Abstract
Plasticity in the central nervous system after cerebral ischemia is a controversial issue; focal cerebral ischemia produces an area of infarction that is surrounded by neurons that may respond to nearby damage by creating new synapses. In the present study the expression of the postsynaptic microtubule-associated protein 2 (MAP2) and the presynaptic marker protein, synaptophysin, was investigated by immunocytochemical techniques in the CA1 sector of hippocampus and in cerebellum of rats made ischemic by bilateral clamping of common carotid arteries and reperfused for 7 and 30 days. In addition, ischemia-induced behavioral alterations were also evaluated after 7 and 30 days of reperfusion. The present study demonstrates a decreased postsynaptic MAP2 immunoreactivity, representative of neuronal loss, particularly in CA1 sector of hippocampus and in cerebellum of ischemic rats reperfused for 7 days. After 30 days of reperfusion, MAP2 immunostaining was similar to control. In the same brain sections an increased presynaptic synaptophysin immunoreactivity has been observed only after 30 days of reperfusion. These data suggest compensatory regenerative changes associated with synaptic remodelling and are supported by behavioral recovery observed under the same experimental conditions.
Original language | English (US) |
---|---|
Pages (from-to) | 457-464 |
Number of pages | 8 |
Journal | Developmental Neuroscience |
Volume | 19 |
Issue number | 6 |
State | Published - Nov 1997 |
Externally published | Yes |
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Keywords
- Behavior
- Cerebral ischemia
- MAP2
- Synaptophysin
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
MAP2, synaptophysin immunostaining in rat brain and behavioral modifications after cerebral postischemic reperfusion. / Martinez, G.; Di Giacomo, C.; Carnazza, M. L.; Sorrenti, V.; Castana, R.; Barcellona, M. L.; Perez-Polo, J. R.; Vanella, A.
In: Developmental Neuroscience, Vol. 19, No. 6, 11.1997, p. 457-464.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - MAP2, synaptophysin immunostaining in rat brain and behavioral modifications after cerebral postischemic reperfusion
AU - Martinez, G.
AU - Di Giacomo, C.
AU - Carnazza, M. L.
AU - Sorrenti, V.
AU - Castana, R.
AU - Barcellona, M. L.
AU - Perez-Polo, J. R.
AU - Vanella, A.
PY - 1997/11
Y1 - 1997/11
N2 - Plasticity in the central nervous system after cerebral ischemia is a controversial issue; focal cerebral ischemia produces an area of infarction that is surrounded by neurons that may respond to nearby damage by creating new synapses. In the present study the expression of the postsynaptic microtubule-associated protein 2 (MAP2) and the presynaptic marker protein, synaptophysin, was investigated by immunocytochemical techniques in the CA1 sector of hippocampus and in cerebellum of rats made ischemic by bilateral clamping of common carotid arteries and reperfused for 7 and 30 days. In addition, ischemia-induced behavioral alterations were also evaluated after 7 and 30 days of reperfusion. The present study demonstrates a decreased postsynaptic MAP2 immunoreactivity, representative of neuronal loss, particularly in CA1 sector of hippocampus and in cerebellum of ischemic rats reperfused for 7 days. After 30 days of reperfusion, MAP2 immunostaining was similar to control. In the same brain sections an increased presynaptic synaptophysin immunoreactivity has been observed only after 30 days of reperfusion. These data suggest compensatory regenerative changes associated with synaptic remodelling and are supported by behavioral recovery observed under the same experimental conditions.
AB - Plasticity in the central nervous system after cerebral ischemia is a controversial issue; focal cerebral ischemia produces an area of infarction that is surrounded by neurons that may respond to nearby damage by creating new synapses. In the present study the expression of the postsynaptic microtubule-associated protein 2 (MAP2) and the presynaptic marker protein, synaptophysin, was investigated by immunocytochemical techniques in the CA1 sector of hippocampus and in cerebellum of rats made ischemic by bilateral clamping of common carotid arteries and reperfused for 7 and 30 days. In addition, ischemia-induced behavioral alterations were also evaluated after 7 and 30 days of reperfusion. The present study demonstrates a decreased postsynaptic MAP2 immunoreactivity, representative of neuronal loss, particularly in CA1 sector of hippocampus and in cerebellum of ischemic rats reperfused for 7 days. After 30 days of reperfusion, MAP2 immunostaining was similar to control. In the same brain sections an increased presynaptic synaptophysin immunoreactivity has been observed only after 30 days of reperfusion. These data suggest compensatory regenerative changes associated with synaptic remodelling and are supported by behavioral recovery observed under the same experimental conditions.
KW - Behavior
KW - Cerebral ischemia
KW - MAP2
KW - Synaptophysin
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UR - http://www.scopus.com/inward/citedby.url?scp=0030830756&partnerID=8YFLogxK
M3 - Article
C2 - 9445083
AN - SCOPUS:0030830756
VL - 19
SP - 457
EP - 464
JO - Developmental Neuroscience
JF - Developmental Neuroscience
SN - 0378-5866
IS - 6
ER -