RESUMO
Iron (Fe) is used in various cellular functions, and a constant balance between its uptake, transport, storage, and use is necessary to maintain its homeostasis in the body. Changes in Fe metabolism with a consequent overload of this metal are related to neurological changes and cover a broad spectrum of diseases, mainly when these changes occur during the embryonic period. This work aimed to evaluate the effect of exposure to Fe overload during the embryonic period of Drosophila melanogaster. Progenitor flies (male and female) were exposed to ferrous sulfate (FeSO4) for ten days in concentrations of 0.5, 1, and 5 âmM. After mating and oviposition, the progenitors were removed and the treatment bottles preserved, and the number of daily hatches and cumulative hatching of the first filial generation (F1) were counted. Subsequently, F1 flies (separated by sex) were subjected to behavioral tests such as negative geotaxis test, open field test, grooming, and aggression test. They have evaluated the levels of dopamine (DA), serotonin (5-HT), octopamine (OA), tryptophan and tyrosine hydroxylase (TH), acetylcholinesterase, reactive species, and the levels of Fe in the progenitor flies and F1. The Fe levels of F1 flies are directly proportional to what is incorporated during the period of embryonic development; we also observed a delay in hatching and a reduction in the number of the hatch of F1 flies exposed during the embryonic period to the 5mM Fe diet, a fact that may be related to the reduction of the cell viability of the ovarian tissue of progenitor flies. The flies exposed to Fe (1 and 5 âmM) showed an increase in locomotor activity (hyperactivity) and a significantly higher number of repetitive movements. In addition to a high number of aggressive encounters when compared to control flies. We can also observe an increase in the levels of biogenic amines DA and 5-HT and an increase in TH activity in flies exposed to Fe (1 and 5 âmM) compared to the control group. We conclude that the hyperactive-like behavior demonstrated in both sexes by F1 flies exposed to Fe may be associated with a dysregulation in the levels of DA and 5-HT since Fe is a cofactor of TH, which had its activity increased in this study. Therefore, more attention is needed during the embryonic development period for exposure to Fe overload.
Assuntos
Drosophila melanogaster/embriologia , Hipercinese/fisiopatologia , Sobrecarga de Ferro/embriologia , Animais , Comportamento Animal/fisiologia , Aminas Biogênicas/metabolismo , Aminas Biogênicas/fisiologia , Proteínas de Drosophila/metabolismo , Drosophila melanogaster/metabolismo , Feminino , Expressão Gênica/genética , Regulação da Expressão Gênica no Desenvolvimento/genética , Hipercinese/etiologia , Ferro/metabolismo , Ferro/fisiologia , Ferro/toxicidade , Sobrecarga de Ferro/metabolismo , Sobrecarga de Ferro/fisiopatologia , Locomoção/efeitos dos fármacos , Masculino , Exposição Materna , Atividade Motora/efeitos dos fármacos , Oxirredução , Exposição PaternaRESUMO
Bipolar disorder is a psychiatric pathology characterized by biphasic mood episodes of mania or hypomania and depression. The pharmacotherapy of bipolar disorder has significant adverse effects impairing treatment adherence and patient quality of life. The N/OFQ-NOP receptor system has been widely implicated with mood disorders. Clinical and preclinical findings suggest antidepressants actions for NOP antagonists. More recently, the administration of NOP agonists has shown to promote depressant states. The present study aimed to investigate the effects of non-peptide NOP ligands in methylphenidate-induced manic-like behavior in mice. The NOP agonist Ro 65-6570 (0.01-1 mg/kg, ip), at the higher dose, did not affect spontaneous locomotion per se, but prevented the methylphenidate (10 mg/kg, sc)-induced hyperlocomotion. The NOP partial agonist AT-090 (0.001-0.03 mg/kg, ip) and the NOP antagonist SB-612111 (1-10 mg/kg, ip) did not significantly affect the psychostimulant-induced hyperactivity. Experiments performed with mice lacking the NOP receptor (NOP(-/-)) demonstrated that the treatment with methylphenidate induced similar hyperlocomotion in NOP(-/-) and NOP(+/+) mice. In conclusion, these findings suggest a potential role for NOP agonists in the prevention of manic states, especially by counteracting the hyperactivity symptom of bipolar patients. However, more studies are necessary in order to evaluate these compounds in other features of bipolar disorder.
