RESUMO
Post-traumatic stress disorder (PTSD) is a psychiatric condition resulting from exposure to a traumatic event. It is characterized by several debilitating symptoms including re-experiencing the past trauma, avoidance behavior, increased fear, and hyperarousal. Key roles in the neuropathology of PTSD and its symptomatology have been attributed to the hippocampus and amygdala. These regions are involved in explicit memory processes and context encoding during fear conditioning. The aim of our study was to investigate whether PTSD is capable of altering the morphology, density and expression of glial fibrillary acidic protein (GFAP) in astrocytes from the CA1 region of the hippocampus and the medial amygdala and correlate the data obtained with the orientation index of the polarity of astrocytes. Thirty male rats were divided in two groups: control (n = 15) and PTSD (n = 15). The inescapable shock protocol, in which the animals are exposed to a single episode of footshock, was used to induce PTSD. Our results show that, in the hippocampus, PTSD is capable of decreasing the density of GFAP+ astrocytes as well as altering astrocytic morphology, as shown by the reductions observed in the total number of primary processes, in the number of primary processes in the lateral quadrants, and the degree of branching in the lateral quadrants. The analysis of the orientation index indicates that PTSD alters the polarity of hippocampal astrocytes. No alterations were observed in the amygdala astrocytes. Therefore, this study demonstrates notable changes in hippocampal astrocytes, supporting the concept that these cells play an important role in PTSD symptomatology.
Assuntos
Astrócitos/patologia , Astrócitos/fisiologia , Região CA1 Hipocampal/patologia , Transtornos de Estresse Pós-Traumáticos/patologia , Animais , Contagem de Células , Polaridade Celular , Complexo Nuclear Corticomedial/metabolismo , Complexo Nuclear Corticomedial/patologia , Proteína Glial Fibrilar Ácida/metabolismo , Masculino , Ratos Wistar , Transtornos de Estresse Pós-Traumáticos/metabolismoRESUMO
Exercise training has neuroprotective effects whereas myocardial infarction (MI) and heart failure (HF) can cause neuronal death and reactive gliosis in the whole amygdala. The posterodorsal medial amygdala (MePD) is involved with cardiovascular reflexes and the central control of sympathetic/parasympathetic responses. Our aim was to study the effects of prior exercise training and of MI-induced HF on the neuronal and glial densities and the glial fibrillary acidic protein-immunoreactivity (GFAP-ir) in the MePD of adult male rats. Animals (n= 5/group) were: control, sedentary submitted to a sham MI (Sed Sham), sedentary submitted to MI/HF (Sed HF), trained on a treadmill and submitted to a sham MI (T Sham) or trained on a treadmill and submitted to MI/HF (T HF). The number of neurons and glial cells in the MePD was estimated using the optical fractionator and the GFAP-ir was quantified by optical densitometry. In the respective groups, treadmill training improved physical performance and MI damaged near 40% of the left ventricle. There was a hemispheric lateralization effect on the density of neurons (higher in the right MePD), but no significant difference in either the neuronal or the glial densities due to experimental condition. Regional GFAP-ir results revealed that the Sed HF group had a higher expression in the left MePD compared to the control and the Sed Sham rats (p⟨0.01). The present data did not evidence the effects of training or MI/HF in the MePD cellular density, but indicate a possible local restructuring of astrocytic cytoskeleton after MI/HF in rats.
Assuntos
Tonsila do Cerebelo/patologia , Proteína Glial Fibrilar Ácida/metabolismo , Insuficiência Cardíaca/metabolismo , Infarto do Miocárdio/metabolismo , Neuroglia/metabolismo , Neurônios/metabolismo , Condicionamento Físico Animal , Tonsila do Cerebelo/fisiologia , Animais , Astrócitos/citologia , Citoesqueleto/metabolismo , Modelos Animais de Doenças , Imuno-Histoquímica , Masculino , Neurônios/patologia , Ratos , Ratos WistarRESUMO
Oral squamous cell carcinoma (OSCC) is a public health problem. The hamster buccal pouch model is ideal for analyzing the development of OSCC. This research analysed the effects of sunitinib (tyrosine kinase inhibitor) in precancerous lesions induced by 7,12-dimethylbenz(a)anthracene (DMBA) in this model. Thirty-four male hamsters, divided into six groups: control-C (n = 7), acetone-A (n = 12), carbamide peroxide-CP (n = 5 ), acetone and CP-A+CP (n = 8), 1% DMBA in acetone and CP-DA+CP (n = 6), and 1% DMBA in acetone and CP and 4-week treatment with sunitinib-DA+CP+S (n = 7). The aspects evaluated were anatomopathological features (peribuccal area, paws, nose, and fur), histological sections of the hamster buccal pouches (qualitatively analyzed), epithelium thickness, and the rete ridge density (estimated). Sunitinib was unable to attenuate the decrease in weight gain induced by DMBA; no increase in volume was detected in the pouch and/or ulceration, observed in 43% of the animals in the DA+CP group. DA+CP groups presented a significant increase in rete ridge density compared to the control groups (P < 0.01) which was reverted by sunitinib in the DA+CP+S group. Sunitinib seems to have important benefits in early stage carcinogenesis and may be useful in chemoprevention.
