The biological basis of the clinical efficacy of lithium in the treatment of mental illness has b... more The biological basis of the clinical efficacy of lithium in the treatment of mental illness has been extensively studied in neurones, but little is known about the effects of the drug on glia. Recently we showed that treatment of rats with clinically relevant doses of lithium chloride results in a 35% increase in the immunocontent of the astrocyte marker GFAP in the hippocampus. Here we studied the cytology of this phenomenon. Rats were treated for 4 weeks with a lithium diet which resulted in serum Li+ concentrations of 0.6-1.2 mmol/l. GFAP immunocytochemistry of the hippocampus revealed a mild gliosis in the CA1 area and the dentate gyrus which was associated with a change in the orientation of astrocytic processes. In control animals astrocyte processes were mainly orientated perpendicular to the stratum pyramidale, whereas in treated animals the cells were predominantly stellar in appearance.
S100B is a calcium-binding protein expressed and secreted by astrocytes, playing a neurotrophic r... more S100B is a calcium-binding protein expressed and secreted by astrocytes, playing a neurotrophic role in neighboring cells. A protective role of the S100B against glutamate-induced excitotoxicity has recently been proposed. We investigated S100B secretion in rat hippocampal astrocytes exposed to high concentrations of glutamate during serum deprivation (stimulated condition) or not (basal condition), for 30 min. Glutamate at 1 mM had no effect on basal secretion of S100B, but it decreased S100B secretion in serum-deprived astrocytes after 1 h. Secretion was inhibited by Rp-cAMPS or H89. In addition, serum deprivation was accompanied by a transitory increase of intracellular content of cAMP. Our results suggest that high levels of glutamate in a serum-deprived condition could impair S100B secretion from hippocampal astrocytes.
This study was undertaken to evaluate the effects of chronic variate stress and lithium treatment... more This study was undertaken to evaluate the effects of chronic variate stress and lithium treatment on glutamatergic activity and neuronal vulnerability of rat hippocampus. Male Wistar rats were simultaneously treated with lithium and submitted to a chronic variate stress protocol during 40 days, and afterwards the hippocampal glutamatergic uptake and release, measured in slices and synaptosomes, were evaluated. We observed an increased synaptosomal [(3)H]glutamate uptake and an increase in [(3)H]glutamate stimulated release in hippocampus of lithium-treated rats. Chronic stress increased basal [(3)H]glutamate release by synaptosomes, and decreased [(3)H]glutamate uptake in hippocampal slices. When evaluating cellular vulnerability, both stress and lithium increased cellular death after oxygen and glucose deprivation (OGD). We suggest that the manipulation of glutamatergic activity induced by stress may be in part responsible for the neuroendangerment observed after stress exposure, and that, in spite of the described neuroprotective effects of lithium, it increased the neuronal vulnerability after OGD.
This study was undertaken to verify the effects of chronic stress and lithium treatments on the h... more This study was undertaken to verify the effects of chronic stress and lithium treatments on the hippocampal Na+,K(+)-ATPase activity of rats, as well as to investigate the effects of stress interruption and post-stress lithium treatment on this enzyme activity and on spatial memory. Two experiments were carried out; in the first experiment, adult male Wistar rats were divided into two groups: control and submitted to a chronic variate stress paradigm, and subdivided into treated or not with LiCl. After 40 days of treatment, rats were killed, and Na+,K(+)-ATPase activity was determined. In the second experiment, rats were stressed during 40 days, and their performance was evaluated in the Water Maze task. The stressed group was then subdivided into four groups, with continued or interrupted stress treatment and treated or not with lithium for 30 additional days. After a second evaluation of performance in the Water Maze, rats were killed and Na+,K(+)-ATPase activity was also measured. Results showed an impairment in Na+,K(+)-ATPase activity and in Water Maze performance of chronically stressed rats, which were prevented by lithium treatment and reversed by lithium treatment and by stress interruption. These results suggest that the modulation of Na+,K(+)-ATPase activity may be one of the mechanisms of action of lithium in the treatment of mood disorders.