Assuntos
Antimaníacos/administração & dosagem , Transtorno Bipolar/fisiopatologia , Hipercinese/fisiopatologia , Imidazóis/administração & dosagem , Metilfenidato/administração & dosagem , Receptores Opioides/fisiologia , Compostos de Espiro/administração & dosagem , Animais , Feminino , Hipercinese/induzido quimicamente , Camundongos , Receptores Opioides/agonistas , Ácido Valproico/administração & dosagem , Receptor de NociceptinaRESUMO
Neonatal hypoxic-ischemic (HI) encephalopathy is a major cause of perinatal morbimortality. There is growing evidence that n-3 polyunsaturated fatty acids, especially docosahexaenoic acid (DHA), attenuate brain injury. This study aimed to investigate the possible neuroprotective effect of maternal intake of flaxseed, rich in DHA׳s precursor α-linolenic acid, in the young male offspring subjected to perinatal HI. Wistar rats were divided in six groups, according to maternal diet and offspring treatment at day 7: Control HI (CHI) and Flaxseed HI (FHI); Control Sham and Flaxseed Sham; Control Control and Flaxseed Control. Flaxseed diet increased offspring׳s hippocampal DHA content and lowered depressive behavior. CHI pups presented brain mass loss, motor hyperactivity and poor spatial memory, which were improved in FHI rats. Maternal flaxseed intake may prevent depressive symptoms in the offspring and promote neuroprotective effects, in the context of perinatal HI, improving brain injury and its cognitive and behavioral impairments.
Assuntos
Encéfalo/efeitos dos fármacos , Linho/química , Hipercinese/prevenção & controle , Hipóxia-Isquemia Encefálica/prevenção & controle , Extratos Vegetais/farmacologia , Memória Espacial/efeitos dos fármacos , Análise de Variância , Animais , Animais Recém-Nascidos , Encéfalo/metabolismo , Encéfalo/patologia , Lesões Encefálicas/fisiopatologia , Lesões Encefálicas/prevenção & controle , Ácidos Docosa-Hexaenoicos/administração & dosagem , Ácidos Docosa-Hexaenoicos/farmacologia , Feminino , Hipercinese/fisiopatologia , Hipóxia-Isquemia Encefálica/fisiopatologia , Masculino , Fármacos Neuroprotetores/administração & dosagem , Fármacos Neuroprotetores/farmacologia , Extratos Vegetais/administração & dosagem , Extratos Vegetais/química , Gravidez , Ratos , Ratos Wistar , Sementes/química , Fatores de Tempo , Ácido alfa-Linolênico/administração & dosagem , Ácido alfa-Linolênico/farmacologiaRESUMO
In this study, we describe three patients who each had an electroclinical overlap of two different epileptic encephalopathies (EE), with onset in a certain age period. Patient 1 had electroclinical features compatible with continuous spikes and waves during slow sleep (CSWSS) syndrome that changed into Lennox-Gastaut syndrome (LGS) (symptomatic, cause porencephalic cyst) at the age of 8.5 years. Patient 2 had LGS which evolved into CSWSS at the age of 6 years (symptomatic, cause polymicrogyria). The third patient had cryptogenic CSWSS syndrome at age the age of 7 years which evolved into LGS at the age of 7.5 years. All three patients could be considered to have two EE: CSWSS syndrome and LGS or to have had overlapping features of these epileptic syndromes.
