TY - JOUR
T1 - Acute increase in expression of growth associated protein GAP-43 following cortical ischemia in rat
AU - Stroemer, R. Paul
AU - Kent, Thomas A.
AU - Hulsebosch, Claire E.
N1 - Funding Information:
This work is supported by NS 01217, NS 07185, NS 11255, RR 03979, and Bristol Myers-Squibb.
PY - 1993/11/12
Y1 - 1993/11/12
N2 - Focal cerebral ischemia creates an area of infarction that is surrounded by neuronal tissue that may respond to nearby damage by creating neurite growth. To determine if axonal sprouting occurs after infarction, antibodies to growth associated protein MW 43,000 (GAP-43), a protein expressed on axonal growth cones, were used to assess the level of GAP-43 immunoreactivity as a measure of sprouting. Cerebral ischemia was induced in spontaneously hypertensive rats by permanently occluding the distal middle cerebral artery and ipsilateral common carotid artery. After I week of recovery, the animals were perfused, the brains removed, processed, and optical densities of the immunuoreaction were measured. The cortex surrounding the infarcted area had increased optical densities ( x ̄ ± S.D. = 14.2% ± 5.5) compared to the optical density values measured in similar areas in the contralateral hemisphere ( x ̄ ± S.D. = 6.0% ± 3.3), a 136% increase that is statistically significant, P < 0.05 Student's t-test. We hypothesize that this increase in GAP-43 reaction product is due to axonal sprouting in the cortex surrounding an area of infarction. These data, coupled with previous work examining synaptophysin levels after cortical infarction, support the hypothesis of sprouting and synaptogenesis in the cortex following cerebral infarction.
AB - Focal cerebral ischemia creates an area of infarction that is surrounded by neuronal tissue that may respond to nearby damage by creating neurite growth. To determine if axonal sprouting occurs after infarction, antibodies to growth associated protein MW 43,000 (GAP-43), a protein expressed on axonal growth cones, were used to assess the level of GAP-43 immunoreactivity as a measure of sprouting. Cerebral ischemia was induced in spontaneously hypertensive rats by permanently occluding the distal middle cerebral artery and ipsilateral common carotid artery. After I week of recovery, the animals were perfused, the brains removed, processed, and optical densities of the immunuoreaction were measured. The cortex surrounding the infarcted area had increased optical densities ( x ̄ ± S.D. = 14.2% ± 5.5) compared to the optical density values measured in similar areas in the contralateral hemisphere ( x ̄ ± S.D. = 6.0% ± 3.3), a 136% increase that is statistically significant, P < 0.05 Student's t-test. We hypothesize that this increase in GAP-43 reaction product is due to axonal sprouting in the cortex surrounding an area of infarction. These data, coupled with previous work examining synaptophysin levels after cortical infarction, support the hypothesis of sprouting and synaptogenesis in the cortex following cerebral infarction.
KW - Cerebral ischemia
KW - GAP-43
KW - Immunohistochemistry
KW - Middle cerebral artery
KW - Plasticity
KW - Sprouting
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U2 - 10.1016/0304-3940(93)90557-2
DO - 10.1016/0304-3940(93)90557-2
M3 - Article
C2 - 8121636
AN - SCOPUS:0027504942
SN - 0304-3940
VL - 162
SP - 51
EP - 54
JO - Neuroscience Letters
JF - Neuroscience Letters
IS - 1-2
ER -