OHSU

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Matthew Frerking, Ph.D.

Associate Professor
Admin Unit: SOM-Behavioral Neuroscience Department
Phone: 503-418-2660
Lab Phone: 503-418-2661
Fax: 503-494-6877
Office: MRB 525
Mail Code: L470
Programs:
Behavioral Neuroscience
Neuroscience Graduate Program
Research Interests:
neuroscience electrophysiology synaptic transmission » PubMed Listing
Preceptor Rotations
Dr. Frerking has not indicated availability for preceptor rotations at this time.
Faculty Mentorship
Dr. Frerking has not indicated availability as a mentor at this time.
Profile

Background

Matt Frerking received his Ph.D. in Zoology in Martin Wilson's lab at UC Davis in 1990. He went on to postdoctoral research in the labs of Roger Nicoll at UC San Francisco, and Yang Dan at UC Berkeley. In 2001, he joined the OHSU faculty as an Assistant Scientist at the Neurological Sciences Institute. In 2008, he joined the Department of Behavioral Neuroscience as an Assistant Professor.

Summary of Current Research

The Frerking lab studies the transmission of signals between neurons, with a particular emphasis on transmission in the hippocampus. The hippocampus is of particular interest for three reasons: first, it is the site in the brain where many forms of learning and memory are initiated, second, it is a common site of seizure initiation during temporal lobe epilepsy, and third, hippocampal dysfunction is implicated in the cognitive defects that underlie some forms of disease.

All of these aspects of hippocampal function and dysfunction are thought to occur through a variety of synaptic mechanisms, which are the major focus of the lab. Three topics of current interest are:

Regulation of circuit excitability. Seizures are thought to be caused when a neural circuit escapes its normal balance of excitation and inhibition and becomes hyperexcitable. In controlling seizures, it is important to understand how circuits maintain this balance normally, and how hyperexcitability is generated during pathological states. Several lines of evidence suggest that excitability in the hippocampus is controlled by local inhibitory interneurons, which release GABA onto the pyramidal cells when active.

The Frerking lab studies the glutamatergic synapses onto these interneurons that drive their activation. They have found that different interneurons generate excitatory postsynaptic currents (EPSCs) that vary across interneuronal types in terms of the kinetics of the EPSC and the receptors that generate it.

Signal processing during behaviorally-relevant activity. Synapses are a site where behaviorally-relevant signals are processed as they pass through the hippocampal network. One form of synaptic signal processing is generated by a dynamic combination of different forms of activity-dependent synaptic plasticity. These synaptic dynamics are a mechanism by which some parts of a behaviorally-relevant pattern of activity will be amplified, while other parts will be suppressed.

The Frerking lab studies how synaptic dynamics can affect signal processing of behaviorally-relevant signals as they pass through the synapse, by examining synaptic responses to the patterns of activity that are observed during the performance of behavioral tasks. Their studies indicate that synaptic output varies over a factor of 2-3 during realistic patterns of activity, and these dynamics can be modified by neuromodulation in a manner that causes location-based signals to pass through the synapse more effectively than olfactory signals. These results suggest that modulation of synaptic dynamics can allow the hippocampus to filter which types of information are most effectively passed through the circuit. 

Neural dysfunction in animal models of disease. Several diseases are known to impact the functions of the hippocampus, but the underlying electrophysiological defects and the computational consequences of these defects that actually lead to impaired function are unknown.

The Frerking lab has begun to examine neural transmission and excitability in mouse models for neurodegenerative diseases and neurodevelopmental diseases, with the goal of identifying specific types of electrophysiological dysfunction that takes place during these diseases. So far, they have identified a defect in the function of the Na+,K+ ATPase in a mouse model for Rett Syndrome, in collaboration with Sergio Ojeda and Larry Sherman. The Frerking lab is also collaborating with Hemachandra Reddy to define synaptic defects in the transgenic APP/PS-1 mouse, a model for Alzheimer's disease.   

Recent Publications

1. Wondolowski J, Frerking M. Subunit-dependent postsynaptic expression of kainate receptors on hippocampal interneurons in area CA1. J. Neurosci. 2009 29:563-74.

2. Yang Y, Wang XB, Frerking M, Zhou Q. Delivery of AMPA receptors to perisynaptic sites precedes the full expression of long-term potentiation. PNAS 2008 105: 11388-93.

3. Yang Y, Wang XB, Frerking M, Zhou Q. Spine expansion and stabilization associated with long-term potentiation. J Neurosci. 2008 May 28;28(22):5740-51.

4. Deng V, Matagne V, Banine F, Frerking M, Ohliger P, Budden S, Pevsner J, Dissen GA, Sherman LS, Ojeda SR. FXYD1 is an MeCP2 target gene overexpressed in the brains of Rett syndrome patients and Mecp2-null mice. Hum Mol Genet. 2007 Mar 15;16(6):640-50.

5. Partovi D, Frerking M. Presynaptic inhibition by kainate receptors converges mechanistically with presynaptic inhibition by adenosine and GABAB receptors. Neuropharmacology. 2006 Nov;51(6):1030-7.

6. Frerking M, Ohliger-Frerking P. Functional consequences of presynaptic inhibition during behaviorally relevant activity. J Neurophysiol. 2006 Oct;96(4):2139-43.

7. Frerking M, Schulte J, Wiebe SP, Stäubli U. Spike timing in CA3 pyramidal cells during behavior: implications for synaptic transmission. J Neurophysiol. 2005 Aug;94(2):1528-40.

8. Ohliger-Frerking P, Wiebe SP, Stäubli U, Frerking M. GABA(B) receptor-mediated presynaptic inhibition has history-dependent effects on synaptic transmission during physiologically relevant spike trains. J Neurosci. 2003 Jun 15;23(12):4809-14.