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ischemia damages more than 90% of CA1 neurons, the dorsolateral
striatal neurons, and about 10% of neocortical neurons, whereas
20 min of ischemia leads to delayed neuronal death in more than
30% of neocortical neurons and also extends delayed neuronal
death to neurons in the CA3 and DG regions.
Figure 4 illustrates typical histopathological changes in the
hippocampal regions after transient cerebral ischemia in the 2
vessel-occlusion (with hypotension) forebrain ischemia (2VO)
model in rat. Male Wistar rats were subjected to either sham-surgery
without ischemia, or 10 min of ischemia followed by 7 days of rep-
erfusion, respectively. Paraffi n-embedded coronal sections (10 mm)
were photographed by light microscopy. Selective neuronal death
is evident in more than 80% of pyramidal neurons in the CA1
region of the hippocampus after 10 min of cerebral ischemia in the
2VO model.
5. Potential
Technical
Diffi culties
and Pitfalls
Even though histology is routinely used by various laboratories, it
is relatively long procedure. Every step in the procedure is important.
High temperature during tissue processing or longer time in cleansing
agents can make tissue brittle and damage tissue integrity.
References
1. Bederson JB et al (1986) Evaluation of 2,3,5-tri-
phenyltetrazolium chloride as a stain for detec-
tion and quantifi cation of experimental cerebral
infarction
improves histopathological outcome after moderate
fl uid percussion brain injury in rats. Neurosurgery
45(3):601-608
4. Bancroft JD, Stevens A (1996) Theory and prac-
tice of histological techniques. Churchill
Livingstone, Edinburgh, p 766
5. Smith ML et al (1984) Models for studying
long-term recovery following forebrain ischemia
in the rat. 2. A 2-vessel occlusion model. Acta
Neurol Scand 69(6):385-401
in
rats.
Stroke
17(6):
1304-1308
2. Sicard KM, Fisher M (2009) Animal models of
focal brain ischemia. Exp Transl Stroke Med
1:7
3. Wada K et al (1999) Early treatment with a novel
inhibitor of lipid peroxidation (LY341122)
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