus as compared to the control group, while lipid fluorescence products were significantly increased in the striatum, thalamus, and hippocampus of the treated animals. These data suggest that in the brain of rats exposed to lead acetate, lead produces a neurotoxic effect with a complex correlation with both lead regional content and lipid peroxidation.     

The effect of prenatal stress on oxidative protein modification in the rat brain in ontogeny

Oxidative protein modification (OPM) was studied in the striatum, hippocampus, and hypothalamus of rats of various ages that were subjected to prenatal stress. The basal level of spontaneous OPM products and the level of OPM products after induction by Fenton??s reagent were measured. The OPM processes in the structures we studied had similar features. Under normal conditions, a gradual increase in the content of OPM products was observed at days 10?C30 of postnatal ontogeny and a decrease in this index was observed in adult animals. Additionally, some differences in the contents of OPM products were revealed in specific brain regions. In the animals that were subjected to prenatal stress, we found substantial differences in the time course of OPM in all brain regions studied. Thus, the level of OPM products in 10-day-old rats that were subjected to prenatal stress was substantially higher compared to that in the control rats. However, the indices of both spontaneous and induced OPM later decreased. Thus, impairments of OPM processes in the striatum, hypothalamus, and hippocampus may be a cause of changes in adaptive behavior, which were observed in adult rats that were subjected to prenatal stress.     

Sepsis facilitates brain serotonin activity and impairs learning ability in rats

Sepsis often provokes various neurological disorders. Because many neurologic symptoms are caused by changes in neurotransmissions, we investigated the relationship between behavioral alterations and changes in activities of the monoaminergic systems in rats. Sepsis was induced by cecal ligation and puncture. A step-through passive avoidance test was used for the behavioral evaluation. Passive avoidance retention in animals subjected to learning immediately before the septic or sham operation was examined after 24 or 48 h. Retention performance in animals subjected to learning 24 h after the operation was also examined after a further 24 h. Plasma concentrations of amino acids were determined 24 h after the operation. The activities of the brain monoaminergic systems were evaluated by ratios of metabolites to monoamines. Marked damage was found in the septic rats in the blood analysis 24 h after the operation. The plasma concentrations of tyrosine and arginine in the septic rats were decreased to 69% and 70% of those in the sham-operated animals, respectively. Retention performance was impaired in the septic rats when they were subjected to learning 24 h after the operation, but it was not impaired when animals were subjected to learning before the septic operation. The brain concentration of serotonin was increased in the cerebral cortex, striatum, and hippocampus 48 h after the septic operation, but not after 24 h. The concentration of 5-hydroxyindoleacetic acid, a metabolite of serotonin, was increased in the above three regions both 24 and 48 h after the operation, but not in the hypothalamus. Facilitation of the serotonergic activity in the telencephalon and hippocampus is suggested to be involved in the impairment of learning ability in sepsis.     

Effect of a combination of pentoxifylline and nimodipine on lipid peroxidation in postischemic rat brain

The authors studied the effects of a combination of pentoxifylline and nimodipine on cerebral lipid peroxidation in postischemic rat brain. Pentoxifylline (40 mg/kg) and nimodipine (3 mg/kg) were administered per os 30 min before 5 min of ischemia (four-vessel occlusion model of transient ischemia). The extent of peroxidation in brain tissue (cerebral cortex, hippocampus, striatum) was then estimated by assay of thiobarbituric acid reactive substances (TBARS). The concentration of TBARS was significantly lower in the cerebral cortex and hippocampus of the group treated with the combination of drugs than in untreated ischemic rats. However, this concentration was not significantly different from that found in the cerebral cortex and hippocampus of other groups premedicated with nimodipine or pentoxifylline alone. The tested drugs had no effect on TBARS in the striatum. The hypothesis that the combination of drugs would have a synergistic effect on postischemic lipid peroxidation was therefore not confirmed.     