RESUMO
Physical exercise has an important influence on brain plasticity, which affects the neuron-glia interaction. Astrocytes are susceptible to plasticity, and induce and stabilize synapses, regulate the concentration of various molecules, and support neuronal energy metabolism. The aim of our study was to investigate whether physical exercise is capable of altering the morphology, density and expression of glial fibrillary acidic protein (GFAP) in astrocytes from the CA1 region of rat hippocampus. Thirteen male rats were divided in two groups: sedentary (n = 6) and exercise (n = 7). The animals in the exercise group were submitted to a protocol of daily physical exercise on a treadmill for four consecutive weeks. GFAP immunoreactivity was evaluated using optical densitometry and the morphological analyses were an adaptation of Sholl's concentric circles method. Our results show that physical exercise is capable of increasing the density of GFAP-positive astrocytes as well as the regional and cellular GFAP expression. In addition, physical exercise altered astrocytic morphology as shown by the increase observed in the degree of ramification in the lateral quadrants and in the length of the longest astrocytic processes in the central quadrants. Our data demonstrate important changes in astrocytes promoted by physical exercise, supporting the idea that these cells are involved in regulating neural activity and plasticity.
Assuntos
Astrócitos/citologia , Astrócitos/metabolismo , Regulação da Expressão Gênica/fisiologia , Proteína Glial Fibrilar Ácida/metabolismo , Hipocampo/citologia , Condicionamento Físico Animal/fisiologia , Animais , Contagem de Células , Masculino , Ratos , Ratos WistarRESUMO
This study investigated the sexual dimorphism in the recurrent laryngeal nerve (RLN) and thyroarytenoid (TA) muscle, which control the vocal fold. The RLN and TA were bilaterally studied in human specimens obtained from necropsies (seven men and seven women). Analysis of the morphometric parameters showed that the RLN of the men were significantly larger, as shown by the intraperineural area (42.5%) (P=0.006), total number of fibers (38.0%) (P=0.0002), axonal area (34.3%) (P=0.0001), axonal diameter (19.0%) (P=0.0001), and the area of the nerve occupied by myelinated fibers (34.9%) (P=0.001). By contrast, in women, our results showed that the area of the RLN occupied by endoneurial connective tissue was larger (5.7%) (P=0.001). Estimation of the fiber area and shape coefficient showed that the histologic organization of TA is similar in men and women. These results may contribute toward enhancing our understanding about the voice neurobiology.
Assuntos
Nervo Laríngeo Recorrente/anatomia & histologia , Prega Vocal/inervação , Idoso , Idoso de 80 Anos ou mais , Feminino , Humanos , Músculos Laríngeos/anatomia & histologia , Masculino , Pessoa de Meia-Idade , Nervo Laríngeo Recorrente/fisiologia , Caracteres Sexuais , Fatores SexuaisRESUMO
Stroke causes disability and mortality worldwide and is divided into ischemic and hemorrhagic subtypes. Although clinical trials suggest distinct recovery profiles for ischemic and hemorrhagic events, this is not conclusive due to stroke heterogeneity. The aim of this study was to produce similar brain damage, using experimental models of ischemic (IS) and hemorrhagic (HS) stroke and evaluate the motor spontaneous recovery profile. We used 31 Wistar rats divided into the following groups: Sham (n=7), ischemic (IS) (n=12) or hemorrhagic (HS) (n=12). Brain ischemia or hemorrhage was induced by endotelin-1 (ET-1) and collagenase type IV-S (collagenase) microinjections, respectively. All groups were evaluated in the open field, cylinder and ladder walk behavioral tests at distinct time points as from baseline to 30 days post-surgery (30 PS). Histological and morphometric analyses were used to assess the volume of lost tissue and lesion length. Present results reveal that both forms of experimental stroke had a comparable long-term pattern of damage, since no differences were found in volume of tissue lost or lesion size 30 days after surgery. However, behavioral data showed that hemorrhagic rats were less impaired at skilled walking than ischemic ones at 15 and 30 days post-surgery. We suggest that experimentally comparable stroke design is useful because it reduces heterogeneity and facilitates the assessment of neurobiological differences related to stroke subtypes; and that spontaneous skilled walking recovery differs between experimental ischemic and hemorrhagic insults.
