scholarly journals Aberrant changes of somatostatin and neuropeptide Y in brain of a genetic rat model for epilepsy: tremor rat

2016 ◽  
Vol 76 (3) ◽  
pp. 165-175
Author(s):  
Xiaoxue Xu ◽  
Feng Guo ◽  
Xinze Cai ◽  
Jun Yang ◽  
Jiuhan Zhao ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Rat Model ◽  
Tremor Rat

Role of neuropeptide Y Y1 and Y2 receptors on behavioral despair in a rat model of depression with co-morbid anxiety

2012 ◽  
Vol 62 (1) ◽  
pp. 200-208 ◽  
Author(s):  
Julio César Morales-Medina ◽  
Yvan Dumont ◽  
Charles-Etienne Benoit ◽  
Stéphane Bastianetto ◽  
Gonzalo Flores ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Rat Model ◽  
Behavioral Despair

Gene therapy mediated seizure suppression in Genetic Generalised Epilepsy: Neuropeptide Y overexpression in a rat model

2018 ◽  
Vol 113 ◽  
pp. 23-32 ◽  
Author(s):  
Kim L. Powell ◽  
Xavier Fitzgerald ◽  
Claire Shallue ◽  
Valentina Jovanovska ◽  
Matthias Klugmann ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Neuropeptide Y ◽  
Rat Model ◽  
Seizure Suppression

Neuropeptide Y system mRNA expression changes in the hippocampus of a type I diabetes rat model

2020 ◽  
Vol 227 ◽  
pp. 151419
Author(s):  
Elisa J. Campos ◽  
João Martins ◽  
Dan Brudzewsky ◽  
David P.D. Woldbye ◽  
António F. Ambrósio
Keyword(s):  
Neuropeptide Y ◽  
Mrna Expression ◽  
Rat Model ◽  
Type I Diabetes ◽  
Type I

scholarly journals Metabolic acetate therapy improves phenotype in the tremor rat model of Canavan disease

2010 ◽  
Vol 33 (3) ◽  
pp. 195-210 ◽  
Author(s):  
Peethambaran Arun ◽  
Chikkathur N. Madhavarao ◽  
John R. Moffett ◽  
Kristen Hamilton ◽  
Neil E. Grunberg ◽  
...  
Keyword(s):  
Rat Model ◽  
Canavan Disease ◽  
Tremor Rat

scholarly journals Long-Term Valproate Treatment Increases Brain Neuropeptide Y Expression and Decreases Seizure Expression in a Genetic Rat Model of Absence Epilepsy

PLoS ONE ◽  
2013 ◽  
Vol 8 (9) ◽  
pp. e73505 ◽  
Author(s):  
Johanna Elms ◽  
Kim L. Powell ◽  
Leena van Raay ◽  
Stefanie Dedeurwaerdere ◽  
Terence J. O’Brien ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Rat Model ◽  
Absence Epilepsy

Neuropeptide Y suppresses absence seizures in a genetic rat model primarily through effects on Y2 receptors

2007 ◽  
Vol 25 (4) ◽  
pp. 1136-1143 ◽  
Author(s):  
Margaret J. Morris ◽  
Emma Gannan ◽  
Leanne M. Stroud ◽  
Annette G. Beck-Sickinger ◽  
Terence J. O'Brien
Keyword(s):  
Neuropeptide Y ◽  
Rat Model ◽  
Absence Seizures

scholarly journals Distribución hipocampal del Neuropeptido Y (NPY) en un modelo animal de demencia senil del tipo Alzheimer inducido por estreptozotocina

2019 ◽  
pp. 172-175
Keyword(s):  
Neuropeptide Y ◽  
Rat Model ◽  
Male Rats ◽  
Mammalian Brain ◽  
Amino Acid Peptide ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Hippocampal Ca1 ◽  
Dementia Of Alzheimer’S Type ◽  
De Medicina

