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Memory Enhancement Involves Activation

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Without question, AnnaLitmanovich is a “Renaissancewoman.” Her first four years ofschool were spent studyingpiano in Uzbekistan, the coun-try of her birth. Since comingto the United States, Anna hasexcelled in both the arts andsciences. For the past six yearsshe has performed for OperaPacific in Costa Mesa,appearing in nine operas andone ballet. While at UCI, shehas investigated the effects ofdrugs and hormones on mem-ory storage and has tutoredstudents ranging from adoptedRussian children who cannotspeak English to fellow under-graduates in such fields asmath, psychology, physics, andbiology. If that’s not enough,she also plays competitive tennis. Anna hopes to pursue acareer in academic medicine.Animals have evolved the amazing ability to store memory betterfor emotionally significant events. This ability depends on a con-vergence of hormonal and neurochemical signals in a small regionof the medial temporal lobe of the brain called the basolateralamygdala (BLA). The neurotransmitter acetylcholine has beenfound to play a critical role in BLA modulation of memory storagevia activation of muscarinic receptors. This project was the firstanalysis of the muscarinic receptor subtypes, which mediate this cholinergic activa-tion of the BLA during consolidation. In collaboration with researchers from mylaboratory, including Dr. Ann E. Power, who was directly responsible for guidingAnna’s research, Anna learned that cholinergic modulation of memory involves acti-vation of both excitatory and inhibitory receptor systems in the BLA. These find-ings enhance our understanding of the neurobiological mechanisms of modulationof memory storage by emotion and arousal.Key Terms Agonists Antagonists Basolateral Amygdala  Inhibitory Avoidance Muscarinic CholinergicAgents Muscarinic ReceptorsMemory Enhancement InvolvesActivation of Both Type 1 and Type2 Muscarinic Cholinergic Receptorsin the Basolateral AmygdalaAnna Litmanovich NeurobiologyThe basolateral amygdala (BLA) is the putative site for integration of neuronaland hormonal signals for emotional learning and memory. The present studyexplored which muscarinic receptor type(s) (M1, M2 or both) mediates the criticalcholinergic activation in the BLA during memory-modulating processes. Sprague-Dawley rats were implanted with bilateral cannulae aimed at the BLA and thentrained on an inhibitory avoidance (IA) task. To selectively activate each receptortype, selective antagonists, methoctramine or telenzipine (50 nmol per side), were co-infused with a general muscarinic receptor agonist, oxotremorine, to stimulate M1 orM2 receptors, respectively. Oxotremorine (50 nmol per side) was infused alone tostimulate both receptor types. A single trial IA task was used in combination withimmediate post-training drug treatments so that the consolidation phase of memorycould be selectively manipulated. The mean retention latency of oxotremorine-onlygroup in the 48-hr retention test was significantly higher than the mean retentionlatencies of the groups that received co-infusion of telenzipine or methoctraminewith the oxotremorine. These findings indicate that both muscarinic receptor typesneed to be activated in order for memory enhancement to occur.31The UCI Undergraduate Research JournalAuthorAbstractFaculty MentorJames L. McGaughSchool of Biological SciencesIntroductionLearning and memory are influenced by the emotional andmotivational state of an organism. Extensive evidence indi-cates that the amygdala is a critical site of integration forsensory, neuromodulatory and hormonal influences onmemory storage (Liang et al., 1986; McGaugh et al., 1996).Electrical or drug-induced stimulation of the amygdalaimmediately after training can produce memory enhance-ment or impairment, depending upon experimental condi-tions (Gold and van Buskirk, 1978; Gallagher et al., 1981;Cahill and McGaugh, 1991). Specifically, the basolateralregion of the amygdala (BLA) plays a central role in influ-encing the strength of memory storage. Post-training mem-ory modulatory treatments are ineffective if the BLA islesioned (Roozendaal et al., 1996), and direct selectivemanipulations of the BLA are sufficient to influence mem-ory strength (Quirarte et al., 1997; Da Cunha et al., 1999;Hatfield et al., 1999; Power et al., 2000).Behavioral pharmacological studies have revealed a robustinfluence of muscarinic cholinergic agents in particular onmemory modulatory processes. Intra-BLA administrationof muscarinic cholinergic agonists facilitate memory stor-age (Vazdarjanova and McGaugh, 1999; Power andMcGaugh, 2002), while intra-BLA administration of mus-carinic cholinergic antagonists block memory enhancementinduced by intra-BLA or peripheral memory-enhancingtreatments (Introini-Collison and McGaugh, 1988; Dalmazet al., 1993; Introini-Collison et al., 1996; Salinas et al., 1997;Power et al., 2000). These findings indicate that activationof amygdaloid muscarinic cholinergic receptors is criticalfor enabling modulatory influences on memory consolida-tion.An abundance of cholinergic synapses and muscariniccholinergic receptors have been observed in the BLA (Mashand Potter, 1986; Spencer et al., 1986). The population ofthese synapses in the BLA is heterogeneous, including bothexcitatory (asymmetric) and inhibitory (symmetric) synaps-es (Li et al., 2001; Wainer et al., 1984). In accordance withthis heterogeneity of synapses, the BLA contains high den-sities of both the major excitatory and inhibitory muscarinicreceptors types, M1 and M2, respectively (Hammer et al.,1980; Peralta et al., 1988; Brann et al., 1987; Pinkas-Kramarski et al., 1988). Recent findings suggest that thenucleus basalis magnocellularis (NBM), which sends densecholinergic projections into the BLA (Mesulam, et al.,1983), is the critical source of cholinergic input to the BLAduring modulation of memory storage (Power andMcGaugh, 2002). However, the neuronal mechanismsunderlying the critical role of cholinergic activation in theBLA during memory modulating processes are not wellunderstood. Therefore, this study investigated which mus-carinic receptor type(s) influence BLA-mediated memorymodulation.Sprague-Dawley rats (Charles River Laboratories) were sur-gically implanted with bilateral cannulae aimed at the BLAand one week later trained on a single trial inhibitory avoid-ance (IA) task. Rats received post-training intra-BLA infu-sions in order to selectively affect the consolidation phase ofmemory. To


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