Mia Lindskog, Ph.D.
Changes in emotional state can affect network excitability and modulate cognitive processes, including learning and memory. This is an important quality of the brain function, as remembering everything we perceive would not be practical and probably detrimental to our cognitive functions. The modulation is often mediated by "slow neurotransmitters" (called "slow" since they act on G-protein coupled receptors and affect signaling pathways in the cells in contrast to the fast effect of opening an ion channel) and that are associated with moods and affective states (e.g. dopamine and reward, histamine and arousal, serotonin and well-being...). Neuromodulators have an important function in enhancing memory encoding during certain circumstances and are well researched from the aspect of neuropharmacology, but it is not until recently that the role of modulation on circuits and synaptic strength has started to be explored.
The recent interest in modulation of neuronal network has gone hand in hand with the network hypothesis for psychiatric disease such as depression. If mood and affective states traditionally have been considered a result of a chemical balance, in contrast to the discrete electrical network activity underlying cognition, affective disorders were regarded as a chemical unbalance where psychopharmaca restores the balance. An alternative way of looking at affective disorders however is as dysfunction of the information-processing network in the brain. A role for psychopharmaca would then be to restore network function by modulating the functional connectivity by modulating the strength of synapses.
In our lab we combine biochemistry, electrophysiology and behavior to study the modulation of the hippocampal network in healthy rats and in depression models.
Dysfunctional hippocampal activity affects emotion and cognition in mood disorders (Review)
Brain Research, Epub ahead of print, April 5, 2012
Dysfunctional astrocytic regulation of glutamate transmission in a rat model of depression.
Molecular Psychiatry, Epub ahead of print, February 28, 2012
Dopamine in the hippocampus is cleared by the norepinephrine transporter.
The International Journal of Neuropsychopharmacology 15: 531-540, 2011
Postsynaptic GluA1 enables acute retrograde enhancement of presynaptic function to coordinate adaptation to synaptic inactivity.
Proceedings of the National Academy of Sciences USA 107: 21806-21811, 2010
Involvement of DARPP-32 phosphorylation in the stimulant action of caffeine.
Nature 418: 774-778, 2002