Distribución hipocampal del Neuropeptido Y (NPY) en un modelo animal de demencia senil del tipo Alzheimer inducido por estreptozotocina Hippocampal distribution of neuropeptide Y in rat model of streptozotocin-induced experimental dementia of Alzheimer’s type Ariza A, Andrade R, Aguilar LA Laboratorio de Neurociencia y Comportamiento, Facultad de Medicina “Alberto Hurtado’’, Universidad Peruana Cayetano Heredia, Lima 31, Perú. DOI: https://doi.org/10.33017/RevECIPeru2011.0041/ RESUMEN La distribución de numerosos neuropéptidos en el cerebro humano sugiere que los sistemas peptidérgicos pueden contribuir a la patogénesis del déficit cognitivo en el envejecimiento patológico tal como trastornos de demencia. El neuropéptido Y (NPY) es un péptido de 36 aminoácidos y además es el neuropéptido conocido más abundante en el cerebro de mamíferos. La estructura primaria del NPY ha sido bien preservada durante la evolución haciendo a este neuropéptido uno de los neuropéptidos mas conservados entre especies. A pesar de que algunos datos divergentes se encuentran disponibles en la bibliografía científica, la mayor parte de las evidencias sugiere que los niveles del NPY en la corteza, hipocampo, ganglio basal y líquido cefalorraquídeo son contradictorios. La inyección intracerebroventricular de estreptozotocina causa insuficiencia de la glucosa cerebral y metabolismo energético junto con el daño oxidativo y disfunción colinérgica, y provee un modelo relevante para la enfermedad de Alzheimer. El presente estudio examinó la presencia de cuerpos celulares inmunoreactivos conteniendo NPY en un modelo animal para la enfermedad de Alzheimer. Ratas machos fueron inyectados bilateralmente con estreptozotocina (0.5mg/kg), mientras que las ratas controles recibieron el mismo volumen del vehículo, luego las ratas fueron sacrificadas para los análisis inmunocitoquímicos. Un mes después de la inyección de estreptozotocina una alta densidad de células inmunoreactivas para NPY fueron encontradas en las regiones CA1, CA2 y CA3 del hipocampo y en el giro dentado (DG). Además, astrocitos activados fueron vistos en el hipocampo y en la corteza. La distribución del NPY indica que el neuropéptido estudiado puede estar involucrado en múltiples funciones como neuroprotección en el cerebro de las ratas. Estos datos sugieren que el neuropéptido Y puede tener funciones importantes en la progresión de la enfermedad de Alzheimer. Descriptores: Selenito de sodio, NPY, estreptozotocina, demecia senil del tipo alzheimer ABSTRACT Distribution of numerous neuropeptides in the human brain suggests that peptidergic systems may contribute to the pathogenesis of cognitive impairment in pathological aging such as dementia disorders. Neuropeptide Y (NPY) is a 36-amino acid peptide and it is the most abundant neuropeptide presently known in the mammalian brain. The primary structure of NPY has been well preserved during evolution making this peptide one of the most conserved among species. Although some divergent data are available, the bulk of evidence suggests that NPY levels in cortex, hippocampus, basal ganglia and cerebrospinal fluid are contradictory. Intracerebroventricular-streptozotocin (ICV-STZ) in rats causes impairment of brain glucose and energy metabolism along with oxidative damage and cholinergic mdysfunction, and provides a relevant model for Alzheimer’s disease (AD). The present study examined the presence of inmmunoreactive cell bodies containing NPY in a rat model of AD. Male rats were injected bilaterally with ICV-STZ (0.5mg/kg), while sham rats received the same volume of vehicle, then rats were sacrificed for immunocytochemical assays. One month after STZ injection a high density of NPY-immunoreactive perikarya was found in the hippocampal CA1 region, CA2 region, CA3 region and dentate gyrus (DG). In addition, activated astrocytes were seen in the hippocampus and in the cortex. This NPY distribution indicates that the neuropeptide studied might be involved in multiple functions like neuroprotection in the rat brain. These finding suggest that NPY may have important roles in the progression of AD. Keywords: Sodium selenite, NPY, Streptozotocin, Sporadic dementia of Alzheimer's type.

Anxiety responses and neurochemical changes in a kaolin-induced rat model of hydrocephalus

2011 ◽  
Vol 7 (4) ◽  
pp. 401-407 ◽  
Author(s):  
Yong Sup Hwang ◽  
Insop Shim ◽  
Jin Woo Chang
Keyword(s):  
Neuropeptide Y ◽  
Rat Model ◽  
Elevated Plus Maze ◽  
Sprague Dawley ◽  
Injection Group ◽  
Abnormal Gait ◽  
Sprague Dawley Rats ◽  
Plus Maze ◽  
Anxiety Response ◽  
Neurochemical Changes

Object Hydrocephalus is a pathological enlargement of the ventricles of the brain, which can result from various diseases of the central nervous system. Patients with hydrocephalus frequently show motor abnormalities, such as abnormal gait and posture, as well as intellectual and emotional impairment. The present study was designed to investigate anxiety responses in rats with kaolin-induced hydrocephalus. Methods A total of 26 Sprague-Dawley rats were used for this study. Hydrocephalus was induced in 14 Sprague-Dawley rats by injecting 0.1 ml of 20% kaolin solution into the cisterna magna; 12 rats were administered the same volume of saline in the same fashion and served as controls. Seven of the rats that were injected with kaolin and 6 of the rats injected with saline were killed 3 days after injection (Group 1); the remaining rats were killed 4 weeks after injection (Group 2) to evaluate effects related to acute and chronic hydrocephalus. The rats were tested in an elevated plus maze after induction of hydrocephalus by kaolin injection. After the animals were killed, brain sections were immunostained for cholecystokinin and neuropeptide Y. In addition, tyrosine hydroxlyase immunoreactivity in the ventral tegmental area was evaluated by immunohistological staining. Results The rats with acute hydrocephalus showed decreased entry into and spent less time in the open arms of the elevated plus maze as compared with the control rats. The hydrocephalic rats had significantly more cholecystokinin-immunoreactive neurons and fewer neuropeptide Y–immunoreactive neurons in their brains. In addition, hydrocephalus progress in this model was positively correlated with the anxiety response. The numbers of tyrosine hydroxlyase–immunoreactive neurons were decreased significantly in the hydrocephalic rats as compared with the control rats. Conclusions These results suggest that the rat model of hydrocephalus is characterized by increased anxiety response and is associated with the functional impairment of the central dopamine system.

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