Key result
56Fe-particle irradiation decreased muscarinic-stimulated low-Km GTPase in the striatum but not the hippocampus, and did not affect alpha 1-adrenergic low-Km GTPase activity in either tissue.
56Fe-particle irradiation specifically reduces muscarinic-stimulated low-Km GTPase activity in the rat striatum without affecting alpha 1-adrenergic pathways.
Highlights selective striatal muscarinic effects in rats after heavy-ion exposure; leaves open translation to human CNS radiation risks.
Initial findings from our laboratory have indicated that muscarinic enhancement of K(+)-evoked release of dopamine from perifused striatal slices is reduced after exposure to 56Fe-particle irradiation. This finding suggested that there is a radiation-induced deficit in muscarinic receptor sensitivity. Subsequent findings have indicated that at least part of the loss in sensitivity may occur as a result of alterations in the initial steps of the signal transduction process and involve muscarinic receptor-G protein coupling/uncoupling. The present study was carried out to localize this deficit further by determining carbachol-stimulated low-Km guanosine triphosphatase (GTPase) activity in striatal and hippocampal tissue obtained from rats exposed to 0, 0.1 or 1.0 Gy of 56Fe-particle irradiation. In addition, to examine the specificity of the effect of 56Fe-particle irradiation, alpha 1-adrenergic-stimulated low-Km GTPase activity was also examined in these tissues. The results showed that there was a high degree of specificity in the effects of 56Fe particles. Decrements were observed in muscarinic-stimulated low-Km GTPase in striatum but not in hippocampus, and 56Fe-particle irradiation did not affect alpha 1-adrenergic low-Km GTPase activity in either brain tissue.
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Villalobos‐Molina et al. (1994) studied this question. 56Fe-particle irradiation vs. 0 Gy was evaluated on Carbachol-stimulated and alpha 1-adrenergic-stimulated low-Km GTPase activity in striatal and hippocampal tissue. 56Fe-particle irradiation decreased muscarinic-stimulated low-Km GTPase in the striatum but not the hippocampus, and did not affect alpha 1-adrenergic low-Km GTPase activity in either tissue.
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