Assuntos
Isquemia Encefálica/psicologia , Encéfalo/patologia , Hemorragias Intracranianas/psicologia , Recuperação de Função Fisiológica , Acidente Vascular Cerebral/patologia , Acidente Vascular Cerebral/psicologia , Animais , Isquemia Encefálica/induzido quimicamente , Isquemia Encefálica/complicações , Isquemia Encefálica/patologia , Colagenases/administração & dosagem , Endotelina-1/administração & dosagem , Hemorragias Intracranianas/induzido quimicamente , Hemorragias Intracranianas/complicações , Hemorragias Intracranianas/patologia , Masculino , Microinjeções , Atividade Motora/efeitos dos fármacos , Destreza Motora/efeitos dos fármacos , Ratos , Acidente Vascular Cerebral/complicações , Acidente Vascular Cerebral/diagnósticoRESUMO
Extra-pyramidal symptoms (EPS) such as akinesia, dystonia, gait alteration and tremors are observed when dopamine D2-receptors are blocked by pharmacological agents such as haloperidol. These alterations produce a Parkinson disease-like state (PLS). Physical exercise has been proven to improve gait and locomotor symptoms in Parkinson's disease; we sought to elucidate the effects of physical exercise on PLS induced by chronic administration of haloperidol in rats. We used 48 rats distributed into four groups: Control, Exercise, Haloperidol, and Hal+Exe. All the animals received a daily injection of saline or haloperidol for 30 days, and the exercise groups underwent a daily 30-minute exercise protocol for 20 days. The animals were subjected to the ink-paw test, bar test and open-field test throughout the training period. The haloperidol-induced akinesia increased throughout the days of injections, but exercise was shown to alleviate it. The assessment showed shortened stride length and increased stance width with the use of haloperidol, which were significantly alleviated by exercise. These results indicate that exercise could be an interesting approach towards reducing unwanted EPS caused by haloperidol.
Assuntos
Antagonistas de Dopamina/efeitos adversos , Haloperidol/efeitos adversos , Coxeadura Animal/induzido quimicamente , Coxeadura Animal/terapia , Condicionamento Físico Animal , Animais , Comportamento Animal/efeitos dos fármacos , Comportamento Animal/fisiologia , Modelos Animais de Doenças , Comportamento Exploratório/efeitos dos fármacos , Comportamento Exploratório/fisiologia , Coxeadura Animal/fisiopatologia , Locomoção/efeitos dos fármacos , Locomoção/fisiologia , Masculino , Condicionamento Físico Animal/fisiologia , Ratos , Ratos WistarRESUMO
Studies have suggested that neuronal loss in Parkinson's disease (PD) could be related to the pacemaker activity of the substantia nigra pars compacta generated by L-type Ca(v) 1.3 calcium channels, which progressively substitute voltage-dependent sodium channels in this region during aging. Besides this mechanism, which leads to increases in intracellular calcium, other factors are also known to play a role in dopaminergic cell death due to overproduction of reactive oxygen species. Thus, dihydropyridines, a class of calcium channel blockers, and resveratrol, a polyphenol that presents antioxidant properties, may represent therapeutic alternatives for the prevention of PD. In the present study, we tested the effects of the dihydropyridines, isradipine, nifedipine, and nimodipine and of resveratrol upon locomotor behavior in Drosophila melanogaster. As previously described, paraquat induced parkinsonian-like motor deficits. Moreover, none of the drugs tested were able to prevent the motor deficits produced by paraquat. Additionally, isradipine, nifedipine, resveratrol, and ethanol (vehicle), when used in isolation, induced motor deficits in flies. This study is the first demonstration that dyhidropyridines and resveratrol are unable to reverse the locomotor impairments induced by paraquat in Drosophila melanogaster.
Assuntos
Antioxidantes , Bloqueadores dos Canais de Cálcio/administração & dosagem , Di-Hidropiridinas , Degeneração Neural/induzido quimicamente , Estilbenos , Animais , Antioxidantes/administração & dosagem , Antioxidantes/metabolismo , Antioxidantes/uso terapêutico , Bloqueadores dos Canais de Cálcio/metabolismo , Bloqueadores dos Canais de Cálcio/uso terapêutico , Canais de Cálcio/efeitos dos fármacos , Canais de Cálcio/metabolismo , Di-Hidropiridinas/administração & dosagem , Di-Hidropiridinas/metabolismo , Di-Hidropiridinas/uso terapêutico , Modelos Animais de Doenças , Dopamina/metabolismo , Drosophila melanogaster/metabolismo , Degeneração Neural/metabolismo , Paraquat , Transtornos Parkinsonianos/induzido quimicamente , Transtornos Parkinsonianos/metabolismo , Resveratrol , Estilbenos/administração & dosagem , Estilbenos/metabolismo , Estilbenos/uso terapêutico , Substância Negra/citologia , Substância Negra/efeitos dos fármacos , Substância Negra/metabolismoRESUMO
NADPH-diaphorase (NADPH-d) is a histochemical marker for nitric oxide synthase (NOS), widely used to identify nitric oxide (NO) producing cells in the nervous system of both vertebrates and invertebrates. Using NADPH-d histochemistry and semi-quantitative optical densitometry, we characterized the NO-producing neurons in the pedal ganglia of young and adult Megalobulimus abbreviatus, subjected to aversive thermal stimulus. The animals were killed at different times (3, 6, 12 and 24 h) following stimulus. The enzymatic activity was detected in different cellular subsets and neuronal processes. In all the studied pedal ganglia subregions, the optical density of positive neurons (P < 0.05) and neuropilar area 1 (P < 0.01) was significantly different in treated animals when compared to controls. The increase in nitrergic activity induced by nociceptive stimulus suggests the involvement of NO in the nociceptive circuit of M. abbreviatus, which is well maintained throughout evolution, and could be helpful in drawing cellular homologies with other gastropods.