Increased lipid peroxidation in vulnerable brain regions after transient forebrain ischemia in rats

We examined cerebral lipid peroxidation, estimated by a thiobarbituric acid test, in rat brain regions after 30 minutes of severe forebrain ischemia and at recirculation periods of up to 72 hours. The lipid peroxide levels remained unaltered in all brain regions during ischemia and during the first hour of recirculation but were selectively increased between 8 and 72 hours of recirculation in the ischemia-sensitive regions of the hippocampus, striatum, and cortex. The most pronounced increases (30-37%) were seen at 48 hours of recirculation. In contrast, lipid peroxide levels were unchanged in infarcted brain regions 24 hours after intracarotid injection of microspheres, indicating that reoxygenation of the ischemic brain is a prerequisite for lipid peroxidation. We assessed the lipid peroxidation capacity of cerebral homogenates obtained from rats subjected to ischemia and recirculation by measuring the production of lipid peroxides after aerobic incubation. The homogenates from rats exposed to 30 minutes of ischemia or to 1 hour of recirculation were not more susceptible to peroxidation. However, the production of lipid peroxides was selectively increased in the hippocampus, striatum, and cortex at 8-48 hours of recirculation, suggesting a loss of efficacy of the antioxidant systems. These results, showing a delayed and long-lasting increase in lipid peroxidation that occurs in ischemia-sensitive brain regions and parallels the development of neuronal necrosis, support the hypothesis that free radical processes participate in postischemic neuronal damage.     

β-endorphin and methionine-enkephalin levels in discrete brain regions, spinal cord, pituitary gland and plasma of morphine tolerant-dependent and abstinent rats

The effect of morphine tolerance-dependence, protracted and naloxone-precipitated abstinence on the levels of β-endorphin and methionine-enkephalin in discrete brain regions, spinal cord, pituitary gland and plasma was determined in the male Sprague-Dawley rats. Among the brain regions examined, the levels of β-endorphin in descending order were: hypothalamus, amygdala, midbrain, hippocampus, corpus striatum, pons and medulla and cortex. The levels of β-endorphin in midbrain, hypothalamus, and pituitary of morphine tolerant-dependent rats were decreased significantly. During protracted withdrawal β-endorphin levels were decreased in amygdala, spinal cord and pituitary. During naloxone-precipitated abstinence β-endorphin levels were increased in corpus striatum, midbrain and cortex. In addition, in naloxone-precipitated abstinence β-endorphin levels were decreased in pituitary gland and hippocampus but increased in plasma. The levels of methionine-enkephalin in brain regions in decreasing order were: corpus striatum, pons and medulla, amygdala, hypothalamus, midbrain, hippocampus and cortex. The levels of methionine-enkephalin in pons and medulla, amygdala, hippocampus and pituitary gland were decreased in morphine tolerant-dependent rats. During protracted abstinence from morphine, methionine-enkephalin levels in spinal cord, amygdala, pons and medulla, midbrain, cortex, corpus striatum and pituitary gland were decreased. The levels of methionine-enkephalin in hypothalamus and corpus striatum of naloxone-precipitated abstinent rats were increased but were decreased in amygdala and pituitary gland. These results suggest that during morphine tolerance-dependence and during protracted abstinence β-endorphin and methionine-enkephalin levels in discrete brain regions and pituitary gland are decreased. During precipitated abstinence β-endorphin levels are increased in brain regions (except hippocampus) and plasma but decreased in pituitary, whereas methionine-enkephalin levels in amygdala and pituitary gland are decreased except in corpus striatum and hypothalamus where they are increased. The pituitary levels of β-endorphin where reduced in all three conditions. However, the levels after withdrawal were not significantly different from those in tolerant—dependent animals.     

Spatial and temporal patterns of oxidative stress in the brain of gerbils submitted to different duration of global cerebral ischemia

The present study was undertaken to examine spatial and temporal patterns of oxidative stress rate in the brain of Mongolian gerbils submitted to different duration of global ischemia/reperfusion. The common carotid arteries of gerbils were occluded for 5, 10, or 15 min. We followed the temporal ischemia-induced oxidative stress rate, the most important factor that exacerbates brain damage by reperfusion, starting from 24 h up to 28 days after reperfusion. The spatial ischemia-induced oxidative stress distribution was measured parallely in different brain regions: forebrain cortex, striatum, hippocampus and cerebellum. Post-ischemic effects were followed in vivo by monitoring the neurological status of whole animals and at the intracellular level by standard biochemical assays in different brain regions. We measured superoxide production, superoxide dismutase activity, nitric oxide production, index of lipid peroxidation, and reduced glutathione. Our results revealed a pattern of dynamic changes in each oxidative stress parameter that corresponded with ischemia duration in all tested brain structures. The highest levels were obtained in the first 24 h after the insult. After that, they slowly returned to nearly control values 28 days after reperfusion (with the exception of SOD activity that returned to control values at fourth day after reperfusion). The most sensitive oxidative stress parameter was index of lipid peroxidation. Our study confirmed spatial distribution of ischemia-induced oxidative stress. Tested brain structures showed different sensitivity to each oxidative stress parameter, although their basal levels were similar. These new findings could be valuable for creation and strategy of post-ischemic therapy.     

