dr. L.M. (Lucia) Talamini - University of Amsterdam

Biographical Sketch

L.M. Talamini obtained a masters in Biology in 1991, at the University of Leiden, with specializations in Medical Biology and Neurobiology. Over the following 3 years she worked on growth factor-induced plasticity, at the Institute of Neurobiology in Rome (with L.Aloe and R. Levi-Montalcini) and on NMDA receptor plasticity at the dept. of Experimental Animal Physiology (with W. Kamphuis and F. Lopez Da Silva). She obtained her PhD in 2000, at the University of Groningen, where she developed an animal model of schizophrenia (with J. Korf). In 1999 she joined the Psychonomics program of the University of Amsterdam, to developed neural network models of memory and schizophrenia, broadening her perspective on human cognition. She left the department in 2002, towork as agroup leaderand cognition specialist in schizophrenia drug discovery at Johnson & Johnson Pharmaceutical Research and Development. In 2004 she returned to her present affliation. Talamini has published widely in the fields of memory, schizophrenia and neural network modeling.

Research interests

Talamini’s current research interests concern the relation between brain and cognition, especially with regard to memory, the role of sleep in memory, and cognitive dysfunctions in schizophrenia. She adopts an integrated approach, involving experimentation (in humans and animals) and neural network modelling, to bridge the gap between brain and behaviour. Examples of her work are the animal (MAM) model of schizophrenia, based on prenatal interference with mediotemporal lobe development, and several neural network models involving mediotemporal lobe structures. The latter models address different features of memory, including recall, recognition and interference, but also sequence learning and novelty detection. They show how these functions emerge from processes at the neural level, involving for instance neurotransmitter interactions, brain oscillatory mechanisms and interplay between mediotemporal lobe subregions. These models can be 'lesioned' to study effects on behavior. It was, for instance, shown how a schizophrenia-like neuropathology leads to memory and context processing deficits that parallel observations in patients. The models often lead to original predictions that can be tested experimentaly, leading to increased understanding of cognitive (dys)function.

Selected publications

Talamini L.M. and Meeter M. (2009) Dominance of objects over context in a mediotemporal lobe model of schizophrenia. PloS ONE, 4(8):e6505.

Atsuko Takashima, Ingrid Nieuwenhuis, Ole Jensen, Lucia Talamini, Mark Rijpkema, Guillen Fernandez. (2009) Shift from hippocampal to neocortical centered retrieval network with consolidation. J. Neurosci., 29(32):10087-93.

Lucia M. Talamini, Ingrid L.C. Nieuwenhuis, Atsuko Takashima and Ole Jensen. (2008) Sleep directly following learning benefits consolidation of spatial associative memory. Learning and Memory. 15(4):233-7.

Meeter M., Riedel W., Schmitt, Talamini L.M. (2006) Effects of 5-HT on memory and the hippocampus: model and data. Neuropsychopharmacology 31(4):712-20.

Lisman JE, Talamini LM, Raffone A. (2005) Recall of memory sequences by interaction of the dentate and CA3: A revised model of the phase precession. Neural Netw. 18: 1191-1201.

Talamini L.M., Meeter M., Elvevåg B., Murre J.M.J., & Goldberg T.E. (2005) Reduced parahippocampal connectivity produces schizophrenia-like memory deficits in simulated neural circuits. Arch Gen Psychiatry. 62(5):485-93.

Meeter M., Murre J.M. J. and Talamini L.M. (2004) Mode shifting between storage and recall based on novelty detection in oscillating hippocampal circuits. Hippocampus, 14, 722-41.

Talamini L.M., Meeter M. and Murre J.M.J. (2003) Combating fuzziness with computational modeling. Behavioral and Brain Sciences, 26, 107-108

Meeter M., Murre J.M.. and Talamini L.M. (2002) A computational approach to memory deficits in schizophrenia. Neurocomputing, 44, 929-936.

Fiore M, Korf J, Antonelli A, Talamini L, Aloe L. (2002) Long-lasting effects of prenatal MAM treatment on water maze performance in rats: Associations with altered brain development and neurotrophin levels. Neurotoxicol Teratol., 24, 179-191.

Talamini L.M., Ellenbroek B., Koch T. and J. Korf. (2000) Impaired sensory gating and attention in rats with developmental abnormalities of the mesocortex. Ann. New York Acad. Sci. 911, 486-495.

Fiore M., Korf J., Angelucci F., Talamini L.M. and Aloe L. (2000) Prenatal exposure to methylazoxymethanol acetate in the rat alters neurotrophin levels and behavior: considerations for neurodevelopmental diseases. Physiol. Behav. 71, 57-67.

Talamini L.M., Koch T., Luiten P.G.M., Koolhaas J.M. and Korf J. (1999) Interruptions of early cortical development affect limbic association areas and social behaviour in rats; possible relevance for neurodevelopmental disorders. Brain Research 847, 105-120.

Fiore M., Talamini L.M., Angelucci F., KochT., AloeL.and KorfJ. (1999) Prenatal methylazoxymethanol acetate alters behaviour and brain NGF levels in young rats: a possible correlation with the development of schizophrenia–like deficits. Neuropharmacology 38, 857-869.

Talamini L.M. Koch T and Korf J. (1998) Methylazoxymethanol acetate-induced abnormalities in the entorhinal cortex of the rat; parallels with morphological findings in schizophrenia. Brain Research 789, 293-306.

Talamini L.M. Louwerens J.W and Korf J. PET versus post mortem studies in schizophrenia research: significance for the pathogenesis and pharmacotherapy. In: Advances in the neurobiology of schizophrenia (eds. J.A. den Boer, H.G.M. Westenberg and H.M. van Praag). John Wiley & Sons, Ltd, 1995. pp. 157-188.