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1.
Eur. j. anat ; 24(1): 17-29, ene. 2020. tab, ilus
Artigo em Inglês | IBECS | ID: ibc-186061

RESUMO

Indirect triple immunolabelling techniques were used to identify the presence of choline acetyl-transferase (ChAT), neuronal nitric oxide synthase (nNOS), Dopamine beta-hydroxylase (DβH), neuromedin U-8 (NMU-8), and neuropeptide Y (NPY) in the ganglionated plexuses of the human gallbladder. Of all the intrinsic cholinergic neurons examined, NMU-8-immunoreactive (-IR) neurons appeared to be the most populous, followed closely by neurons containing NPY-IR. nNOS-IR neurons were often observed to coexist with ChAT, NMU, and NPY. Occasionally, these nNOS positive neurons were seen triple labeled with ChAT, NMU-8, and NPY. Results also indicate that not all nNOS and NMU-8-IR coexistent neurons express NPY immunoposi-tivity. Our findings suggest that these intrinsic neurons may be categorized into a distinct population of neurons that express both inhibitory and excita-tory capabilities.Intrinsic cholinergic neurons that were ChAT-IR displayed a spectrum of immunopositivity. Interestingly, a small subpopulation of these neurons ap-peared to be extremely weak ChAT-IR or simply ChAT-immunonegative. These occasionally obser-ved ChAT-immunonegative neurons at times ex-pressed single immunopositivity for NMU-8 or nNOS, while more frequently, these ChAT-immunonegative neurons were found to be single immunopositive, or at times, double immunopositi-ve for NMU-8-, NPY-, or nNOS-IR.Dopamine beta-hydroxylase (DβH) antibodies were used to confirm the lack of intrinsic sympat-hetic innervation in the human gallbladder. As suspected, in all the sections examined, DβH-IR neu-rons were not detected. The only indication of DβH immunopositivity was noted among delicate fibers surrounding the neurons and blood vessels within the organ


No disponible


Assuntos
Humanos , Feminino , Adulto , Pessoa de Meia-Idade , Vesícula Biliar/anatomia & histologia , Imuno-Histoquímica/métodos , Coleta de Tecidos e Órgãos , Colina O-Acetiltransferase , Óxido Nítrico , Dopamina beta-Hidroxilase , Vesícula Biliar/enzimologia , Colecistectomia Laparoscópica , Colelitíase/cirurgia , Microscopia Confocal/métodos
2.
Eur. j. anat ; 19(1): 1-7, ene. 2015.
Artigo em Inglês | IBECS | ID: ibc-133884

RESUMO

The human adult parotid duct is the longest of all major salivary gland ducts, approximately 6-8 cm in length. Its unique structure extends over the masseter muscle, penetrates through the buccinator muscle and opens into the oral cavity. Salivary secretion is under basic control of the sympathetic and parasympathetic divisions of the autonomic nervous system. Scarce reporting on the parotid duct nerve distribution led us to this study; to investigate the nervous distribution in the human adult and fetal parotid ducts using an antibody against protein gene product 9.5 (PGP9.5), a molecular marker for nerve cells and fibers. In order to identify the nerve fibers distributed throughout the parotid duct and confirm them to be part of the autonomic nervous system, we stained adult parotid ducts with tyrosine hydroxylase (TH) and choline acetyltransferase (ChAT) for observation. PGP9.5 staining of the parotid duct’s inside wall where it traverses over the masseter prior to penetrating the buccinator revealed a dense concentration of nerve fibers in the area. Staining revealed both sympathetic and parasympathetic nerve fibers in the same area, with the majority of the sympathetic nerve fibers surrounding blood vessels. However, the section of the duct penetrating the buccinator showed less concentration of nerve fibers in both adult and fetal specimens. The difference in the nerve distribution of the parotid duct suggests its direct association with the salivary transport function of the duct. PGP9.5 expression in fetuses over five months of age further suggests that the nerve distribution in the human parotid duct is fully established at six months of gestation


No disponible


Assuntos
Humanos , Masculino , Feminino , Adulto , Região Parotídea/inervação , Ductos Salivares/inervação , Desenvolvimento Fetal , Feto/inervação , Tirosina 3-Mono-Oxigenase/análise , Colina O-Acetiltransferase/análise
4.
Eur. j. anat ; 13(3): 133-143, dic. 2009. ilus
Artigo em Inglês | IBECS | ID: ibc-107639