Increased anxiety level induced by social crowding stress in rats is not related to changes in the nitrergic system of the brain

In our previous studies, we have shown that stress induced by early social deprivation or total isolation, increases nitric oxide synthase activity in the brain regions of laboratory animals, and possible links between this phenomenon and stress-induced psychoemotional disturbances have been discussed. In the present study, we studied the effects of chronic psychosocial stress (housing under crowding conditions for 6 weeks) on the anxiety behavior and the indices of nitrergic system and intensity of free radical-mediated processes. Stress significantly increased anxiety levels, primarily influencing the exploratory components of animal behavior. Nitric oxide synthase activity and the levels of nitric oxide stable metabolites did not differ in the cerebral cortex, hippocampus, striatum and cerebellum of the control and stressed rats. Stress moderately increased the content of lipid peroxidation products in the cerebellum, whereas the levels of protein- and nonprotein thiol groups remained unchanged. Thus, the increased anxiety level in rats subjected to a long-term crowding was not accompanied by changes in the nitrergic system in the brain.     

Memory impairments and oxidative stress in the hippocampus of in-utero cocaine-exposed rats

We examined whether significant oxidative stress is induced in the brain of juvenile rats exposed in utero to cocaine, and contributes to their mnesic difficulties. We measured nitric oxide generation, using electron paramagnetic resonance, and the thiobarbituric acid reactive species as specific indexes of lipid peroxidation. Both nitric oxide and lipid peroxidation were elevated in the hippocampus of in-utero cocaine-exposed rats as compared with control animals. In-utero cocaine-exposed rats developed significant learning impairments in the water-maze, shown by probe test retrieval deficits. In parallel, behavioural sessions resulted in increases of thiobarbituric acid reactive species levels only in control animals. Therefore, in-utero cocaine exposure resulted in a significant oxidative stress in basal conditions, which may be related to impaired learning ability.     

Learning deficits and brain monoamines in rats with congenital hyperbilirubinemia

At 28 days of age, rats with congenital hyperbilirubinemia (homozygous Gunn strain) were submitted to an active learning task (two-way shuttlebox avoidance) and a passive learning task (step-down avoidance) and the results compared with controls (heterozygous littermates). Jump thresholds to painful footshock were used as measures of pain sensitivity. After testing, the concentration of dopamine and norepinephrine was measured in eight brain regions. The jaundiced Gunn rat demonstrated significant learning retardation on both avoidance tasks compared with their controls. Because jump thresholds to shock were similar in hyperbilirubinemic animals and their controls, these differences in learning performance could not be attributed to differences in sensitivity to footshock. Norepinephrine concentrations in hypothalamus and hippocampus were elevated in jaundiced rats compared with controls. In jaundiced rats, dopamine concentrations in striatum and pons-medulla were diminished. Cerebella in jaundiced rats were significantly smaller, and total content of both dopamine and norepinephrine significantly lower in jaundiced rats compared with controls. Learning deficits in young jaundiced Gunn rats may be associated with the changes in brain catecholamine concentrations found in these animals. To determine whether or not any recovery from hyperbilirubinemia occurs, similar behavioral and biochemical testing could be applied to homozygous Gunn rats at different stages in development.     

The relationship between the level of neuroactive steroids in the brain, behavior, and anxiety in male rats with different hormonal status

We investigated the levels of neuroactive steroids, behavior, and anxiety in the brains of male rats with different hormonal status. We revealed a correlation between motor and exploratory activities, emotionality, and anxiety and the concentrations of corticosterone, testosterone, and estradiol in the hypothalamus, hippocampus, amygdala, cingulated gyrus, and frontal cortex in intact male rats, as well as in animals with experimentally high or low levels of sex steroids. The correlation analysis confirmed the selective involvement of different brain structures and neuroactive steroids in brain functioning and behavioral adaptation.     

