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School of Behavioral and Brain Sciences - The University of Texas at Dallas

Sven Kroener

 

Sven Kroener

Assistant Professor

PhD, Ruhr-University Bochum (Germany)

Synaptic Transmission in the Prefrontal Cortex, Schizophrenia, Drug Addiction

 

JO 4.204

972-883-2039 phone

kroener@utdallas.edu email

 

Cellular and Synaptic Physiology Lab website

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Research Interests

 

My lab studies the neuronal circuitry of the prefrontal cortex (PFC) and how alterations in synaptic transmission are related to schizophrenia and drug addiction.

 

Pathological dysfunctions that disrupt the intrinsic circuitry of the PFC and impair working memory have been implicated in numerous mental illnesses, most notably schizophrenia. More recently, the importance of the PFC in executive functions and behavioral flexibility have also made it a focus for studies into the mechanisms that underlie drug addiction.

 

An important cognitive feature of higher organisms is their ability to temporarily structure their behavior and to actively hold in mind information relevant for goal-attainment. This so called "working memory" is closely related to the functions of the PFC and its innervation by dopaminergic fibers.

 

I study the network properties that underlie the persistent neuronal activity required for working memory, using electrophysiological recordings and high-resolution calcium-imaging (Kroener et al., 2009). I am particularly interested in the functional role of inhibition in the PFC circuit, and how the activity of GABAergic interneurons (which have been identified as a main locus of change in schizophrenia) is modulated by dopamine (Kroener et al., 2007).

 

Projects in my laboratory also examine how drugs of abuse (specifically cocaine and alcohol) can alter PFC function. The most recent studies currently underway in my lab use an animal model of alcohol addiction to study changes in glutamatergic synaptic transmission and NMDA receptor function in the PFC. Chronic ethanol exposure induces homeostatic increases in NMDA receptors, which may affect the interplay between backpropagating action potentials and localized calcium-spikes required for spike timing-dependent plasticity, a physiologically relevant model of synaptic plasticity. Thus changes at the NMDA receptor could alter integrative properties and synaptic plasticity in PFC pyramidal neurons and they may represent pathological neuroadaptations that underlie alcohol dependence. These studies will provide insights into the mechanisms that contribute to a loss of response inhibition in the PFC during the development and maintenance of addiction to alcohol.

 

Recent Publications

 

Kroener S., Mulholland P.J., New N.N., Gass J.T., Becker H.C., Chandler L.J. (2012). Chronic alcohol exposure alters behavioral and synaptic plasticity of the rodent prefrontal cortex. PLoS One. 7(5):e37541.

 

Herold C., Palomero-Gallagher N., Hellmann B., Kröner S., Theiss C, Güntürkün O, Zilles K (2011). The receptor architecture of the pigeons' nidopallium caudolaterale: an avian analogue to the mammalian prefrontal cortex. Brain Struct Funct 216(3): 239-254.

 

Kroener, S., Lavin, A. (2010) Altered dopamine modulation of inhibition in the prefrontal cortex of cocaine-sensitized rats. Neuropsychopharmacology. 2010 Oct;35(11):2292-304.

 

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