TY - JOUR
T1 - Decrease of somatostatin receptor binding in the rat cerebral cortex after ibotenic acid lesion of the nucleus basalis magnocellularis
T2 - a quantitative autoradiographic study
AU - Bogdanovic, Nenad
AU - Nilsson, Lars
AU - Adem, Abdu
AU - Winblad, Bengt
AU - Bergström, Lena
N1 - Funding Information:
Acknowledgements. The authors wish to thank Mrs. Inga Volkmann for expert technical assistance and Dr. Eric Messamore for valuable discussion and revising the manuscript. The financial support of the Swedish Medical Research Council, Axelsson Johnsson Foundation, Sandoz Foundation for Gerontological Research, Swedish Institute, King Gustaf V:s and 9ueen Victorias Foundation, Gun and Bertil Stohnes Foundation, Ake Wibergs Foundation, Claes Groschinskys Foundation, Ahl6ns Foundation, Loo and Hans Ostermans Foundation and the Swedish Alzheimer Foundation, are gratefully acknowledged.
PY - 1993/11/19
Y1 - 1993/11/19
N2 - The specific binding of 125I-Tyr11-somatostatin-14 (125I-Tyr11-SS-14) was measured in different cortical regions after unilateral ibotenic acid lesion of the rat nucleus basalis magnocellularis (NBM). A marked loss of acetylcholinesterase-positive fibers was observed in the frontal, parietal, temporal and occipital cortices ipsilateral to the lesion. The loss of cholinergic cell bodies in the NBM was further investigated with cholineacetyltransferase (ChAT) immunohistochemistry which indeed demonstrated a loss of ChAT-positive magnocellular perikarya. Autoradiographic analyses of specific binding of 125I-Tyr11-SS-14 demonstrated a significant reduction in binding density in the denervated parts of the neocortex. The decrease in specific binding was most pronounced (40-50%) in the superficial layers (I-III) of the frontal, parietal and temporal cortices 2 and 4 weeks after lesion. A significant loss in 125I-Tyr11-SS-14 binding in the deeper layers was only observed in the frontal cortex after 2 and 4 weeks. In the occipital cortex a significant decrease was measured in the superficial layers only after 4 weeks. The specific binding in all cortical regions returned to normal after 6 weeks. The results suggested that 125I-Tyr11-SS-14 binding sites are localized on cholinergic afferents in the rat neocortex and that an up-regulation of number of binding sites, alternatively an increased binding affinity occured with time after lesion.
AB - The specific binding of 125I-Tyr11-somatostatin-14 (125I-Tyr11-SS-14) was measured in different cortical regions after unilateral ibotenic acid lesion of the rat nucleus basalis magnocellularis (NBM). A marked loss of acetylcholinesterase-positive fibers was observed in the frontal, parietal, temporal and occipital cortices ipsilateral to the lesion. The loss of cholinergic cell bodies in the NBM was further investigated with cholineacetyltransferase (ChAT) immunohistochemistry which indeed demonstrated a loss of ChAT-positive magnocellular perikarya. Autoradiographic analyses of specific binding of 125I-Tyr11-SS-14 demonstrated a significant reduction in binding density in the denervated parts of the neocortex. The decrease in specific binding was most pronounced (40-50%) in the superficial layers (I-III) of the frontal, parietal and temporal cortices 2 and 4 weeks after lesion. A significant loss in 125I-Tyr11-SS-14 binding in the deeper layers was only observed in the frontal cortex after 2 and 4 weeks. In the occipital cortex a significant decrease was measured in the superficial layers only after 4 weeks. The specific binding in all cortical regions returned to normal after 6 weeks. The results suggested that 125I-Tyr11-SS-14 binding sites are localized on cholinergic afferents in the rat neocortex and that an up-regulation of number of binding sites, alternatively an increased binding affinity occured with time after lesion.
KW - Autoradiography
KW - Cerebral cortex
KW - Ibotenic acid lesion
KW - Nucleus basalis magnocellularis
KW - Somatostatin receptor binding
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U2 - 10.1016/0006-8993(93)90934-F
DO - 10.1016/0006-8993(93)90934-F
M3 - Article
C2 - 8313162
AN - SCOPUS:0027452286
SN - 0006-8993
VL - 628
SP - 31
EP - 38
JO - Brain Research
JF - Brain Research
IS - 1-2
ER -