Professor Amy MiltonUniversity positionProfessor Professor Amy Milton is pleased to consider applications from prospective PhD students. DepartmentsInstitutesBehavioural and Clinical Neuroscience Institute Home pagehttp://www.psychol.cam.ac.uk/directo... Research ThemesInterestsMemory is a critical function of the brain, but little is known about the mechanisms by which memories are modified, adapted, and persist. Memories are known to 'reconsolidate' undergoing updating and strengthening following their destabilisation at retrieval. I study the neurochemical, molecular and intracellular basis of the reconsolidation process, for aversive (fear) and appetitive (addictive drug) memories. Using translationally relevant animal models of neuropsychiatric disorders, such as post-traumatic stress disorder and drug addiction, I also focus on using this knowledge of memory reconsolidation mechanisms to develop treatments for these disorders, based on the disruption of maladaptive memories. Research Focus
EquipmentBehavioural analysis Collaborators
Associated News Items
Key publicationsMilton AL, Holmes EA (2018), “Of mice and mental health: facilitating dialogue and seeing further.” Phil Trans R Soc Lond B Biol Sci 373(1742): pii: 20170022 Milton AL, Merlo E, Ratano P, Gregory BL, Dumbreck JK, Everitt BJ (2013), “Double dissociation of the requirement for GluN2B- and GluN2A-containing NMDA receptors in the destabilization and restabilization of a reconsolidating memory.” J Neurosci 33(3):1109-15 Details Milton AL, Everitt BJ (2012), “The persistence of maladaptive memory: addiction, drug memories and anti-relapse treatments.” Neurosci Biobehav Rev 36(4):1119-39 Details Milton AL, Everitt BJ (2010), “The psychological and neurochemical mechanisms of drug memory reconsolidation: implications for the treatment of addiction.” Eur J Neurosci 31(12):2308-19 Details Milton AL, Lee JL, Butler VJ, Gardner R, Everitt BJ (2008), “Intra-amygdala and systemic antagonism of NMDA receptors prevents the reconsolidation of drug-associated memory and impairs subsequently both novel and previously acquired drug-seeking behaviors.” J Neurosci 28(33):8230-7 Details Publications2018Cahill EN, Vousden GH, Exton-McGuinness MTJ, Beh IRC, Swerner CB, Macak M, Abas S, Cole CC, Kelleher BF, Everitt BJ, Milton AL (2018), “Knockdown of Zif268 in the posterior dorsolateral striatum alone does not enduringly disrupt a response memory of a rewarded T-maze task.” Neuroscience 370: 112-120 Merlo E, Milton AL, Everitt BJ (2018), “A novel retrieval-dependent memory process revealed by the arrest of ERK1/2 activation in the basolateral amygdala.” J Neurosci 38(13): 3199-3207 Puaud M, Ossowska Z, Barnard J, MIlton AL (2018), “Saccharin fading is not required for the acquisition of alcohol self-administration, and can alter the dynamics of cue-alcohol memory reconsolidation.” Psychopharmacology 235(4): 1069-82 2017Vousden GH, Milton AL (2017), “The chains of habits: too strong to be broken by reconsolidation blockade? ” Curr Opin Behav Sci 13: 158-163 2016Schramm MJW, Everitt BJ, Milton AL (2016), “Bidirectional Modulation of Alcohol-Associated Memory Reconsolidation through Manipulation of Adrenergic Signaling.” Neuropsychopharm 41(4): 1103-1111 2015James EL, Bonsall MB, Hoppitt L, Tunbridge EM, Geddes JR, Milton AL, Holmes EA (2015), “Computer Game Play Reduces Intrusive Memories of Experimental Trauma via Reconsolidation-Update Mechanisms.” Psych Sci 26(8): 1201-1215 Merlo E, Milton AL, Everitt BJ (2015), “Enhancing cognition by affecting memory reconsolidation.” Curr Opin Behav Sci 4:41-47 Merlo E, Ratano P, Ilioi EC, Robbins MALS, Everitt BJ, Milton AL (2015), “Amygdala dopamine receptors are required for the destabilization of a reconsolidating appetitive memory.” eNeuro e0024-14.2015 2014Merlo E, Milton AL, Goozée ZY, Theobald DE, Everitt BJ (2014), “Reconsolidation and extinction are dissociable and mutually exclusive processes: behavioral and molecular evidence.” J Neurosci 34(7):2422-31 Details Ratano P, Everitt BJ, Milton AL (2014), “The CB1 Receptor Antagonist AM251 Impairs Reconsolidation of Pavlovian Fear Memory in the Rat Basolateral Amygdala.” Neuropsychopharmacology Details 2013Corlett PR, Cambridge V, Gardner JM, Piggot JS, Turner DC, Everitt JC, Arana FS, Morgan HL, Milton AL, Lee JL, Aitken MR, Dickinson A, Everitt BJ, Absalom AR, Adapa R, Subramanian N, Taylor JR, Krystal JH, Fletcher PC (2013), “Ketamine effects on memory reconsolidation favor a learning model of delusions.” PLoS One 8(6):e65088 Details Fernando AB, Murray JE, Milton AL (2013), “The amygdala: securing pleasure and avoiding pain.” Front Behav Neurosci 7:190 Details Milton AL (2013), “Drink, drugs and disruption: memory manipulation for the treatment of addiction.” Curr Opin Neurobiol 23(4):706-12 Details 2012Milton AL, Everitt BJ (2012), “Neuroscience. Wiping drug memories.” Science 336(6078):167-8 Details Milton AL, Schramm MJ, Wawrzynski JR, Gore F, Oikonomou-Mpegeti F, Wang NQ, Samuel D, Economidou D, Everitt BJ (2012), “Antagonism at NMDA receptors, but not ?-adrenergic receptors, disrupts the reconsolidation of pavlovian conditioned approach and instrumental transfer for ethanol-associated conditioned stimuli.” Psychopharmacology (Berl) 219(3):751-61 Details 2010Théberge FR, Milton AL, Belin D, Lee JL, Everitt BJ (2010), “The basolateral amygdala and nucleus accumbens core mediate dissociable aspects of drug memory reconsolidation.” Learn Mem 17(9):444-53 Details 2008Milton AL, Lee JLC, Everitt BJ (2008), “Reconsolidation of appetitive memories for both natural and drug reinforcement is dependent on b-adrenergic receptors” Learning & Memory 15:88-92 2006Lee JLC, Milton AL, Everitt BJ (2006), “Reconsolidation and extinction of conditioned fear: inhibition and potentiation” The Journal of Neuroscience 26:10051-10056 Lee JLC, Milton AL, Everitt BJ (2006), “Cue-induced cocaine seeking and relapse are reduced by disruption of drug memory reconsolidation” The Journal of Neuroscience 26:5881-5887 2004Milton AL, Marshall JW, Cummings RM, Baker HF, Ridley RM (2004), “Dissociation of hemi-spatial and hemi-motor impairments in a unilateral primate model of Parkinson's disease.” Behav Brain Res 150(1-2):55-63 Details |