Assuntos
Encefalopatias/fisiopatologia , Eletroencefalografia , Epilepsia/fisiopatologia , Agressão/psicologia , Encefalopatias/complicações , Cistos do Sistema Nervoso Central/complicações , Cistos do Sistema Nervoso Central/psicologia , Criança , Pré-Escolar , Progressão da Doença , Epilepsia/etiologia , Epilepsia Rolândica/fisiopatologia , Epilepsia Tônico-Clônica/fisiopatologia , Transtornos Neurológicos da Marcha/etiologia , Transtornos Neurológicos da Marcha/fisiopatologia , Humanos , Hipercinese/etiologia , Hipercinese/fisiopatologia , Deficiência Intelectual/fisiopatologia , Deficiências da Aprendizagem/etiologia , Deficiências da Aprendizagem/psicologia , Síndrome de Lennox-Gastaut , Masculino , Malformações do Desenvolvimento Cortical/complicações , Malformações do Desenvolvimento Cortical/psicologia , Transtornos dos Movimentos/complicações , Transtornos dos Movimentos/psicologia , Convulsões/fisiopatologia , Sono/fisiologia , Transtornos do Sono-Vigília/fisiopatologia , Espasmos Infantis/fisiopatologiaRESUMO
The interaction between sleep deprivation and epilepsy has been well described in electrophysiological studies, but the mechanisms underlying this association remain unclear. The present study evaluated the effects of sleep deprivation on locomotor activity and genetic damage in the brains of rats treated with saline or pilocarpine-induced status epilepticus (SE). After 50 days of pilocarpine or saline treatment, both groups were assigned randomly to total sleep deprivation (TSD) for 6 h, paradoxical sleep deprivation (PSD) for 24 h, or be kept in their home cages. Locomotor activity was assessed with the open field test followed by resection of brain for quantification of genetic damage by the single cell gel electrophoresis (comet) assay. Status epilepticus induced significant hyperactivity in the open field test and caused genetic damage in the brain. Sleep deprivation procedures (TSD and PSD) did not affect locomotor activity in epileptic or healthy rats, but resulted in significant DNA damage in brain cells. Although PSD had this effect in both vehicle and epileptic groups, TSD caused DNA damage only in epileptic rats. In conclusion, our results revealed that, despite a lack of behavioral effects of sleep deprivation, TSD and PSD induced genetic damage in rats submitted to pilocarpine-induced SE.
Assuntos
Hipercinese/fisiopatologia , Atividade Motora/fisiologia , Privação do Sono/fisiopatologia , Sono REM/fisiologia , Estado Epiléptico/fisiopatologia , Animais , Dano ao DNA , Hipercinese/genética , Masculino , Pilocarpina , Ratos , Ratos Wistar , Privação do Sono/genética , Estado Epiléptico/induzido quimicamente , Estado Epiléptico/genéticaRESUMO
Non-competitive N-methyl-D-aspartate receptor (NMDA-R) antagonists have been extensively used in rodents to model psychotic symptoms of schizophrenia. Although the motor syndrome induced by acute and systemic administration of low doses of dizocilpine (MK-801) has been extensively characterized, its neurobiological basis is not fully understood. NMDA-R antagonists can disinhibit excitatory inputs in certain brain areas, but the precise circuitry is not fully known. We examined the involvement of the anterior thalamic nucleus (ATN) in hyperlocomotion and other related behaviors (stereotypies, ataxia signs) induced after acute systemic administration of MK-801. Since GABAergic neurons of the reticular thalamic nucleus (RTN) exert the main inhibitory control on thalamic projection neurons, we hypothesized that systemically injected MK-801 might block NMDA-R on RTN GABAergic neurons. This effect would subsequently result in disinhibition of GABAergic inputs onto ATN projections to cortical motor areas, thereby inducing behavioral effects. We evaluated the behavioral syndrome induced by the systemic administration MK-801 (0.2 mg/kg) in control rats and in rats subjected to a bilateral stereotaxic infusion of the GABA(A) agonist muscimol (0.2 µl of 2.5 and 5.0 mM; 0.5-1 nmol per application, respectively) into the ATN. As previously reported, MK-801-induced hyperlocomotion in parallel with disorganized movements (e.g. not guided by normal exploration) slight ataxia signs and stereotypies. All responses were antagonized by pre-infusion of muscimol but not saline into the ATN. According to our results we suggest that the ATN plays a role on hyperlocomotion evoked by MK-801 and could involve a thalamic GABAergic disinhibition mechanism.
