4 results on '"Cibelle de Melo Bastos Cavalcante"'
Search Results
2. Role of Modulation of Hippocampal Glucose Following Pilocarpine-Induced Status Epilepticus
- Author
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Jucilene Freitas-Santos, Amanda Larissa Dias Pacheco, Ana Catarina Rezende Leite, Igor Santana de Melo, Reginaldo Correia Silva-Filho, Daniel Góes Leite Gitaí, Yngrid Mickaelli Oliveira dos Santos, Maisa de Araújo Costa, Robinson Sabino-Silva, Vanessa de Oliveira Silva, Alexandre Urban Borbely, Marcelo Duzzioni, Cibelle de Melo Bastos Cavalcante, and Olagide W. Castro
- Subjects
0301 basic medicine ,medicine.medical_specialty ,Glucose uptake ,Neuroscience (miscellaneous) ,Hippocampus ,Status epilepticus ,Hippocampal formation ,Amygdala ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,0302 clinical medicine ,Internal medicine ,medicine ,Premovement neuronal activity ,business.industry ,Subiculum ,030104 developmental biology ,Endocrinology ,medicine.anatomical_structure ,nervous system ,Neurology ,Pilocarpine ,medicine.symptom ,business ,030217 neurology & neurosurgery ,medicine.drug - Abstract
Status epilepticus (SE) is defined as continuous and self-sustaining seizures, which trigger hippocampal neurodegeneration, mitochondrial dysfunction, oxidative stress, and energy failure. During SE, the neurons become overexcited, increasing energy consumption. Glucose uptake is increased via the sodium glucose cotransporter 1 (SGLT1) in the hippocampus under epileptic conditions. In addition, modulation of glucose can prevent neuronal damage caused by SE. Here, we evaluated the effect of increased glucose availability in behavior of limbic seizures, memory dysfunction, neurodegeneration process, neuronal activity, and SGLT1 expression. Vehicle (VEH, saline 0.9%, 1 μL) or glucose (GLU; 1, 2 or 3 mM, 1 μL) were administered into hippocampus of male Wistar rats (Rattus norvegicus) before or after pilocarpine to induce SE. Behavioral analysis of seizures was performed for 90 min during SE. The memory and learning processes were analyzed by the inhibitory avoidance test. After 24 h of SE, neurodegeneration process, neuronal activity, and SGLT1 expression were evaluated in hippocampal and extrahippocampal regions. Modulation of hippocampal glucose did not protect memory dysfunction followed by SE. Our results showed that the administration of glucose after pilocarpine reduced the severity of seizures, as well as the number of limbic seizures. Similarly, glucose after SE reduced cell death and neuronal activity in hippocampus, subiculum, thalamus, amygdala, and cortical areas. Finally, glucose infusion elevated the SGLT1 expression in hippocampus. Taken together our data suggest that possibly the administration of intrahippocampal glucose protects brain in the earlier stage of epileptogenic processes via an important support of SGLT1.
- Published
- 2020
3. Role of Modulation of Hippocampal Glucose Following Pilocarpine-Induced Status Epilepticus
- Author
-
Igor Santana, de Melo, Yngrid Mickaelli Oliveira, Dos Santos, Amanda Larissa Dias, Pacheco, Maisa Araújo, Costa, Vanessa, de Oliveira Silva, Jucilene, Freitas-Santos, Cibelle, de Melo Bastos Cavalcante, Reginaldo Correia, Silva-Filho, Ana Catarina Rezende, Leite, Daniel Góes Leite, Gitaí, Marcelo, Duzzioni, Robinson, Sabino-Silva, Alexandre Urban, Borbely, and Olagide Wagner, de Castro
- Subjects
Male ,Neurons ,Cell Death ,Pilocarpine ,Hippocampus ,Severity of Illness Index ,Antioxidants ,Oxidative Stress ,Glucose ,Sodium-Glucose Transporter 1 ,Status Epilepticus ,Animals ,Rats, Wistar ,Biomarkers ,Memory Consolidation - Abstract
Status epilepticus (SE) is defined as continuous and self-sustaining seizures, which trigger hippocampal neurodegeneration, mitochondrial dysfunction, oxidative stress, and energy failure. During SE, the neurons become overexcited, increasing energy consumption. Glucose uptake is increased via the sodium glucose cotransporter 1 (SGLT1) in the hippocampus under epileptic conditions. In addition, modulation of glucose can prevent neuronal damage caused by SE. Here, we evaluated the effect of increased glucose availability in behavior of limbic seizures, memory dysfunction, neurodegeneration process, neuronal activity, and SGLT1 expression. Vehicle (VEH, saline 0.9%, 1 μL) or glucose (GLU; 1, 2 or 3 mM, 1 μL) were administered into hippocampus of male Wistar rats (Rattus norvegicus) before or after pilocarpine to induce SE. Behavioral analysis of seizures was performed for 90 min during SE. The memory and learning processes were analyzed by the inhibitory avoidance test. After 24 h of SE, neurodegeneration process, neuronal activity, and SGLT1 expression were evaluated in hippocampal and extrahippocampal regions. Modulation of hippocampal glucose did not protect memory dysfunction followed by SE. Our results showed that the administration of glucose after pilocarpine reduced the severity of seizures, as well as the number of limbic seizures. Similarly, glucose after SE reduced cell death and neuronal activity in hippocampus, subiculum, thalamus, amygdala, and cortical areas. Finally, glucose infusion elevated the SGLT1 expression in hippocampus. Taken together our data suggest that possibly the administration of intrahippocampal glucose protects brain in the earlier stage of epileptogenic processes via an important support of SGLT1.
