Elizabete Rocha - Academia.edu (original) (raw)

Papers by Elizabete Rocha

Research paper thumbnail of Lithium treatment causes gliosis and modifies the morphology of hippocampal astrocytes in rats

NeuroReport, 1998

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.

Research paper thumbnail of The nociceptive response of stressed and lithium-treated rats is differently modulated by different flavors

Physiology & Behavior, 2006

Pleasant and unpleasant flavors and odors can modulate pain perception, and the efficacy of sweet... more Pleasant and unpleasant flavors and odors can modulate pain perception, and the efficacy of sweet flavors in reducing pain seems to be related to its hedonic value. Chronic variate stress paradigm is a model of depression, and is suggested to induce anhedonia. We observed previously that lithium may prevent behavioral and neurochemical alterations induced by chronic stress; so we hypothesized that chronically stressed animals may present different nociceptive response to pleasant and unpleasant tastes that could be prevented by lithium treatment. Adult male Wistar rats were divided into four groups, control and stressed, treated or not with lithium. A Chronic Variate Stress paradigm was used, and lithium was added to the chow. After 40 days of treatment, the tail flick latency of the animals was evaluated, and rats were immediately placed in a box with access to a 5% acetic acid solution (acid flavor). After 5 min, tail flick latency was measured again. On the following day, animals were submitted to the same procedure, with the substitution of acetic acid by condensed sweet milk (sweet flavor). The stressed group was the only group who did not present analgesia after sweet taste exposition. All groups, except the control group, presented increased tail flick latency after exposition to the acid flavor. These results indicate that pleasant and unpleasant flavors present different relevance for the induction of antinociception in stressed animals, and the absence of sweet flavor-induced analgesia may represent an anhedonic effect of the chronic variate stress paradigm. On the other hand, perception of different flavors may be more prominent in animals treated with lithium.

Research paper thumbnail of Chronic treatment with lithium increases the ecto-nucleotidase activities in rat hippocampal synatosomes

Neuroscience Letters, 2004

Lithium is a mood-stabilizing treatment used in bipolar and other psychiatric disorders. The mole... more Lithium is a mood-stabilizing treatment used in bipolar and other psychiatric disorders. The molecular mechanisms underlying lithium action remain poorly understood. Adenosine is a neuromodulator that possesses anticonvulsant and neuroprotective properties and the ectonucleotidase pathway is a metabolic source of the extracellular adenosine. Here we investigated the effect of lithium on the ecto-nucleotidase pathway in synaptosomes from hippocampus and cerebral cortex of adult rats. Male Wistar rats received standard rat chow with lithium chloride (2.5 mg/g of chow) and NaCl (17 mg/g of chow) during 4 weeks. The serum lithium levels were 1.18 ± 0.05 mEq./L. ATP and AMP hydrolysis was significantly increased (20 and 35%, respectively) in hippocampal synaptosomes of rats chronically treated with lithium chloride. No significant differences were observed in the hydrolysis of the three nucleotides by cortical synaptosomes. In conclusion, the modulation of the ecto-nucleotidase pathway may be a new explanation for the potential neuroprotective lithium action in hippocampal lesions.

Research paper thumbnail of High glutamate decreases S100B secretion stimulated by serum deprivation in astrocytes

Neuroreport, 2002

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.

Research paper thumbnail of Lithium and Valproate Protect Hippocampal Slices Against ATP-induced Cell Death

Neurochemical Research, 2007

Lithium and valproate (VPA) are the most commonly prescribed mood-stabilizing drugs. Recently, se... more Lithium and valproate (VPA) are the most commonly prescribed mood-stabilizing drugs. Recently, several studies have reported their neuroprotective properties in several models of neural toxicity and, in some pathological conditions, large amounts of intracellular ATP can be released from damaged cells. In the present study, we investigate the potential neuroprotective effect of lithium and VPA against ATP-induced cell death in hippocampal slices of adult rats. Acute (in vitro) and chronic (in vivo) treatment at therapeutic doses with lithium or VPA significantly prevent the ATP-induced cell death. Lithium and VPA also exerted a synergic effect in the prevention of ATP-induced cell death. Moreover, hippocampal slices prepared from rats chronically treated with lithium or VPA presented a significant reduction in cell death in the presence of cytotoxic extracellular ATP. Although further investigations are necessary, our results show the neuroprotective effect of lithium and VPA against neuronal death induced by extracellular ATP, probably through a different pathway, and suggest novel uses of these drugs in neurogenerative diseases.