Assuntos
Núcleos Anteriores do Tálamo/efeitos dos fármacos , Núcleos Anteriores do Tálamo/fisiologia , Maleato de Dizocilpina/administração & dosagem , Maleato de Dizocilpina/toxicidade , Hipercinese/induzido quimicamente , Animais , Hipercinese/fisiopatologia , Masculino , Ratos , Ratos WistarRESUMO
Dopamine (DA) D2 receptors expressed in DA neurons (D2 autoreceptors) exert a negative feedback regulation that reduces DA neuron firing, DA synthesis and DA release. As D2 receptors are mostly expressed in postsynaptic neurons, pharmacological and genetic approaches have been unable to definitively address the in vivo contribution of D2 autoreceptors to DA-mediated behaviors. We found that midbrain DA neurons from mice deficient in D2 autoreceptors (Drd2(loxP/loxP); Dat(+/IRES-cre), referred to as autoDrd2KO mice) lacked DA-mediated somatodendritic synaptic responses and inhibition of DA release. AutoDrd2KO mice displayed elevated DA synthesis and release, hyperlocomotion and supersensitivity to the psychomotor effects of cocaine. The mice also exhibited increased place preference for cocaine and enhanced motivation for food reward. Our results highlight the importance of D2 autoreceptors in the regulation of DA neurotransmission and demonstrate that D2 autoreceptors are important for normal motor function, food-seeking behavior, and sensitivity to the locomotor and rewarding properties of cocaine.
Assuntos
Cocaína/administração & dosagem , Inibidores da Captação de Dopamina/administração & dosagem , Motivação/fisiologia , Receptores de Dopamina D2/deficiência , Recompensa , Análise de Variância , Animais , Autorradiografia , Baclofeno/farmacologia , Comportamento de Escolha/fisiologia , Condicionamento Operante , Di-Hidroxifenilalanina/metabolismo , Dopamina/metabolismo , Agonistas de Dopamina/farmacologia , Antagonistas de Dopamina/farmacologia , Interações Medicamentosas , Inibidores Enzimáticos/farmacologia , Comportamento Exploratório/fisiologia , Alimentos , Agonistas dos Receptores de GABA-B/farmacologia , Hidrazinas/farmacologia , Hipercinese/tratamento farmacológico , Hipercinese/fisiopatologia , Técnicas In Vitro , Aprendizagem em Labirinto/fisiologia , Potenciais da Membrana/efeitos dos fármacos , Potenciais da Membrana/genética , Mesencéfalo/citologia , Camundongos , Camundongos Knockout , Atividade Motora/genética , Neurônios/fisiologia , Quimpirol/farmacologia , Esquema de Reforço , Sulpirida/farmacologiaRESUMO
Altered corticostriatal information processing associated with early dopamine systems dysfunction may contribute to attention deficit/hyperactivity disorder (ADHD). Mice with neonatal dopamine-depleting lesions exhibit hyperactivity that wanes after puberty and is reduced by psychostimulants, reminiscent of some aspects of ADHD. To assess whether the maturation of corticostriatal functional connectivity is altered by early dopamine depletion, we examined preadolescent and postadolescent urethane-anesthetized mice with or without dopamine-depleting lesions. Specifically, we assessed (1) synchronization between striatal neuron discharges and oscillations in frontal cortex field potentials and (2) striatal neuron responses to frontal cortex stimulation. In adult control mice striatal neurons were less spontaneously active, less responsive to cortical stimulation, and more temporally tuned to cortical rhythms than in infants. Striatal neurons from hyperlocomotor mice required more current to respond to cortical input and were less phase locked to ongoing oscillations, resulting in fewer neurons responding to refined cortical commands. By adulthood some electrophysiological deficits waned together with hyperlocomotion, but striatal spontaneous activity remained substantially elevated. Moreover, dopamine-depleted animals showing normal locomotor scores exhibited normal corticostriatal synchronization, suggesting that the lesion allows, but is not sufficient, for the emergence of corticostriatal changes and hyperactivity. Although amphetamine normalized corticostriatal tuning in hyperlocomotor mice, it reduced horizontal activity in dopamine-depleted animals regardless of their locomotor phenotype, suggesting that amphetamine modified locomotion through a parallel mechanism, rather than that modified by dopamine depletion. In summary, functional maturation of striatal activity continues after infancy, and early dopamine depletion delays the maturation of core functional capacities of the corticostriatal system.
