Description of research and teaching

We are interested in neuronal mechanisms of investigational drugs potentially useful in treatment of psychiatric diseases.

Our behavioral neuropharmacology team consists of Anni-Maija Talvio (former Linden), PhD (Pharm), and PhD student Mira Lainiola, M.Sc and undergraduate students. Our behavioral team is a part of a larger Neuropsychopharmacological research group (Department of Pharmacology, Faculty of Medicine). Our main projects are listed below. 

Metabotropic glutamate receptors (mGluRs). Glutamate is the main excitatory neurotransmitter in the brain. Pharmacological compounds modulating metabotropic glutamate receptors (mGluRs) can fine tune glutamatergic system when its function is abnormal and therefore could be beneficial in many psychiatric diseases including addiction, depression and schizophrenia. We study how emotional and cognitive behaviors are affected by modulating glutamatergic neurotransmission through metabotropic glutamate receptor 2 (mGluR2, GRM2) and 3 (mGluR3, GRM3). Recent findings indicate important roles for these receptors in neuronal plasticity in the prefrontal cortex and hippocampus. Antagonists for mGluR2/3 produce antidepressant-like effects in behavioral models. We have shown that the lack of mGluR3 produces defects in working memory and alcohol conditioned place preference (Lainiola et al., 2014; Lainiola et al., 2019). Our aim is to study mechanisms how mGluR3-mediated plasticity affects reward memory acquisition and expression to better understand potential of pharmacological ligands modulating mGluR3 in treatment of diseases where reward regulation is aberrant including addiction and depression.

Neuroinflammation in reward. Motivation and reward-related functions are also modulated by inflammatory reactions, such as microglia activation, in the brain. Neuroinflammation regulates neurotransmission in multiple ways and may play a role in the development of depression and addiction. We investigate mechanisms how activation of innate immune system by the Toll-like receptor 4 agonist lipopolysaccharide (LPS) alters reward-related behaviors in preclinical mouse models (Lainiola et al., 2017; Lainiola et al., 2020).