RESUMO

During recent years a key role as morphogen has been postulated for the neurotransmitter acetylcholine in the developing Central Nervous System. Acetylcholine released from growing axons regulates growth, differentiation and plasticity. The acetylcholine distribution is frequently defined by acetylcholinesterase and choline acetyltransferase expression patterns. The cholinergic/cholinoceptive system in the adult zebrafish retina has been described. Nevertheless, there are no data regarding the developing retina. The acetylcholinesterase and choline acetyltransferase distribution patterns during zebrafish retinal development are very similar. In both cases the first positive elements appear in the plexiform layers and in later stages reactive amacrine cells have been observed in the ganglion cell layer and inner nuclear layer. In the adult retina a cholinergic and cholinoceptive neuropile band is observed in the inner plexiform layer. Displaced amacrine cells and amacrine cells positive to both markers have been observed. Transient expressions of choline acetyltransferase in the optic nerve and outer plexiform layer and of acetylcholinesterase in amacrine cells and displaced amacrine cells are observed during retinal development coinciding with the arrangement of the pioneering retinal projections into the optic tectum. The mature distribution pattern of the cholinergic/ cholinoceptive system in the adult retina is conserved along the phylogenetic scale, thus it seems to be a primary feature acquired relatively early during the evolution of vertebrates (AU)


No disponible


Assuntos
Animais , Acetilcolinesterase , Colina O-Acetiltransferase , Retina/fisiologia , Células Amácrinas/fisiologia , Células Ganglionares da Retina/fisiologia , Peixes/fisiologia , Diferenciação Celular , Plasticidade Neuronal , Nervo Óptico/crescimento & desenvolvimento
5.
Rev. neurol. (Ed. impr.) ; 37(2): 155-163, 16 jul., 2003. tab
Artigo em Espanhol | IBECS | ID: ibc-155818

RESUMO

Los signos neuropatológicos característicos de la enfermedad de Alzheimer (EA) son la presencia de placas seniles o neuríticas (PN) y ovillos neurofibrilares (ON), pérdida de sinapsis y pérdida de neuronas. Las neuronas grandes se afectan más que las pequeñas. Los pacientes de EA también pueden padecer otras lesiones no específicas, como degeneración granulovacuolar, cuerpos de Hirano y cuerpos de Lewy. Estos pacientes presentan una gran pérdida de neuronas colinérgicas, especialmente las que están situadas en el núcleo basal de Meynert, así como una disminución de la actividad de la colina acetil transferasa (CAT), lo que sugirió que la mayoría de los trastornos cognitivos de la EA estaban provocados por la pérdida del sistema colinérgico. Curiosamente, unos estudios realizados recientemente en sujetos con un deterioro cognitivo leve (DCL) –se piensa que estos pacientes están en riesgo de desarrollar la EA– han demostrado que estos sujetos pueden tener PN y ON en el neocórtex y los sistemas límbicos y paralímbicos, con niveles relativamente normales de CAT en varias regiones cerebrales. Esto sugiere que las estructuras del sistema colinérgico están relativamente preservadas en las primeras etapas de la enfermedad. Los científicos han hecho avances significativos en la comprensión de las manifestaciones clínicas y las patobiológicas de la EA; sin embargo, se desconocen los mecanismos que explican la vulnerabilidad específica del sistema colinérgico a la EA, así como el proceso inicial que conduce a las complejas lesiones neuropatológicas (AU)


The neuropathological hallmarks of Alzheimer’s disease (AD) are the presence of senile (neuritic) plaques (NP), neurofibrillary tangles (NFT), synapse loss, and neuronal cell loss. Large neurons are more affected than small ones. AD patients can also have other non-specific lesions, such as granulovacuolar degeneration, Hirano bodies, and Lewy bodies. AD patients present a loss of many cholinergic neurons, especially those located in the nucleus basalis of Meynert, as well as a decrease of choline acetyl transferase (ChAT) activity, which suggested that the core of the cognitive deficits of AD was caused by the loss of cholinergic input. Interestingly, recent studies conducted in subjects with mild cognitive impairment (MCI) (these are patients that are at risk of developing AD) have shown that these subjects can have NP and NFT in the neocortex and allocortex, with relatively normal levels of ChAT in a variety of brain regions. This suggests the structures of the cholinergic system are preserved in early stages of the disease. Scientists have made significant advances in understanding both the clinical manifestations and pathobiological manifestations of AD. However, the mechanisms of specific vulnerability of the cholinergic system to AD, as well as the initial process that leads to the complex neuropathological lesions are unknown (AU)


Assuntos
Humanos , Idoso , Doença de Alzheimer/patologia , Encéfalo/patologia , Transtornos Cognitivos/patologia , Doença de Alzheimer/enzimologia , Encéfalo/enzimologia , Colina O-Acetiltransferase/análise , Colina O-Acetiltransferase/deficiência , Proteínas do Tecido Nervoso/análise , Neurotransmissores/fisiologia
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