Arachidonate transport through the blood-retina and blood-brain barrier of the rat after reperfusion of varying duration following complete cerebral ischemia

The permeability-surface area product (PS) of [1-¹⁴C]arachidonate at the blood-retina and blood-brain barrier was determined by short carotid perfusion in young Wistar rats 1 or 6 h after recovery period following complete cerebral ischemia induced by temporary cardiac arrest. For the retina and structures of visual system, hypothalamus and olfactory bulb there was no significant difference over sham-operated rats among mean PSs. For cortex, hippocampus and striatum, significant increases were found at both time intervals of recovery after cardiac arrest. The ischemia-reperfusion model was characterized by a significant increase in tissue conjugated diene in the hippocampus and microsomal lysophosphatidylcholine acyltransferase activity in the cortex. Consistent with these findings, we also show ultrastructural evidence mainly represented by partial opening of interendothelial junctions and mild signs of tissue edema in surrounding neuropil, suggesting barrier leakiness predominantly in the cortex, hippocampus and striatum but almost absent in the retina microvessels. Our results indicate that ischemia-reperfusion does affect influx through blood-brain barrier into regional structures of rat central nervous system of arachidonate, a metabolic substrate and lipid mediator rapidly incorporated into microcapillary and brain lipids. The data also suggested that : (i) reactive oxyradicals were moderately generated during the early phase of ischemic-reperfusion process in the rat ; (ii) after reperfusion, in vitro susceptibility of different brain regions to iron-induced peroxidation was highest in the hippocampus and lowest in the cortex and striatum ; (iii) membrane phospholipid repair mechanisms were activated at the same time.     

Prenatal exposure to noise stress: Anxiety,impaired spatial memory,and deteriorated hippocampal plasticity in postnatal life

Sound pollution is known as an annoying phenomenon in modern life. Especially, development of organisms during fetal life is more sensitive to environmental tensions. To address a link between the behavioral and electrophysiological aspects of brain function with action of hypothalamus‐pituitary‐adrenal (HPA) axis in stressed animals, this study was carried out on the male Wistar rats prenatally exposed to sound stress. Groups of pregnant rats were exposed to noise stress for 1, 2, and 4 hour(s). The degree of anxiety and the spatial memory were evaluated by elevated plus maze and Morris water maze, respectively. Basic synaptic activity and long‐term potentiation (LTP) induction were assessed in the CA3‐CA1 pathway of hippocampus. The serum level of corticosterone was measured in the pregnant mothers and the offspring. The behavioral experiments appeared that the stressed animals performed considerably weaker than the control rats. The prenatal stress negatively affected the basic synaptic responses and led to a lower level of LTP. The pregnant animals showed an increased serum corticosterone in comparison with the nonpregnant females. Also the offspring exposed to the noise stress had a more elevated level of corticosterone than the control rats. Our findings indicate that the corticosterone concentration changes markedly coincides the results of behavioral and electrophysiological experiments. We conclude that, similar to other environmental stresses, the sound stress during fetal life efficiently disturbs both cognitive abilities and synaptic activities. The changes in action of HPA axis may contribute to problems of the brain function in the prenatally stress exposed animals. © 2014 Wiley Periodicals, Inc.     

Differences in brain area concentrations of dopamine and serotonin in myers' high ethanol preferring (mHEP) and outbred rats

Both male and female mHEP rats consume excessive amounts of ethanol and thus offer a rational model for examining biochemical and behavioral differences with non-drinking rat lines. Differences in basal concentrations of 5-hydroxytryptamine (5-HT) and dopamine (DA) correlate with the consumption of ethanol in some ethanol-preferring rat lines. The concentrations of 5-HT and DA were examined by HPLC in five brain areas (prefrontal cortex, hippocampus, nucleus accumbens, striatum and hypothalamus) of ethanol-n?ive rats and after the oral administration of 0.25 or 1.0 g ethanol/kg in the male and female mHEP rat, the male Wistar rat, and the female Sprague-Dawley rat. The mHEP and control rats that received ethanol were screened for drinking in a 10-day "step-up" 3% to 30% ethanol solutions beginning at postnatal days 40 and 80, and then tested at 150 days of age. The levels of DOPAC in females were lower in the hippocampus of both na?ve mHEP and ethanol-treated Sprague-Dawley rats. In striatum, the concentrations of 5-HT and DA were elevated in both mHEP and ethanol-treated Sprague-Dawley female rats. The concentrations of 5-HT and its metabolite, 5-HIAA, were lower in the nucleus accumbens of the ethanol-n?ive female mHEP rat relative to the female outbred control. In the male rats, the levels of DA, HVA and DOPAC, as well as 5-HT and 5-HIAA were reduced in the hypothalamus of both ethanol-n?ive mHEP rats and Wistar rats receiving ethanol by gavage. These data demonstrate differences in neurotransmitter activity between the selectively bred mHEP rat and the outbred rat strains. There are few common features found in both the male and the female mHEP rat when compared to their respective controls. Differences in neurotransmitter function in these brain areas may account for some of the behavioral differences previously demonstrated between the two sexes of the mHEP rat.     

