Sham Vehicle Drug pERK ERK Novel taste pERK ERK Water

Fig. 21 Controls at two *levels of analysis of 'conditioned taste aversion. (a) Microinfusion into the taste 'cortex of scopolamine (Drug), an inhibitor of the 'receptor for 'acetylcholine, during training, blocks the formation of long-term memory of conditioned taste aversion in the rat (black bar).A control, in which only a drug-free solution (the vehicle) is microinfused into the taste cortex, has no such effect (grey bar).The 'sham' control (i.e. surgery but no microinfusion into the brain) is also shown for comparison (open bar). Hence the effect on memory is due to the drug and not to the manipulations involved in its administration. Data from Naor and Dudai (1996). (b) Sampling a novel taste, but not a familiar taste (water), causes activation of the enzyme mitogen-activated 'protein kinase (ERK) in the taste cortex of the rat. This activation is caused by the phosphorylation of the ERK, and it can detected by the use of specific antibodies, that bind only to the phosphorylated form of the enzyme (pERK, black bar). However, the population of the ERK molecules includes a certain proportion of pERK even in the absence of any taste stimulus. This implies that the increase in the number of molecules detected by the anti-pERK antibodies after the experience of the novel taste, could be due to an increase in the overall number of the ERK molecules ('protein synthesis), without a change in the proportion of the pERK molecules. A control is therefore necessary in which the overall number of ERK molecules is measured in parallel, with antibodies that recognize the ERK molecule regardless of whether it is phosphorylated or not (grey bar). Such a control shows that the total number of ERK molecules does not change, and that the effect of the novel taste experience is activation of the existing ERK molecules. Data from Berman etal. (1998).


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