Research paper thumbnail of Chronic Lithium Treatment has Antioxidant Properties but does not Prevent Oxidative Damage Induced by Chronic Variate Stress

Neurochemical Research, 2006

This study evaluated the effects of chronic stress and lithium treatments on oxidative stress par... more This study evaluated the effects of chronic stress and lithium treatments on oxidative stress parameters in hippocampus, hypothalamus, and frontal cortex. Adult male Wistar rats were divided into two groups: control and submitted to chronic variate stress, and subdivided into treated or not with LiCl. After 40 days, rats were killed, and lipoperoxidation, production free radicals, total antioxidant reactivity (TAR) levels, and superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities were evaluated. The results showed that stress increased lipoperoxidation and that lithium decreased free radicals production in hippocampus; both treatments increased TAR. In hypothalamus, lithium increased TAR and no effect was observed in the frontal cortex. Stress increased SOD activity in hippocampus; while lithium increased GPx in hippocampus and SOD in hypothalamus. We concluded that lithium presented antioxidant properties, but is not able to prevent oxidative damage induced by chronic variate stress.

Research paper thumbnail of Chronic Stress and Lithium Treatments Alter Hippocampal Glutamate Uptake and Release in the Rat and Potentiate Necrotic Cellular Death After Oxygen and Glucose Deprivation

Neurochemical Research, 2011

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.

Research paper thumbnail of Na+,K+-ATPase activity is reduced in hippocampus of rats submitted to an experimental model of depression: Effect of chronic lithium treatment and possible involvement in learning deficits

Neurobiology of Learning and Memory, 2005

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.

Research paper thumbnail of Pain Reactivity and Somatization in Kindergarten-Age Children

Journal of Pediatric Psychology, 2003

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.

Research paper thumbnail of Temperament and Pain Reactivity Predict Health Behavior Seven Years Later

Journal of Pediatric Psychology, 2006

Objective Minor illnesses and major diseases are affected by individual, environmental, and socia... more Objective Minor illnesses and major diseases are affected by individual, environmental, and social factors. We sought to determine if children's temperament and pain reactivity (individual response styles) measured in kindergarten are related to future health behavior. Methods Seven-year follow-up measures of health behavior were gathered in 42 children (mean age M ¼ 11 years) who participated in a previous study of pain reactivity and somatization. Current health behavior was compared with children's pain reactivity and temperament measured in kindergarten. Results Pain reactivity in kindergarten was associated with children's self-reports of somatization 7 years later, independent of their temperament. Temperament was related to children's self-reports of somatization and to maternal reports of health care utilization and psychosocial health status. Conclusions Early response styles (i.e., heightened pain reactivity and difficulty adjusting) may indicate risk for increased health care utilization and poorer health and well-being later in childhood.

Research paper thumbnail of Children's memory for pain: overview and implications for practice

The Journal of Pain, 2004

Children's memories of painful experiences can have long-term consequences for their reaction to ... more Children's memories of painful experiences can have long-term consequences for their reaction to later painful events and their acceptance of later health care interventions. This review surveys research on children's memory for pain, emphasizing implications for clinical practice. Topics reviewed include consequences of children's memories of pain; the development of memory; differences between explicit (declarative, verbal, autobiographic) memory and implicit (nondeclarative, nonverbal) memory; and individual differences, situational, and methodologic factors affecting memories of pain. Methods to prevent the adverse consequences of remembered pain are addressed with reference to current research on editing or reframing memories.

Research paper thumbnail of High Levels of Vicarious Exposure Bias Pain Judgments

The Journal of Pain, 2010

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.

Research paper thumbnail of Effect of chronic stress on spatial memory in rats is attenuated by lithium treatment

Physiology & Behavior, 2003

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

Research paper thumbnail of An investigation of the neuroprotective effect of lithium in organotypic slice cultures of rat hippocampus exposed to oxygen and glucose deprivation

Neuroscience Letters, 2001

Brain ischemia results in cellular degeneration and loss of function. Here we investigated the ne... more Brain ischemia results in cellular degeneration and loss of function. Here we investigated the neuroprotective effect of lithium in an in vitro model of ischemia. Organotypic hippocampal slice cultures were exposed to oxygen and glucose deprivation. Cellular death was quantified by measuring uptake of propidium iodide (PI). Lithium chloride (0.2-1.2 mM) was added to the medium before, during and after lesion induction. A decrease in incorporation of PI was observed, indicating a neuroprotective effect in all doses tested. We also studied the effect of lithium on the phosphorylation of HSP27, a heat shock protein involved in cellular protection in its dephosphorylated state. In the lesioned hippocampus, 0.4 mM lithium chloride decreased the proportion of phosphorylated HSP27 to total HSP27. These results suggest that lithium may be useful in the treatment of brain ischemia. q

Research paper thumbnail of Lithium treatment causes gliosis and modifies the morphology of hippocampal astrocytes in rats

NeuroReport, 1998

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.