To evaluate predictors of somatization and pain reactivity in childhood. Facial expressions of ch... more To evaluate predictors of somatization and pain reactivity in childhood. Facial expressions of children undergoing inoculation were scored for pain reactivity. Measures of temperament, pain experience, pain models, parental behavior, and parental ability to decode pain were examined for their ability to predict pain reactivity and somatization in a structural modeling analysis. Pain reactivity was associated positively with parental reports of their child's somatization. Child temperament, previous negative experiences with medical procedures, and maternal responses to their children's pain were positively associated with pain reactivity. Temperament and pain experience may play a role in children's pain reactivity, and reactivity may contribute to the development of somatization. Although the model that guided the analysis proved to be a reasonable description of the outcomes, several anticipated relationships were not significant. We discuss implications for a refined model of somatization and for early identification and prevention.
The present study evaluated the effects of exposure to facial expression of pain, on observers&am... more The present study evaluated the effects of exposure to facial expression of pain, on observers' perceptions of pain expression. Participants were undergraduates shown brief video clips of the facial expressions of shoulder-pain patients displaying no pain or moderate pain. Participants were randomly allocated to either a high preexposure condition in which each clip was preceded by 10 other clips showing strong pain or a no-exposure control. On each test trial, participants indicated whether they thought the person they saw was in pain or not. Data were analyzed using signal detection theory methods. High prior exposure to pain was unrelated to sensitivity to pain expression, but did significantly diminish the likelihood of judging the other to be in pain. Results are discussed in terms of their implications for pain judgments of health-care professionals, adaptation-level theory, and the psychophysical method of selective adaptation. This paper provides an experimental demonstration that, when people have large amounts of exposure to others' expressions of pain, their estimation of others' pain is reduced. The findings offer 1 explanation for the widely observed underestimation bias in pain judgments and may suggest ways of changing it.
Stress is known to alter cognitive functions, such as memory, and it has been linked to the patho... more Stress is known to alter cognitive functions, such as memory, and it has been linked to the pathophysiology of mood and anxiety disorders. Chronic lithium treatment is used in some psychiatric disorders and has been suggested to act upon mechanisms which can enhance neuronal viability. The purpose of this work is to investigate a possible effect of lithium treatment in
The biological basis of the clinical efficacy of lithium in the treatment of mental illness has b... more The biological basis of the clinical efficacy of lithium in the treatment of mental illness has been extensively studied in neurones, but little is known about the effects of the drug on glia. Recently we showed that treatment of rats with clinically relevant doses of lithium chloride results in a 35% increase in the immunocontent of the astrocyte marker GFAP in the hippocampus. Here we studied the cytology of this phenomenon. Rats were treated for 4 weeks with a lithium diet which resulted in serum Li+ concentrations of 0.6-1.2 mmol/l. GFAP immunocytochemistry of the hippocampus revealed a mild gliosis in the CA1 area and the dentate gyrus which was associated with a change in the orientation of astrocytic processes. In control animals astrocyte processes were mainly orientated perpendicular to the stratum pyramidale, whereas in treated animals the cells were predominantly stellar in appearance.
S100B is a calcium-binding protein expressed and secreted by astrocytes, playing a neurotrophic r... more S100B is a calcium-binding protein expressed and secreted by astrocytes, playing a neurotrophic role in neighboring cells. A protective role of the S100B against glutamate-induced excitotoxicity has recently been proposed. We investigated S100B secretion in rat hippocampal astrocytes exposed to high concentrations of glutamate during serum deprivation (stimulated condition) or not (basal condition), for 30 min. Glutamate at 1 mM had no effect on basal secretion of S100B, but it decreased S100B secretion in serum-deprived astrocytes after 1 h. Secretion was inhibited by Rp-cAMPS or H89. In addition, serum deprivation was accompanied by a transitory increase of intracellular content of cAMP. Our results suggest that high levels of glutamate in a serum-deprived condition could impair S100B secretion from hippocampal astrocytes.