Assuntos
Córtex Cerebral/fisiopatologia , Corpo Estriado/fisiopatologia , Dopamina/metabolismo , Hipercinese/metabolismo , Hipercinese/patologia , Hipercinese/fisiopatologia , Vias Neurais/fisiopatologia , Potenciais de Ação/efeitos dos fármacos , Potenciais de Ação/fisiologia , Fatores Etários , Anfetamina , Animais , Animais Recém-Nascidos , Córtex Cerebral/efeitos dos fármacos , Córtex Cerebral/crescimento & desenvolvimento , Córtex Cerebral/patologia , Corpo Estriado/efeitos dos fármacos , Corpo Estriado/metabolismo , Corpo Estriado/patologia , Modelos Animais de Doenças , Dopamina/deficiência , Estimulação Elétrica/métodos , Hipercinese/induzido quimicamente , Locomoção/efeitos dos fármacos , Locomoção/fisiologia , Camundongos , Vias Neurais/metabolismo , Vias Neurais/patologia , Neurônios/efeitos dos fármacos , Neurônios/fisiologia , Oxidopamina , Serotonina/metabolismoRESUMO
Aripiprazole is an atypical antipsychotic that acts as a partial agonist at the dopamine D(2) receptor. It has been mainly investigated in dopamine-based models of schizophrenia, while its effects on glutamate-based paradigms have remained to be further characterized. Due to its unique mechanism of action, aripiprazole has also been considered as a replacement medication for psychostimulant abuse. Thus, in the present study we tested the hypothesis that aripiprazole would prevent the motor hyperactivity induced by psychostimulant and psychotomimetic drugs that act either by dopaminergic or glutamatergic mechanisms. Male Swiss mice received injections of aripiprazole (0.1-1 mg/kg) followed by drugs that enhance the dopamine-mediated neurotransmission, amphetamine (3 mg/kg) or cocaine (5 mg/kg), or by glutamate NMDA-receptor antagonists, ketamine (60 mg/kg) or MK-801 (0.4 mg/kg). Independent groups also received aripiprazole (0.1-1 mg/kg) or haloperidol (0.5 mg/kg) and were tested for catalepsy. All doses of aripiprazole were effective in preventing the motor stimulant effects of amphetamine and cocaine. Moreover, the higher dose also prevented the effects of ketamine and MK-801. The present study reports the effects of aripiprazole in dopaminergic and glutamatergic models predictive of antipsychotic activity, suggesting that both may be useful for screening novel partial agonists with antipsychotic activity. It also shows that aripiprazole may prevent the acute effects of psychostimulant drugs without significant motor impairment.
Assuntos
Antipsicóticos/farmacologia , Estimulantes do Sistema Nervoso Central/toxicidade , Antagonistas de Aminoácidos Excitatórios/toxicidade , Hipercinese/prevenção & controle , Atividade Motora/efeitos dos fármacos , Piperazinas/farmacologia , Quinolonas/farmacologia , Anfetamina/toxicidade , Animais , Antipsicóticos/toxicidade , Aripiprazol , Catalepsia/induzido quimicamente , Cocaína/toxicidade , Maleato de Dizocilpina/toxicidade , Dopamina/metabolismo , Relação Dose-Resposta a Droga , Avaliação Pré-Clínica de Medicamentos/métodos , Agonismo Parcial de Drogas , Glutamina/metabolismo , Haloperidol/farmacologia , Hipercinese/induzido quimicamente , Hipercinese/metabolismo , Hipercinese/fisiopatologia , Ketamina/toxicidade , Locomoção/efeitos dos fármacos , Masculino , Camundongos , Piperazinas/toxicidade , Quinolonas/toxicidade , Receptores de Dopamina D2/efeitos dos fármacos , Receptores de Dopamina D2/metabolismo , Receptores de N-Metil-D-Aspartato/antagonistas & inibidores , Receptores de N-Metil-D-Aspartato/metabolismo , Fatores de TempoRESUMO
The goal of this study was to analyze the effects of prenatal exposure to the pesticides paraquat (PQ) and mancozeb (MZ) on the development of synaptic transmission in mouse cerebellar cortex. Pregnant NMRI mice were treated with either saline, 10 mg/kg PQ, 30 mg/kg MZ or the combination of PQ + MZ, between gestational days 12 (E12) and E20. Variation in the levels of amino acid neurotransmitters was determined by HPLC, between postnatal day 1 (P1) and P30. Motor coordination was assessed by locomotor activity evaluation of control and experimental pups at P14, P21 and P30. Significant reductions in the levels of excitatory neurotransmitters, aspartate and glutamate, were observed in PQ-, MZ- or combined PQ + MZ-exposed pups, with respect to control, during peak periods of excitatory innervation of Purkinje cells: between P2-P5 and P11-P15. However, at P30, lower aspartate contents, in contrast with increased glutamate levels, were detected in all experimental groups. During the first two postnatal weeks, delays in GABA and glycine ontogenesis were observed in PQ- and PQ + MZ-exposed pups, whereas notable decrements in GABA and glycine levels were seen in PQ + MZ-exposed animals. Decreased taurine contents were detected at P3 and P11 in PQ- and PQ + MZ-exposed mice. Pups in different experimental groups all showed hyperactivity at P14 and then exhibited reduced locomotor activity at P30. Taken together, our results indicate that prenatal exposure to either PQ or MZ or the combination of both could alter the chronology and magnitude of synaptic transmission in developing mouse cerebellar cortex.