Research paper thumbnail of The nociceptive response of stressed and lithium-treated rats is differently modulated by different flavors

Physiology & Behavior, 2006

Pleasant and unpleasant flavors and odors can modulate pain perception, and the efficacy of sweet... more Pleasant and unpleasant flavors and odors can modulate pain perception, and the efficacy of sweet flavors in reducing pain seems to be related to its hedonic value. Chronic variate stress paradigm is a model of depression, and is suggested to induce anhedonia. We observed previously that lithium may prevent behavioral and neurochemical alterations induced by chronic stress; so we hypothesized that chronically stressed animals may present different nociceptive response to pleasant and unpleasant tastes that could be prevented by lithium treatment. Adult male Wistar rats were divided into four groups, control and stressed, treated or not with lithium. A Chronic Variate Stress paradigm was used, and lithium was added to the chow. After 40 days of treatment, the tail flick latency of the animals was evaluated, and rats were immediately placed in a box with access to a 5% acetic acid solution (acid flavor). After 5 min, tail flick latency was measured again. On the following day, animals were submitted to the same procedure, with the substitution of acetic acid by condensed sweet milk (sweet flavor). The stressed group was the only group who did not present analgesia after sweet taste exposition. All groups, except the control group, presented increased tail flick latency after exposition to the acid flavor. These results indicate that pleasant and unpleasant flavors present different relevance for the induction of antinociception in stressed animals, and the absence of sweet flavor-induced analgesia may represent an anhedonic effect of the chronic variate stress paradigm. On the other hand, perception of different flavors may be more prominent in animals treated with lithium.

Research paper thumbnail of Chronic treatment with lithium increases the ecto-nucleotidase activities in rat hippocampal synatosomes

Neuroscience Letters, 2004

Lithium is a mood-stabilizing treatment used in bipolar and other psychiatric disorders. The mole... more Lithium is a mood-stabilizing treatment used in bipolar and other psychiatric disorders. The molecular mechanisms underlying lithium action remain poorly understood. Adenosine is a neuromodulator that possesses anticonvulsant and neuroprotective properties and the ectonucleotidase pathway is a metabolic source of the extracellular adenosine. Here we investigated the effect of lithium on the ecto-nucleotidase pathway in synaptosomes from hippocampus and cerebral cortex of adult rats. Male Wistar rats received standard rat chow with lithium chloride (2.5 mg/g of chow) and NaCl (17 mg/g of chow) during 4 weeks. The serum lithium levels were 1.18 ± 0.05 mEq./L. ATP and AMP hydrolysis was significantly increased (20 and 35%, respectively) in hippocampal synaptosomes of rats chronically treated with lithium chloride. No significant differences were observed in the hydrolysis of the three nucleotides by cortical synaptosomes. In conclusion, the modulation of the ecto-nucleotidase pathway may be a new explanation for the potential neuroprotective lithium action in hippocampal lesions.

Research paper thumbnail of High glutamate decreases S100B secretion stimulated by serum deprivation in astrocytes

Neuroreport, 2002

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.

Research paper thumbnail of Lithium and Valproate Protect Hippocampal Slices Against ATP-induced Cell Death

Neurochemical Research, 2007

Lithium and valproate (VPA) are the most commonly prescribed mood-stabilizing drugs. Recently, se... more Lithium and valproate (VPA) are the most commonly prescribed mood-stabilizing drugs. Recently, several studies have reported their neuroprotective properties in several models of neural toxicity and, in some pathological conditions, large amounts of intracellular ATP can be released from damaged cells. In the present study, we investigate the potential neuroprotective effect of lithium and VPA against ATP-induced cell death in hippocampal slices of adult rats. Acute (in vitro) and chronic (in vivo) treatment at therapeutic doses with lithium or VPA significantly prevent the ATP-induced cell death. Lithium and VPA also exerted a synergic effect in the prevention of ATP-induced cell death. Moreover, hippocampal slices prepared from rats chronically treated with lithium or VPA presented a significant reduction in cell death in the presence of cytotoxic extracellular ATP. Although further investigations are necessary, our results show the neuroprotective effect of lithium and VPA against neuronal death induced by extracellular ATP, probably through a different pathway, and suggest novel uses of these drugs in neurogenerative diseases.

