“…Chronic treatment with carbamates and organophosphorus com pounds causes behavioral modifications such as changes in memory and learning ability and affects the cholinergic system such as causing changes in HAChT and [3H] QN B binding (28)(29)(30)(31)(32)(33)(34). We speculate that there is some relationship between the change in HAChT or [3H]QNB binding and rotarod performance in the present experiments.…”
Abstract-Propoxur, an anticholinesterase carbamate, was injected singly (10 mg/ kg, s.c.) or chronically (5 mg/kg/day, s.c., for 10 days) into mice. Animals were examined for effects on the cholinergic system in brain tissue and on behavior. Single injection caused an increase in brain acetylcholine (ACh) content at 10 and 60 min; and it caused decreases in acetylcholinesterase (AChE) activity at 10, 60 and 180 min, high-affinity choline uptake into synaptosomes at 10 and 60 min, and [3H]quinuclidinyl benzilate (QNB) binding at 10 min without causing any change in choline acetyltransferase (ChAT) activity. Open-field behavior and rotarod performance were depressed at 10 min and rectal temperature was decreased at 10,
“…Chronic treatment with carbamates and organophosphorus com pounds causes behavioral modifications such as changes in memory and learning ability and affects the cholinergic system such as causing changes in HAChT and [3H] QN B binding (28)(29)(30)(31)(32)(33)(34). We speculate that there is some relationship between the change in HAChT or [3H]QNB binding and rotarod performance in the present experiments.…”
Abstract-Propoxur, an anticholinesterase carbamate, was injected singly (10 mg/ kg, s.c.) or chronically (5 mg/kg/day, s.c., for 10 days) into mice. Animals were examined for effects on the cholinergic system in brain tissue and on behavior. Single injection caused an increase in brain acetylcholine (ACh) content at 10 and 60 min; and it caused decreases in acetylcholinesterase (AChE) activity at 10, 60 and 180 min, high-affinity choline uptake into synaptosomes at 10 and 60 min, and [3H]quinuclidinyl benzilate (QNB) binding at 10 min without causing any change in choline acetyltransferase (ChAT) activity. Open-field behavior and rotarod performance were depressed at 10 min and rectal temperature was decreased at 10,
“…Several pervious in vivo studies reported a reduction in the number of muscarinic receptors in certain brain areas as a result of chronic exposure to various OPs (Schiller, 1979;Costa et al, 1982;Russell and Overstreet, 1987).…”
Section: Discussionmentioning
confidence: 99%
“…Muscarinic receptor subtypes differ in synaptic and tissue localization, agonist and antagonist affinity, and the second messenger systems associated with them (Caulfield and Birdsall, 1998). By far the most common and consistent finding on repeated exposure to OP antiAChEs has been a reduction in the number of mAChRs (Schiller, 1979;Costa et al, 1982;Yamada et al, 1983;Churchill et al, 1984aChurchill et al, , 1984b. It has been suggested as the primary mechanism by which animals adapt to or compensate for sustained mAChR activation (Russell and Overstreet, 1987;Hoskins and Ho, 1992).…”
-The neurochemical and behavioral effects of repeated subdermal administration of methyl parathion (MP) at low doses were investigated. Adult male rats were treated repeatedly with either vehicle or MP subcutaneously (3 mg/kg/day) and observed for the signs of toxicity during the treatment period. The toxic sign, tremor, reached maximum right after 9 th injection in MP-treated rats, and declined thereafter. Animals were sacrificed and brains were taken 1 week or 3 weeks after the daily treatment for measurement of acetylcholinesterase (AChE) 3 H]AF-DX384 binding (6 ~ 38%) in different brain regions, including striatum, hippocampus, frontal cortex, thalamus and midbrain. After 1 week of treatment, the inhibition of AChE in brain regions was from 54 to 74%, whereas receptor densities were only marginally affected in a few regions. The timing of the changes in receptor population correlates well with the changes in behaviors during the repeated MP exposure. Our findings suggest that down-regulation of muscarinic receptors plays a role in the development of tolerance to MP. And, the regulations of muscarinic receptors were different among receptor subtypes and brain regions.
“…By far the most common and consistent finding among the reports on chronic exposure to organophosphate compounds has been a reduction in the number of muscarinic AChRs 1.5 EFFECTS ON ACETYLCHOLINE RECEPTORS (Churchill et al, 1984a(Churchill et al, , 1984bCosta et al, 1982aCosta et al, , 1982bGupta et al, 1985;Kobayashi et al, 2007;Russell and Overstreet, 1987;Schiller, 1979;Sun et al, 2003;Yamada et al, 1983). Previous studies have shown that repeated postnatal exposure of rats to organophosphates resulted in persistent inhibition of brain AChE and transient reductions of total and M2/M4 mAChR (Liu et al, 1999;Tang et al, 1999).…”
Section: Effects On Muscarinic Receptorsmentioning
confidence: 98%
“…These homeostatic mechanisms involve modulation of both presynaptic and/or postsynaptic components of the cholinergic synapse. These may involve changes in HACU, ChAT, and the vesicular VAChT in the presynaptic terminal and modifications of mAChRs and nAChRs for both the postsynaptic and presynaptic components (Costa et al, 1981a(Costa et al, , 1981b(Costa et al, , 1982a(Costa et al, , 1982bKobayashi et al, 1986Kobayashi et al, , 1997Padilla, 1995;Richardson and Chambers, 2003Russell and Overstreet, 1987;Schwab et al, 1981Schwab et al, , 1983Whalley and Shih, 1988).…”
Section: Effects On Release Synthesis and Storage Of Acetylcholinementioning
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