Prof. Dr. Thomas Wolbers

Dr. Motoharu Yoshida

Group Leader

German Center for Neurodegenerative Diseases (DZNE)
Leipziger Str. 44 / Haus 64
39120 Magdeburg

+49 (0) 391 / 672-4538

Group Members

Name Phone Fax
Sandra Dittmann, Assistant +49 (0) 391 / 67-24536 +49 (0) 391 / 67-24536
Frederik Theissen, PhD student +49 (0) 391 / 67-24615 +49 (0) 391 / 67-24536
Alberto Arboit, PhD student +49 (0) 391 / 67-24616 +49 (0) 391 / 67-24536

Curriculum Vitae

Dr. Motoharu Yoshida obtained his B.Sc (1999), M.Sc (2001) and Ph.D (2004) degrees in information technology at Kyushu Institute of Technology, Fukuoka, Japan. His Ph.D work focused on the memory function of the hippocampus based on dynamical neural activity of the hippocampal CA3-CA1 region, in the lab of Prof. Hatsuo Hayashi. He then conducted his post-doctoral study at McGill University, Montreal Neurological Institute, Canada, from 2004 to 2006 in the lab of Prof. Angel Alonso. From 2006 to 2008, he was supported by a post-doctoral fellowship from Japan Society for the Promotion of Science. From 2006 to 2009, he was a post-doctoral researcher at Boston University, Center for Memory and Brain, in the lab of Prof. Michael Hasselmo. From 2010 to 2016, Dr. Yoshida was a W1 professor at Ruhr-University Bochum, Faculty of Psychology, heading the Neural Dynamics Laboratory.

Since April 2016, Dr. Yoshida is a group leader of the Cognitive Neurophysiology research group at DZNE Magdeburg and LIN Magdeburg.

Key publications

Valero-Aracama MJ, Sauvage MM, Yoshida M (2015) Environmental enrichment modulates intrinsic cellular excitability of hippocampal CA1 pyramidal cells in a housing duration and anatomical location-dependent manner. Behav Brain Res. 2015 4328(15)00361-7.

Jochems A and Yoshida M (2015) A robust in vivo-like persistent firing supported by the CAN current in a recurrent neural network, PLoS ONE, 10(4):e0123799.

Saravanan V, Arabali D, Jochems A, Cui AX, Gootjes-Dreesbach L, Cutsuridis V, Yoshida M (2015) Transition between encoding and consolidation/replay dynamics via cholinergic modulation of CAN current: a modelling study. Hippocampus, Feb 9. doi: 10.1002/hipo.22429.

Yoshida M, Cutsuridis V (2014) Memory Processes in Medial Temporal Lobe: Experimental, Theoretical and Computational Approaches. Frontiers in Systems Neuroscience.

Yoshida M, Jochems A,  Hasselmo ME (2013) Comparison of properties of medial entorinal cortex layer II neurons in two anatomical dimensions with and without cholinergic activation. PLoS ONE 8(9): e73904.

Jochems A, Reboreda A, Hasselmo ME, Yoshida M (2013) Cholinergic receptor activation supports persistent firing in layer III neurons in the medial entorhinal cortex. Behav. Brain Res., 254:108-15.

Knauer B, Jochems A, Valero-Aracama MJ, Yoshida M (2013) Long-lasting intrinsic persistent firing in rat CA1 pyramidal cells: a possible mechanism for active maintenance of memory. Hippocampus, 23(9):820-31.

Jochems A, Yoshida M (2013) Persistent firing supported by an intrinsic cellular mechanism in the hippocampal CA3 pyramidal cells. Eur J Neurosci,  38(2):2250-9.

Engelbrecht JR, Loncich K, Mirollo R, Hasselmo ME, Yoshida M (2013) Rhythm-induced spike-timing patterns characterized by 1D firing maps. J Comput Neurosci. 34(1):59-71.

Yoshida M, Knauer B, Jochems A (2012) Cholinergic modulation of the CAN current may adjust neural dynamics for active memory maintenance, spatial navigation and time-compressed replay. Front Neural Circuits. 6:10.

Yoshida M, Giocomo LM, Boardman I and Hasselmo ME (2011) Frequency of subthreshold oscillations at different membrane potential voltages in neurons at different anatomical positions on the dorso-ventral axis in the rat medial entorhinal cortex, J Neurosci. 31:12683-94.

