Tuomo Mäki‐Marttunen

This study develops a spiking network model of auditory novelty detection and shows how SCZ-related cellular changes impair mismatch negativity.

The paper integrates gene expression analysis with computational modeling to show region-specific energy metabolism dysregulation in schizophrenia, identifying key genes and metabolite changes in ACC and DLPFC.

The paper uses computational modeling to show schizophrenia-associated changes in ion-channel expression reduce delta-band power in neural simulations.

The paper investigates how CACNA1C variants affect single-cell dynamics in computational models of cortical pyramidal cells, identifying altered calcium regulation and dendritic retraction in Timothy Syndrome type II.

The paper develops a computational model of GABAB receptor signaling to study pre- and postsynaptic mechanisms of neuronal inhibition and validates it using electrophysiological data.

The paper uses computational modeling and post-mortem gene expression data to show that schizophrenia-associated genes impair PKA-mediated LTP in GluR1-containing synapses, linking genetic factors to synaptic plasticity deficits.

This study uses computational models to show that HCN channels have opposing effects on excitability of layer V pyramidal cells depending on dendritic location and neuromodulation.

This study shows that common schizophrenia-associated genetic variants can reduce gamma power in auditory steady-state responses through computational modeling of ion channels.

The paper develops a data-driven framework to model spiking neuronal networks and analyze how synaptic and cellular mechanisms influence network bursts in postnatal rat cortical cultures.

This study investigates the functional effects of two CACNA1C mutations in zebrafish, showing altered mRNA levels, neurotransmitter profiles, and behavioral and electrophysiological changes linked to psychiatric disorders.

The paper assesses LTP-like visual cortical plasticity in schizophrenia and bipolar disorder using VEP modulation, finding impaired N1b modulation in SZ and BDI but not BDII, linked to symptom severity.

The paper examines VEP modulation in 415 healthy individuals, finding significant effects for several components and age-related correlations, supporting VEP as a measure of synaptic plasticity.

The paper develops a biochemically detailed computational model of cortical post-synaptic plasticity that integrates multiple signalling pathways and reproduces observed plasticity phenomena.