Research paper thumbnail of Chronic Lithium Treatment has Antioxidant Properties but does not Prevent Oxidative Damage Induced by Chronic Variate Stress

Neurochemical Research, 2006

This study evaluated the effects of chronic stress and lithium treatments on oxidative stress par... more This study evaluated the effects of chronic stress and lithium treatments on oxidative stress parameters in hippocampus, hypothalamus, and frontal cortex. Adult male Wistar rats were divided into two groups: control and submitted to chronic variate stress, and subdivided into treated or not with LiCl. After 40 days, rats were killed, and lipoperoxidation, production free radicals, total antioxidant reactivity (TAR) levels, and superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities were evaluated. The results showed that stress increased lipoperoxidation and that lithium decreased free radicals production in hippocampus; both treatments increased TAR. In hypothalamus, lithium increased TAR and no effect was observed in the frontal cortex. Stress increased SOD activity in hippocampus; while lithium increased GPx in hippocampus and SOD in hypothalamus. We concluded that lithium presented antioxidant properties, but is not able to prevent oxidative damage induced by chronic variate stress.

Research paper thumbnail of Chronic Stress and Lithium Treatments Alter Hippocampal Glutamate Uptake and Release in the Rat and Potentiate Necrotic Cellular Death After Oxygen and Glucose Deprivation

Neurochemical Research, 2011

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.

Research paper thumbnail of Na+,K+-ATPase activity is reduced in hippocampus of rats submitted to an experimental model of depression: Effect of chronic lithium treatment and possible involvement in learning deficits

Neurobiology of Learning and Memory, 2005

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.

Research paper thumbnail of Pain Reactivity and Somatization in Kindergarten-Age Children

Journal of Pediatric Psychology, 2003

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.

Research paper thumbnail of Temperament and Pain Reactivity Predict Health Behavior Seven Years Later

Journal of Pediatric Psychology, 2006

Objective Minor illnesses and major diseases are affected by individual, environmental, and socia... more Objective Minor illnesses and major diseases are affected by individual, environmental, and social factors. We sought to determine if children's temperament and pain reactivity (individual response styles) measured in kindergarten are related to future health behavior. Methods Seven-year follow-up measures of health behavior were gathered in 42 children (mean age M ¼ 11 years) who participated in a previous study of pain reactivity and somatization. Current health behavior was compared with children's pain reactivity and temperament measured in kindergarten. Results Pain reactivity in kindergarten was associated with children's self-reports of somatization 7 years later, independent of their temperament. Temperament was related to children's self-reports of somatization and to maternal reports of health care utilization and psychosocial health status. Conclusions Early response styles (i.e., heightened pain reactivity and difficulty adjusting) may indicate risk for increased health care utilization and poorer health and well-being later in childhood.

Research paper thumbnail of Children's memory for pain: overview and implications for practice

The Journal of Pain, 2004

Children's memories of painful experiences can have long-term consequences for their reaction to ... more Children's memories of painful experiences can have long-term consequences for their reaction to later painful events and their acceptance of later health care interventions. This review surveys research on children's memory for pain, emphasizing implications for clinical practice. Topics reviewed include consequences of children's memories of pain; the development of memory; differences between explicit (declarative, verbal, autobiographic) memory and implicit (nondeclarative, nonverbal) memory; and individual differences, situational, and methodologic factors affecting memories of pain. Methods to prevent the adverse consequences of remembered pain are addressed with reference to current research on editing or reframing memories.

Research paper thumbnail of High Levels of Vicarious Exposure Bias Pain Judgments

The Journal of Pain, 2010

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.

Research paper thumbnail of Effect of chronic stress on spatial memory in rats is attenuated by lithium treatment

Physiology & Behavior, 2003

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

Research paper thumbnail of An investigation of the neuroprotective effect of lithium in organotypic slice cultures of rat hippocampus exposed to oxygen and glucose deprivation

Neuroscience Letters, 2001

Brain ischemia results in cellular degeneration and loss of function. Here we investigated the ne... more Brain ischemia results in cellular degeneration and loss of function. Here we investigated the neuroprotective effect of lithium in an in vitro model of ischemia. Organotypic hippocampal slice cultures were exposed to oxygen and glucose deprivation. Cellular death was quantified by measuring uptake of propidium iodide (PI). Lithium chloride (0.2-1.2 mM) was added to the medium before, during and after lesion induction. A decrease in incorporation of PI was observed, indicating a neuroprotective effect in all doses tested. We also studied the effect of lithium on the phosphorylation of HSP27, a heat shock protein involved in cellular protection in its dephosphorylated state. In the lesioned hippocampus, 0.4 mM lithium chloride decreased the proportion of phosphorylated HSP27 to total HSP27. These results suggest that lithium may be useful in the treatment of brain ischemia. q