Assuntos
Córtex Cerebelar/efeitos dos fármacos , Córtex Cerebelar/fisiopatologia , Maneb/efeitos adversos , Paraquat/efeitos adversos , Efeitos Tardios da Exposição Pré-Natal/fisiopatologia , Transmissão Sináptica/efeitos dos fármacos , Zineb/efeitos adversos , Animais , Ácido Aspártico/efeitos dos fármacos , Ácido Aspártico/metabolismo , Córtex Cerebelar/metabolismo , Modelos Animais de Doenças , Regulação para Baixo/efeitos dos fármacos , Regulação para Baixo/fisiologia , Feminino , Fungicidas Industriais/efeitos adversos , Ácido Glutâmico/efeitos dos fármacos , Ácido Glutâmico/metabolismo , Glicina/efeitos dos fármacos , Glicina/metabolismo , Herbicidas/efeitos adversos , Hipercinese/induzido quimicamente , Hipercinese/metabolismo , Hipercinese/fisiopatologia , Camundongos , Atividade Motora/efeitos dos fármacos , Atividade Motora/fisiologia , Inibição Neural/efeitos dos fármacos , Inibição Neural/fisiologia , Gravidez , Efeitos Tardios da Exposição Pré-Natal/metabolismo , Transmissão Sináptica/fisiologia , Ácido gama-Aminobutírico/efeitos dos fármacos , Ácido gama-Aminobutírico/metabolismoRESUMO
The basal ganglia are a group of subcortical nuclei classically thought to be involved in the control of movement, and they have reciprocal connections with the cortex, thalamus and structures in the brainstem. Recent findings suggest that the basal ganglia interact with structures involved in the control of the sleep-waking cycle. The pedunculopontine tegmental nucleus (PPN) maintains a close relationship with the basal ganglia and is intimately involved in the regulation of wakefulness and REM sleep. This study evaluated changes in activity of PPN neurons following striatal kainic acid-induced lesions. Rats were injected in the anterodorsal striatum with either kainic acid or vehicle and allowed to recover for 7 or 30 days. The results showed an increase in the number of c-Fos+ cells in the PPN 30 days but not 7 days after the striatal lesion, when motor hyperactivity was no longer detected. In addition, we found a significant correlation between the ventricular brain ratio, as an indicator of lesion size, and the number of c-Fos+ cells in the PPN. Furthermore, the spatial distribution of cell types suggested that most c-Fos+ cells in the PPN were not cholinergic. These results provide new insights into the functional relationship between the basal ganglia and the PPN and suggest that the striatum, through its indirect influence on the PPN, may contribute to the regulation of wakefulness and cortical activation.
