Neuroscience 2004 Abstract
| Presentation Number: | 218.10 |
|---|---|
| Abstract Title: | The fraction 25-35 of β amyloid in neonatal rats enhances nitric oxide levels into hippocampus. |
| Authors: |
Limon Perez De Leon, I. D.*1
; Osorio Espinoza, A. E.1
; Cuevas Martinez, E.1
; Gonzalez Xelo, C.1
; Diaz Fonseca, A.1
; Parra Cid, M.1
; Camacho Abrego, I.1
; Guevara Fonseca, J.2
1Departamento de Farmacia, Benemerita Universidad Autonoma de Puebla FCQ, Puebla, Mexico 2Mexico, 14 sur y Av. Sn Claudio Edif. 139/110 C.U., 72570, Mexico |
| Primary Theme and Topics |
Neurological and Psychiatric Conditions - Neurodegenerative Disorders -- Alzheimer's Disease: Neuropharmacology and neurotransmitters |
| Secondary Theme and Topics | Neurological and Psychiatric Conditions<br />- Neurodegenerative Disorders<br />-- Alzheimer's Disease: Experimental models |
| Session: |
218. Ab Toxicity: Mechanisms II Poster |
| Presentation Time: | Sunday, October 24, 2004 9:00 AM-10:00 AM |
| Location: | San Diego Convention Center - Hall A-H, Board # TT1 |
| Keywords: | Alzheimer'disease, Neurotoxicity, Beta amyloid, Nitric Oxide |
The toxicity of the protein β-amyloid (βA) is correlated with the production of oxidative stress by nitric oxide (NO) production. The last meeting we show that this fraction increase the neural death into hippocampus (Limon et al.,Abs 842.5, SFN 2003). NO is a free radical that produce cellular damage and cellular death. The βA damage is present into the frontal cortex (CX) and hippocampus (Hp) in senile patients with Alzheimer’s Disease (AD). However is unclear about the effect on early stages. The aim of this investigation was evaluate the effect of 25-35 βA fraction on nitric oxide levels into CX and Hp of neonatal rats. Males and females Wistar rats of seven postnatal day (PD7), were used. We injected 1 µl of 25-35 β A fraction [100µM] previously incubated at 37°C x 24 hrs was by stereotaxic surgery into CX. The groups with four, eight and sixteen hours post-administration were sacrificed and measure the NO levels by the Griess reaction in CX and Hp.
Four hours post-administration, we found that NO levels enhanced 121% into CX male rats and 309% into Hp females rats. However there were not changes in the groups with eight and sixteen hours post-administration in both sex.
The results indicate that 25-35 βA into CX and Hp produce neurotoxicity in neonatal rats. The 25-35 βA can be present since early stages increasing NO production.
Four hours post-administration, we found that NO levels enhanced 121% into CX male rats and 309% into Hp females rats. However there were not changes in the groups with eight and sixteen hours post-administration in both sex.
The results indicate that 25-35 βA into CX and Hp produce neurotoxicity in neonatal rats. The 25-35 βA can be present since early stages increasing NO production.
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2004 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2004. Online.
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