Early Changes in Prodynorphin mRNA and ir-Dynorphin A Levels after Kindled Seizures in the Rat

Prodynorphin mRNA and immunoreactive dynorphin A (ir-dynorphin A) levels were measured in different brain areas at various time points after amygdala kindled seizures. In the hippocampus, striatum and hypothalamus, prodynorphin mRNA levels were not significantly changed in kindled rats (killed 1 week after the last stimulus-evoked seizure), but they were significantly increased 1 h after seizures. The relative increase was the highest in the hippocampus (∼3-fold). In the brainstem, midbrain and cerebral cortex no changes in prodynorphin mRNA were detected in kindled rats, 1 h or 1 week after a kindled seizure. ir-Dynorphin A levels were significantly reduced in the hippocampus and in the striatum of kindled rats, as well as 5 and 60 min after kindled seizures, but they were increased back to control levels after 120 min. In the hypothalamus, ir-dynorphin A levels were significantly increased 120 min after a kindled seizure. ir-Dynorphin A levels were also significantly reduced in the brainstem and in the frontal, parietal and temporal cortex 120 min, but not 5 or 60 min, after a kindled seizure. Taken together, these data support the hypothesis that the dynorphinergic system is activated after amygdala kindled seizures, with different kinetics in different brain areas.     

Oxidative Stress Biomarkers in Some Rat Brain Structures and Peripheral Organs Underwent Cocaine

Oxidative stress (OS) generates or intensifies cocaine-evoked toxicity in the brain and peripheral organs. The aim of this study was to examine superoxide dismutase (SOD) activity and lipid peroxidation [measured by malondialdehyde (MDA) levels] in rats during maintenance of cocaine self-administration and after withdrawal by a yoked-triad procedure. Our results indicate that repeated cocaine self-administration provoked an elevation of SOD activity in the hippocampus, frontal cortex, dorsal striatum, and liver. MDA levels were reduced in the brain, increased in the liver, kidney, and heart during maintenance of self-administration, and increased in the kidney in cocaine-yoked rats. In addition, following extinction training, we found enhanced MDA levels and SOD activity in the rat hippocampus, while changes in the activity of OS biomarkers in other brain structures and peripheral tissues were reminiscent of the changes seen during cocaine self-administration. These findings highlight the association between OS biomarkers in motivational processes related to voluntary cocaine intake in rats. OS participates in memory and learning impairments that could be involved in drug toxicity and addiction mechanisms. Therefore, further studies are necessary to address protective mechanisms against cocaine-induced brain and peripheral tissue damage.     

Oxidative stress parameters in different rat brain structures after electroconvulsive shock-induced seizures

Electroconvulsive therapy has been used in the treatment of psychiatric disorders since the 1930s, but little progress has been made in understanding the cellular mechanisms underlying its therapeutic and adverse effects. Electroconvulsive shock (ECS) in animals provides a common experimental model for studying the effects of electroconvulsive therapy in humans. In order to examine the changes of the brain oxidative stress parameters in several brain structures in the early time period after ECS-induced seizures, the levels of lipid peroxidation as well as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in the rat hippocampus, cerebellum, frontal cortex and the pons/medulla region were determined at different time points during the first 24 h after single ECS-induced seizures. In the hippocampus and cerebellum the levels of lipid peroxidation were unchanged, while the SOD and GSH-Px activities were significantly increased. Levels of lipid peroxidation and the activities of SOD and GSH-Px were not statistically changed in the pons/medulla region. Levels of lipid peroxidation in the frontal cortex were significantly higher in comparison to the control group at all time points examined while the SOD and GSH-Px activities were not statistically changed. In conclusion, the results of the present study indicate that single ECS causes the rat brain structure-specific alterations in the levels of lipid peroxidation as well as in the SOD and GSH-Px activities at different time points within the first 24 h after the seizures induction. Oxidative lipid damage was evident only in the frontal cortex, while the hippocampus, cerebellum and the pons/medulla region remained oxidatively unaffected in our experimental conditions.     