Assuntos
Ritmo Circadiano/fisiologia , Corpo Estriado/fisiologia , Vias Neurais/fisiologia , Neurônios/metabolismo , Núcleo Tegmental Pedunculopontino/metabolismo , Proteínas Proto-Oncogênicas c-fos/metabolismo , Acetilcolina/metabolismo , Animais , Denervação , Hipercinese/metabolismo , Hipercinese/fisiopatologia , Imuno-Histoquímica , Ácido Caínico , Masculino , Inibição Neural/fisiologia , Neurônios/citologia , Núcleo Tegmental Pedunculopontino/citologia , Ratos , Ratos Sprague-Dawley , Sono REM/fisiologia , Fatores de Tempo , Vigília/fisiologia , Ácido gama-Aminobutírico/metabolismoRESUMO
Arsenic is an environmental contaminant found in soil, water and air in some zones of the world. It has been widely studied for its effects as a human carcinogenic agent, but few studies have dealt with neurobehavioral effects. In addition, studies of arsenic effects on development have only addressed its effects on embryotoxicity and teratogenicity after a single oral, gavage or intraperitoneal exposure. Among the behavioral alterations reported after intoxication with arsenic are both increased and decreased locomotor activity and learning deficits in a delayed alternation task [Toxicol. Lett. 54 (1990) 345; Bull. Environ. Contam. Toxicol. 50 (1993) 100; Brain Res. Bull. 55 (2001) 301]. To further characterize developmental and behavioral alterations induced by arsenic exposure, Sprague-Dawley rats were exposed to arsenite (36.70 mg arsenic/l in drinking water) from gestation day 15 (GD 15) or postnatal day 1 (PND 1), until approximately 4 months old. The pregnant or lactating dams received either the arsenic solution or regular drinking water and once pups were weaned, they continued receiving the same solution as drinking water. Animals exposed from GD 15 showed increased spontaneous locomotor activity and both exposed groups showed increased number of errors in a delayed alternation task in comparison to the control group. Total arsenic (TA) content in brain was similar for both exposed groups and significantly different from the control group. These results indicate that rats exposed to arsenic during development present deficits in spontaneous locomotor activity and alterations in a spatial learning task.
Assuntos
Intoxicação por Arsênico/fisiopatologia , Comportamento Animal/efeitos dos fármacos , Transtornos Cognitivos/induzido quimicamente , Discinesia Induzida por Medicamentos/fisiopatologia , Hipercinese/induzido quimicamente , Efeitos Tardios da Exposição Pré-Natal , Animais , Animais Recém-Nascidos , Arsenitos/toxicidade , Comportamento Animal/fisiologia , Peso Corporal/efeitos dos fármacos , Peso Corporal/fisiologia , Encéfalo/efeitos dos fármacos , Encéfalo/crescimento & desenvolvimento , Encéfalo/metabolismo , Transtornos Cognitivos/fisiopatologia , Insuficiência de Crescimento/induzido quimicamente , Insuficiência de Crescimento/fisiopatologia , Feminino , Hipercinese/fisiopatologia , Masculino , Aprendizagem em Labirinto/efeitos dos fármacos , Aprendizagem em Labirinto/fisiologia , Atividade Motora/efeitos dos fármacos , Atividade Motora/fisiologia , Gravidez , Ratos , Ratos Sprague-Dawley , Reflexo/efeitos dos fármacos , Reflexo/fisiologia , Compostos de Sódio/toxicidadeRESUMO
At different times post-lesion, the excitotoxically lesioned striatum has been shown to undergo significant neuroanatomical and neurochemical changes, which could be expressed behaviorally. Gender and dose of excitotoxin are other variables that may modify the behavioral effects of the lesion. Consequently, the purpose of this study was to determine the effect of dose, gender, and time post-lesion on spontaneous and drug-induced locomotor behavior after intrastriatal KA lesions. Results showed that dose and time post-lesion had a significant effect on the deficits observed. Hyperactivity induced by the lesion with KA (5 nm) subsided as time post-lesion increased. Both the pattern of spontaneous and MK-801-induced locomotor activity were different for male and female rats. In female animals with KA lesions (5 nm), MK-801 did not stimulate ambulatory activity nor reduce vertical activity. Both female and male rats lesioned with KA (5 nm) showed an exaggerated response to amphetamine, at a time when spontaneous locomotor activity was reduced to control levels. Haloperidol significantly reduced locomotor activity in all groups.