This study was undertaken to evaluate the effects of chronic variate stress and lithium treatment... more This study was undertaken to evaluate the effects of chronic variate stress and lithium treatment on glutamatergic activity and neuronal vulnerability of rat hippocampus. Male Wistar rats were simultaneously treated with lithium and submitted to a chronic variate stress protocol during 40 days, and afterwards the hippocampal glutamatergic uptake and release, measured in slices and synaptosomes, were evaluated. We observed an increased synaptosomal [(3)H]glutamate uptake and an increase in [(3)H]glutamate stimulated release in hippocampus of lithium-treated rats. Chronic stress increased basal [(3)H]glutamate release by synaptosomes, and decreased [(3)H]glutamate uptake in hippocampal slices. When evaluating cellular vulnerability, both stress and lithium increased cellular death after oxygen and glucose deprivation (OGD). We suggest that the manipulation of glutamatergic activity induced by stress may be in part responsible for the neuroendangerment observed after stress exposure, and that, in spite of the described neuroprotective effects of lithium, it increased the neuronal vulnerability after OGD.
This study was undertaken to verify the effects of chronic stress and lithium treatments on the h... more This study was undertaken to verify the effects of chronic stress and lithium treatments on the hippocampal Na+,K(+)-ATPase activity of rats, as well as to investigate the effects of stress interruption and post-stress lithium treatment on this enzyme activity and on spatial memory. Two experiments were carried out; in the first experiment, adult male Wistar rats were divided into two groups: control and submitted to a chronic variate stress paradigm, and subdivided into treated or not with LiCl. After 40 days of treatment, rats were killed, and Na+,K(+)-ATPase activity was determined. In the second experiment, rats were stressed during 40 days, and their performance was evaluated in the Water Maze task. The stressed group was then subdivided into four groups, with continued or interrupted stress treatment and treated or not with lithium for 30 additional days. After a second evaluation of performance in the Water Maze, rats were killed and Na+,K(+)-ATPase activity was also measured. Results showed an impairment in Na+,K(+)-ATPase activity and in Water Maze performance of chronically stressed rats, which were prevented by lithium treatment and reversed by lithium treatment and by stress interruption. These results suggest that the modulation of Na+,K(+)-ATPase activity may be one of the mechanisms of action of lithium in the treatment of mood disorders.
To evaluate predictors of somatization and pain reactivity in childhood. Facial expressions of ch... more To evaluate predictors of somatization and pain reactivity in childhood. Facial expressions of children undergoing inoculation were scored for pain reactivity. Measures of temperament, pain experience, pain models, parental behavior, and parental ability to decode pain were examined for their ability to predict pain reactivity and somatization in a structural modeling analysis. Pain reactivity was associated positively with parental reports of their child's somatization. Child temperament, previous negative experiences with medical procedures, and maternal responses to their children's pain were positively associated with pain reactivity. Temperament and pain experience may play a role in children's pain reactivity, and reactivity may contribute to the development of somatization. Although the model that guided the analysis proved to be a reasonable description of the outcomes, several anticipated relationships were not significant. We discuss implications for a refined model of somatization and for early identification and prevention.
The present study evaluated the effects of exposure to facial expression of pain, on observers&am... more The present study evaluated the effects of exposure to facial expression of pain, on observers' perceptions of pain expression. Participants were undergraduates shown brief video clips of the facial expressions of shoulder-pain patients displaying no pain or moderate pain. Participants were randomly allocated to either a high preexposure condition in which each clip was preceded by 10 other clips showing strong pain or a no-exposure control. On each test trial, participants indicated whether they thought the person they saw was in pain or not. Data were analyzed using signal detection theory methods. High prior exposure to pain was unrelated to sensitivity to pain expression, but did significantly diminish the likelihood of judging the other to be in pain. Results are discussed in terms of their implications for pain judgments of health-care professionals, adaptation-level theory, and the psychophysical method of selective adaptation. This paper provides an experimental demonstration that, when people have large amounts of exposure to others' expressions of pain, their estimation of others' pain is reduced. The findings offer 1 explanation for the widely observed underestimation bias in pain judgments and may suggest ways of changing it.
Stress is known to alter cognitive functions, such as memory, and it has been linked to the patho... more Stress is known to alter cognitive functions, such as memory, and it has been linked to the pathophysiology of mood and anxiety disorders. Chronic lithium treatment is used in some psychiatric disorders and has been suggested to act upon mechanisms which can enhance neuronal viability. The purpose of this work is to investigate a possible effect of lithium treatment in
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