Petersson ME, Yoshida M, Fransén EA (2011) Low-frequency summation of synaptically activated TRP channel-mediated depolarizations. Eur J Neurosci., 34:578-93

Hasselmo ME, Giocomo LM, Yoshida M (2010) Cellular dynamical mechanisms for encoding the time and place of events along spatiotemporal trajectories in episodic memory. Behav Brain Res., 215:261-274.

Zilli EA, Yoshida M, Tahvildari B, Giocomo LM and Hasselmo ME (2009) Evaluation of the oscillatory interference model of grid cell firing through analysis and measured period variance of some biological oscillators, PLoS Computational Biology, e1000573.

Hasselmo ME, Brandon MP, Yoshida M, Giocomo LM, Heys JG, Fransen E, Newman EL, Zilli EA (2009) A phase code for memory could arise from circuit mechanisms in entorhinal cortex, Neural Netw., 22, 1129-1138.

Yoshida M and Hasselmo M (2009) Persistent firing in rat postsubiculum supported by intrinsic single cell mechanisms, J Neurosci., 29, 4945-4952.

Yoshida M, Fransén E and Hasselmo M (2008) mGluR-dependent persistent firing in entorhinal cortex layer III neurons, Eur J Neurosci., 28, 1116-1126.

Yoshida M and Alonso A (2007) Cell-type specific modulation of intrinsic firing properties and subthreshold membrane oscillations by the M(Kv7)-current in neurons of the entorhinal cortex, J Neurophysiol, 98:2779-2794.

Yoshida M and Hayashi H (2007) Emergence of sequence sensitivity in a hippocampal CA3-CA1 model, Neural Netw., 20:653-667.

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Areas of investigation/research focus

The hippocampus and entorhinal cortex, which are part of the medial temporal lobe (MTL), support memory and spatial navigation functions. Our research focuses on neural computation underlying cognitive functions of the MTL, combining in vitro and in vivo electrophysiological recordings with computational simulations. Since the MTL is crucially involved in Alzheimer’s disease and temporal lobe epilepsy, studying neural computation in the MTL is central not only to understanding of cognitive functions and its engineering applications, but also to developing treatments for dementia and epilepsy.

Fig1. (A) Immunohistochemical staining of TRPC5 channel in hippocampal CA1 cells. (B) Persistent firing in a hippocampal CA1 pyramidal cell.
Click on the magnifying glass for a large image.

Temporal association memory:
The ability to associate events that are temporally apart, requires an intact hippocampus. Our current major focus is on the roles of transient receptor potential cation (TRPC) channels in temporal association memory. TRPC channels are abundant in hippocampal principal cells (Fig. 1A). We have recently shown that TRPC channels modulate dynamical properties of hippocampal pyramidal cells known as persistent firing (Fig. 1B). Computational simulations have indicated that TRPC channels play crucial roles in shaping neural network activity, allowing persistent firing to co-exist with the theta oscillations. We plan to further our understandings of the contributions of TRPC channels on behavioral levels using TRPC channel manipulations in vivo.

Fig2. (A1-3) Subthreshold membrane potential oscillations recorded from an MEC layer II neuron at different baseline membrane potentials. (B) Power spectra of subthreshold oscillations measured at different baseline membrane potentials.
Click on the magnifying glass for a large image.

Spatial navigation:
Grid cells in the medial entorhinal cortex (MEC) are believed to support spatial navigation. It has been proposed that grid cell firing emerges through path integration, which is the ability to update spatial representation by using idiothetic cues. MEC layer II has mainly two different types of cells: pyramidal and stellate cells. However, the cellular mechanisms supporting path integration and grid cell formation remain unknown. Oscillatory properties of MEC layer II neurons and persistent firing may support path integration (Fig. 2). We have recently shown that properties of MEC layer II neurons such as the spike adaptation ratio are different along the dorso-ventral axis, indicating these cellular properties may underlie differences in grid cell spacing.

Fig3. Schematic drawing of neural network activity during consolidation (replay activity) and encoding stages (place and time cell firing).
Click on the magnifying glass for a large image.

Memory encoding and consolidation:
It has been suggested that the MTL supports memory formation through two distinct processes: encoding and consolidation. Hippocampal neurons switch their firing mode from "place cell" or "time cell" activity during encoding to the temporally compressed "replay" activity during consolidation. The prevailing theory suggests that the level of the neuromodulator acetylcholine triggers this transition of operational modes. Our theoretical and computational work suggests that cholinergic modulations of intrinsic cellular properties, including the TRPC and potassium channels, may support the transition (Fig. 3).