Beta-endorphin and methionine-enkephalin levels in discrete brain regions, spinal cord, pituitary gland and plasma of morphine tolerant-dependent and abstinent rats

The effect of morphine tolerance-dependence, protracted and naloxone-precipitated abstinence on the levels of beta-endorphin and methionine-enkephalin in discrete brain regions, spinal cord, pituitary gland and plasma was determined in the male Sprague-Dawley rats. Among the brain regions examined, the levels of beta-endorphin in descending order were: hypothalamus, amygdala, midbrain, hippocampus corpus striatum, pons and medulla and cortex. The levels of beta-endorphin in midbrain, hypothalamus, and pituitary of morphine tolerant-dependent rats were decreased significantly. During protracted withdrawal beta-endorphin levels were decreased in amygdala, spinal cord and pituitary. During naloxone-precipitated abstinence beta-endorphin levels were increased in corpus striatum, midbrain and cortex. In addition, in naloxone-precipitated abstinence beta-endorphin levels were decreased in pituitary gland and hippocampus but increased in plasma. The levels of methionine-enkephalin in brain regions in decreasing order were: corpus striatum, pons and medulla, amygdala, hypothalamus, midbrain, hippocampus and cortex. The levels of methionine-enkephalin in pons and medulla, amygdala, hippocampus and pituitary gland were decreased in morphine tolerant-dependent rats. During protracted abstinence from morphine, methionine-enkephalin levels in spinal cord, amygdala, pons and medulla, midbrain, cortex, corpus striatum and pituitary gland were decreased. The levels of methionine-enkephalin in hypothalamus and corpus striatum of naloxone-precipitated abstinent rats were increased but were decreased in amygdala and pituitary gland. These results suggest that during morphine tolerance-dependence and during protracted abstinence beta-endorphin and methionine-enkephalin levels in discrete brain regions and pituitary gland are decreased.(ABSTRACT TRUNCATED AT 250 WORDS)     

Vasopressin and oxytocin in brain areas of rats with high or low behavioral performance

Animals were selected from a population of 55 rats which differed significantly in their ability to perform a behavioral task, a foot-shock motivated brightness discrimination (BD). Using highly specific and sensitive radioimmunoassays, the contents of arginine vasopressin (AVP) and oxytocin (OXT) were measured in 5 brain areas and the plasma of these animals. AVP levels in the septum/striatum and posterior pituitary of rats with high performance significantly exceeded those of the low performance group. Compared to the low performance rats, the OXT content of the high performance rats was higher in the septum/striatum, but was lower in the hippocampus. No significant differences between the groups were found in the hypothalamus, motor cortex and the plasma. The results suggest that both AVP and OXT are signals in central pathways involved in information processing. In particular, high endogenous AVP and OXT levels in neurons of the septum/striatum and low OXT levels within hippocampal neurons might be prerequisites for high performance in the conditioned BD reaction.     

Synaptosomal Membrane Fluidity, Lipid Peroxidation and Superoxide Dismutase Activity in the Brain of Amygdala-Kindled Rats

Abstract: Synaptosomal membrane fluidity, lipid peroxide (LPO) and cytosolic superoxide dismutase (SOD) activity were examined in various brain regions (amygdala, hippocampus, striatum and frontal cortex) of amygdala-kindled rats. At 24 h after the last seizure, a significant increase of membrane fluidity was observed in all the regions examined, whereas the LPO level was sigdflcantly decreased in the four regions with enhanced activity of cytosolic SOD. At 7 days after the last seizure, membrane fluidity was decreased only in the hippocampus. At 6 weeks after the last seizure, there were no changes in membrane fluidity between control and kindled rats. These results suggest that membrane fluidity and lipid peroxidation are modulated transiently by a kindled seizure, but not at a steady state of kindling with enduring seizure susceptibility.