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[Abstract Title]. - Society for Neuroscience

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To determine the involvement of acetylcholine in dorsolateral prefrontal cortex function, we then<br />

trained these monkeys on the spatial delayed response task (Goldman, 1970; Bachevalier and<br />

Mishkin, 1986) in a manual testing apparatus. In this task the monkey watches as an<br />

experimenter places a small food reward in one of two wells of a test tray and then covers both<br />

wells with identical gray plaques. After a brief delay (1-5 sec) during which an opaque screen is<br />

interposed between the monkey and experimenter, the monkey is allowed to obtain the reward by<br />

displacing the plaque covering the well that was baited by the experimenter. Thus, the monkey<br />

must maintain the baited location (left or right) in memory during the brief delay interval in order<br />

to choose correctly. Per<strong>for</strong>mance of this task is devastated by ablation of dorsolateral prefrontal<br />

cortex. The monkeys with cholinergic depletion of lateral and orbital prefrontal cortex were also<br />

unable to learn the task to criterion, which four unoperated control monkeys learned readily.<br />

This finding suggests that acetylcholine, although not critical <strong>for</strong> functions of ventrolateral and<br />

orbital prefrontal cortex, is essential <strong>for</strong> dorsolateral prefrontal cortex function. An alternative<br />

explanation, which we are currently investigating, is that acetylcholine is necessary <strong>for</strong> the<br />

prefrontal cortex to adapt to the different task demands of delayed response, relative to the tests<br />

of discrimination learning with which these monkeys had extensive experience. This would be<br />

consistent with a role <strong>for</strong> cholinergic input to neocortex in cortical plasticity and remodeling.<br />

Disclosures: M.G. Baxter, None; D.A. Kyriazis, None; P.L. Croxson, None.<br />

Poster<br />

292. Acetylcholine, Neurotrophins, and Cognition<br />

Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm<br />

Program#/Poster#: 292.10/SS23<br />

Topic: F.02.d. Cognitive learning and memory systems<br />

Support: NIDA Grant DA023209 to AM<br />

<strong>Title</strong>: Mice lacking the β4 subunit of the nicotinic acetylcholine receptor show long-term<br />

memory deficits in hippocampus-dependent tasks<br />

Authors: H. M. JARRELL, S. SEMENOVA, *A. MARKOU;<br />

Psychiatry, Univ. of Cali<strong>for</strong>nia, La Jolla, CA<br />

<strong>Abstract</strong>: Nicotine binds to nicotinic acetylcholine receptors (nAChRs) throughout the brain and<br />

elicits a range of behavioral responses related to cognition, including enhancement of learning<br />

and memory. However, the role of specific nAChRs subtypes in regulating behavior in the<br />

absence of nicotine is still not clear. The present work investigated the role of β4-containing<br />

nAChRs in learning and memory using wildtype (WT, β4 +/+ ) and null mutant (KO, β4 -/- ) mice <strong>for</strong>

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