Assuntos
Maleato de Dizocilpina/farmacologia , Antagonistas de Aminoácidos Excitatórios/farmacologia , Hipercinese/induzido quimicamente , Neostriado/efeitos dos fármacos , Neurônios/efeitos dos fármacos , Neurotoxinas/farmacologia , Caracteres Sexuais , Animais , Modelos Animais de Doenças , Agonistas de Aminoácidos Excitatórios/farmacologia , Feminino , Doença de Huntington/patologia , Doença de Huntington/fisiopatologia , Hipercinese/fisiopatologia , Ácido Caínico/farmacologia , Masculino , Atividade Motora/efeitos dos fármacos , Atividade Motora/fisiologia , Neostriado/patologia , Neostriado/fisiopatologia , Neurônios/metabolismo , Neurônios/patologia , Ratos , Ratos WistarRESUMO
En algunas ocasiones el lenguaje escrito se ve comprometido en niños que presentan Deficit Atencional con o sin Hipercinesia. Este cuadro no constituye un trastorno especifico del aprendizaje, pero sus sintomas podrian interferir significativamente. Algunos niños presentan sintomas de alteraciones del aprendizaje ademas de los que se describen como constitutivos del cuadro, mientras que otros presentarian problematicas de este orden como consecuencia de su hiperactividad, dado que la misma al comprometer la atencion y los mecanismos de control de la impulsividad, incrementaria la cantidad de errores al momento de escribir- creencia que se intenta exponer en la presente investigacion-. En este trabajo se investigo a 16 niños diagnosticados con deficit atencional con o sin hipercinesia de 8 a 12 años. Los mismos fueron evaluados a partir de sus producciones escritas, producidas a traves de un dictado y de un escrito referido a un texto narrativo leido previamente al niño por el investigador. A partir de las mismas se identificaron errores manifestados en los niveles graficos y ortograficos. En la ortografia se evidencio que: - en cuanto a los errores que transgreden al principio alfabetico, en 3 niños se encontraron dificultades minimas, 4 manifestaron dificultades medias, y 9 dificultades maximas. En cuanto a los errores que trasgreden a la segmentacion convencional, 8 niños segmentaron las palabras de acuerdo a la normativa y 8 niños manifestaron fenomenos de hipo y/o hipersegmentacion. En la grafia se evidencio que 7 niños no presentaron dificultades y los 9 restantes si(AU)
Assuntos
Humanos , Criança , Idioma , Transtorno do Deficit de Atenção com Hiperatividade/diagnóstico , Hipercinese/diagnóstico , Hipercinese/fisiopatologiaRESUMO
Del estudio retrospectivo de 147 historias clinicas (abril 1981 a abril 1991), se aislan 30 casos de sindrome hipercinetico en niños comprendidos entre 1 y 12 años de edad. Se analizan las variables de sexo, antecedentes eredologicos y personales, rendimiento escolar, sintomatologia basica y asociada al sindrome, asi como las anomalias registradas en el estudio electroencefalografico de 21 niños, ademas el tratamiento afectuado. no existen antecedentes de studio similar, en nuestro medio. Se debe alertar hacia esta patologia a traves de la actividad profesional pediatrica para detectar precozmente el sindrome y asumir la terapeutica que el caso requiere. Por los resultados del trbajo, la prevencion a traves de un cuidado pre y perinatal que garantice un parto normal, son aconsejables asi como el tratamiento de los progenitores que presentan rasgos de personalidad anormales y consumo abusivo o dependencia a bebidas alcoholicas.
Assuntos
Humanos , Masculino , Feminino , Pré-Escolar , Hipercinese/fisiopatologia , Bolívia , Eletroencefalografia/métodos , Prontuários Médicos/classificação , Baixo Rendimento EscolarRESUMO
This investigation examined the relationships among measures of childhood physical activity and their association with measures of weight and blood pressure in a sample (n = 222) of preschool children. A multimethod factored approach to the assessment of physical activity was used; this approach included direct observation, motion sensor evaluation, and several parental reports of the subjects' activity levels. Analysis of these data revealed three highly significant activity factors: general activity, hyperactivity, and direct-observation-competitiveness activity. When the association between physical activity factors and cardiovascular risk was explored, no consistent relationship was found between the various childhood physical activity factors and the cardiovascular risk factors of weight and blood pressure. Individual (nonfactored) physical activity measures also failed to correlate with children's physical activity. The results indicate that physical activity is not related to obesity and blood pressure in children. However, other interpretations (i.e., that the activity protocol was insufficiently accurate to detect subtle differences, or that children are not participating in enough physical activity to affect their cardiovascular health) are also possible.