Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A simple hypothesis can explain the results obtained to date if we disregard those results when we wait 30 minutes after original learning to inject. The hypothesis is that, as a result of learning, the postsynaptic endings at a specific set of synapses become more sensitive to transmitter. This sensitivity increases with time after initial learning and then declines. The rate at which such sensitivity increases depends on the amount of initial learning. If the curve of transmission plotted against time is displaced upward with anticholinesterases then the very low portions will show facilitation, and the high portions will cause block (Fig. 8). The middle portions will appear unaffected (unless special experimental tests are made). If the curve of transmission is displaced down with anticholinergics, then the middle portion will appear unaffected and only the very early or late components will show block. The results are evidence that synaptic conductance is altered as a result of learning. So far it seems (i) that cholinergic synapses are modified as a result of learning and that it probably is the postsynaptic membrane that becomes increasingly more sensitive to acetylcholine with time after learning, up to a certain point. (ii) After this point, sensitivity declines, leading to the phenomenon of forgetting. (iii) There is also good evidence that there is an initial phase of declining sensitivity to cholinesterase or increasing sensitivity to anticholinergics. This could reflect the existence of a parallel set of synapses with fast decay that serve as a shortterm store. (iv) Increasing the amount of learning leads to an increase in conductance in each of a set of synapses without an increase in their number. (v) Both original learning and extinction are subserved by cholinergic synapses.
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PMID:The cholinergic synapse and the site of memory. 433 Apr 69

Female Long-Evans rats were gavaged 5 days a week for 4 weeks with chlorpyrifos in oil at dosages of 0, 1, 3, and 10 mg/kg/day. Clinical observations were conducted, and memory was tested with a delayed matching-to-position task (DMTP). Before exposure started, the rats were divided into four groups of ten of comparable overall performance. Then, they were tested during four weeks of dosing and for another four weeks thereafter. The observer was not provided information about each rat's dose group identification. Miosis was a prominent sign observed in the 3 and 10 mg/kg/day groups. Rectal temperature was reduced in the 10 mg/kg/day group. Noncognitive performance measures in the DMTP test (e.g., actual total delay, void trials) were affected and consistent with decreased motor activity. There was a statistically significant difference in the intercept at the zero delay (i.e., a measure of encoding/motivation/attention), which was attributed to deviations from controls in the high-dosage group during dosing weeks 2 and 3 (in opposite directions). This difference was not considered treatment related. The slope of the retention gradient (i.e., a measure of forgetting rate) did not show any statistically significant difference between groups at dosages that inhibited brain cholinesterase by up to approximately 85%. In conclusion, chlorpyrifos decreased motor activity but had no effects on short-term memory (i.e., information retention capability) and on encoding/motivation/attention.
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PMID:Chlorpyrifos: lack of cognitive effects in adult Long-Evans rats. 1075 53