- Published
- 2020
4. Maternal crack cocaine use in rats leads to depressive- and anxiety-like behavior, memory impairment, and increased seizure susceptibility in the offspring
- Author
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Fernanda Maria Araujo de Souza, Jucilene Freitas-Santos, Amanda Larissa Dias Pacheco, Yngrid Mickaelli Oliveira dos Santos, Maisa de Araújo Costa, Daniel Leite Góes Gitaí, Alexandre Urban Borbely, Olagide W. Castro, José Gomes dos Santos Neto, Ashok K. Shetty, Igor Santana de Melo, Dannyele Cynthia Santos Pimentel Nicacio, Robinson Sabino-Silva, Claudio Torres de Miranda, Cibelle de Melo Bastos Cavalcante, and Marcelo Duzzioni
- Subjects
Male ,medicine.medical_specialty ,Offspring ,Status epilepticus ,Anxiety ,Irritability ,03 medical and health sciences ,Epilepsy ,Cocaine-Related Disorders ,0302 clinical medicine ,Status Epilepticus ,Pregnancy ,Seizures ,Internal medicine ,medicine ,Memory impairment ,Animals ,Pharmacology (medical) ,Biological Psychiatry ,Pharmacology ,Memory Disorders ,business.industry ,Pilocarpine ,medicine.disease ,030227 psychiatry ,Rats ,Psychiatry and Mental health ,Endocrinology ,Neurology ,Premature birth ,Crack Cocaine ,Female ,Neurology (clinical) ,medicine.symptom ,business ,030217 neurology & neurosurgery ,medicine.drug - Abstract
Crack users suffer the effects of cocaine present in the drug and the action of other active compounds from its pyrolysis. An emergent fact is an increase in the number of pregnant crack cocaine users. Studies suggest that crack cocaine and its metabolites cross the placenta, promoting premature birth, fever, irritability, sweating, and seizures in the early months of life. In children, the effects of crack cocaine have been associated with cognitive deficits, difficulty in verbalization, aggressiveness, and depression, besides enhancing the susceptibility to epileptic seizures, including status epilepticus (SE) in adulthood. Therefore, we investigated the effect of maternal exposure to smoke crack cocaine on several behavioral parameters in the offspring during adulthood. A series of behavioral tests and intrahippocampal pilocarpine (H-PILO) microinjection at sub-convulsive and convulsive doses in a rat model demonstrated that exposure to crack cocaine during the embryonic period leads to anxiogenic-like behavior and long-term memory impairment in both genders and promotes depressive-like behavior in the female. Besides, crack cocaine offspring exposed to a sub-convulsive H-PILO dose showed higher susceptibility to SE, increased seizure frequency, and neurodegeneration, while animals that received a convulsive dose of H-PILO displayed no alteration in SE severity. Taken together, our data suggest that crack cocaine exposure during the gestational period leads to an increased predilection for anxiety and depression, long-term memory deficits, and reduction in the threshold for developing epileptic seizures associated with neuronal death, which predispose crack cocaine babies to develop neuropsychological disorders.
- Published
- 2020
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