Baseline temperature in an animal model of schizophrenia: Long-term effects of perinatal phencyclidine administration

2008 ◽  
Vol 93 (3) ◽  
pp. 437-443 ◽  
Author(s):  
Nevena V. Radonjić ◽  
Nataša D. Petronijević ◽  
Sonja M. Vučković ◽  
Milica Š. Prostran ◽  
Zorica I. Nešić ◽  
...  
Keyword(s):  
Animal Model ◽  
Long Term Effects ◽  
Baseline Temperature

The long-term effects of the dopamine agonist pramipexole in a proposed restless legs syndrome animal model

2011 ◽  
Vol 12 (1) ◽  
pp. 41-46 ◽  
Author(s):  
Feifei Luo ◽  
Chao Li ◽  
William G. Ondo ◽  
Pingyi Xu ◽  
Wenjie Xie ◽  
...  
Keyword(s):  
Animal Model ◽  
Dopamine Agonist ◽  
Restless Legs Syndrome ◽  
Long Term Effects ◽  
Restless Legs

Development of 5-HT transporter density and long-term effects of methylphenidate in an animal model of ADHD

2009 ◽  
Vol 10 (4-2) ◽  
pp. 581-585 ◽  
Author(s):  
Veit Roessner ◽  
Till Manzke ◽  
Andreas Becker ◽  
Aribert Rothenberger ◽  
Nathalie Bock
Keyword(s):  
Animal Model ◽  
Long Term Effects

scholarly journals Long-Term Effects of Maternal Deprivation on the Neuronal Soma Area in the Rat Neocortex

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Milan Aksić ◽  
Nevena V. Radonjić ◽  
Dubravka Aleksić ◽  
Gordana Jevtić ◽  
Branka Marković ◽  
...  
Keyword(s):  
Animal Model ◽  
Morphological Changes ◽  
Maternal Deprivation ◽  
Retrosplenial Cortex ◽  
Control Group ◽  
Long Term Effects ◽  
Adult Rats ◽  
Adult Age ◽  
Neuronal Soma

Early separation of rat pups from their mothers (separatio a matrem) is considered and accepted as an animal model of perinatal stress. Adult rats, separated early postnatally from their mothers, are developing long-lasting changes in the brain and neuroendocrine system, corresponding to the findings observed in schizophrenia and affective disorders. With the aim to investigate the morphological changes in this animal model we exposed 9-day-old (P9) Wistar rats to a 24 h maternal deprivation (MD). At young adult age rats were sacrificed for morphometric analysis and their brains were compared with the control group bred under the same conditions, but without MD. Rats exposed to MD had a 28% smaller cell soma area in the prefrontal cortex (PFCX), 30% in retrosplenial cortex (RSCX), and 15% in motor cortex (MCX) compared to the controls. No difference was observed in the expression of glial fibrillary acidic protein in the neocortex of MD rats compared to the control group. The results of this study demonstrate that stress in early life has a long-term effect on neuronal soma size in cingulate and retrosplenial cortex and is potentially interesting as these structures play an important role in cognition.

Decreased glutathione levels and altered antioxidant defense in an animal model of schizophrenia: Long-term effects of perinatal phencyclidine administration

2010 ◽  
Vol 58 (4-5) ◽  
pp. 739-745 ◽  
Author(s):  
Nevena V. Radonjić ◽  
Iva D. Knežević ◽  
Urosh Vilimanovich ◽  
Tamara Kravić-Stevović ◽  
Ljiljana V. Marina ◽  
...  
Keyword(s):  
Animal Model ◽  
Antioxidant Defense ◽  
Long Term Effects

scholarly journals Increased Beta-Hydroxybutyrate Level Is Not Sufficient for the Neuroprotective Effect of Long-Term Ketogenic Diet in an Animal Model of Early Parkinson’s Disease. Exploration of Brain and Liver Energy Metabolism Markers

2021 ◽  
Vol 22 (14) ◽  
pp. 7556
Author(s):  
Katarzyna Z. Kuter ◽  
Łukasz Olech ◽  
Urszula Głowacka ◽  
Martyna Paleczna
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Animal Model ◽  
Energy Metabolism ◽  
Locomotor Activity ◽  
Ketogenic Diet ◽  
Long Term Effects ◽  
Beta Hydroxybutyrate ◽  
The Brain

The benefits of a ketogenic diet in childhood epilepsy steered up hope for neuroprotective effects of hyperketonemia in Parkinson’s disease (PD). There are multiple theoretical reasons but very little actual experimental proof or clinical trials. We examined the long-term effects of the ketogenic diet in an animal model of early PD. A progressive, selective dopaminergic medium size lesion was induced by 6-OHDA injection into the medial forebrain bundle. Animals were kept on the stringent ketogenic diet (1% carbohydrates, 8% protein, 70% fat) for 3 weeks prior and 4 weeks after the brain operation. Locomotor activity, neuron count, dopaminergic terminal density, dopamine level, and turnover were analyzed at three time-points post-lesion, up to 4 weeks after the operation. Energy metabolism parameters (glycogen, mitochondrial complex I and IV, lactate, beta-hydroxybutyrate, glucose) were analyzed in the brain and liver or plasma. Protein expression of enzymes essential for gluconeogenesis (PEPCK, G6PC) and glucose utilization (GCK) was analyzed in the liver. Despite long-term hyperketonemia pre- and post-lesion, the ketogenic diet did not protect against 6-OHDA-induced dopaminergic neuron lesions. The ketogenic diet only tended to improve locomotor activity and normalize DA turnover in the striatum. Rats fed 7 weeks in total with a restrictive ketogenic diet maintained normoglycemia, and neither gluconeogenesis nor glycogenolysis in the liver was responsible for this effect. Therefore, potentially, the ketogenic diet could be therapeutically helpful to support the late compensatory mechanisms active via glial cells but does not necessarily act against the oxidative stress-induced parkinsonian neurodegeneration itself. A word of caution is required as the stringent ketogenic diet itself also carries the risk of unwanted side effects, so it is important to study the long-term effects of such treatments. More detailed metabolic long-term studies using unified diet parameters are required, and human vs. animal differences should be taken under consideration.

scholarly journals Long-term effects of cerebral hypoperfusion on neural density and function using misery perfusion animal model

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Asuka Nishino ◽  
Yosuke Tajima ◽  
Hiroyuki Takuwa ◽  
Kazuto Masamoto ◽  
Junko Taniguchi ◽  
...  
Keyword(s):  
Animal Model ◽  
Cerebral Hypoperfusion ◽  
Long Term Effects ◽  
Misery Perfusion ◽  
And Function
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