Emma Louise Louth,1,2 Rasmus Langelund Jørgensen,3 Anders Rosendal Korshoej,3 Jens Christian Hedemann Sørensen,3 and Marco Capogna1,2,4,*
1Department of Biomedicine, Aarhus University, Aarhus, Denmark
2DANDRITE, The Danish Research Institute of Translational Neuroscience, Aarhus University, Aarhus, Denmark
3Department of Neurosurgery, Aarhus University Hospital, Aarhus, Denmark
4Center for Proteins in Memory–PROMEMO, Danish National Research Foundation, Aarhus University, Aarhus, Denmark
Edited by: Dominique Debanne, INSERM U1072 Neurobiologie des Canaux Ioniques et de la Synapse, France
Reviewed by: Yanis Inglebert, McGill University, Canada; Antonio Rodriguez Moreno, Universidad Pablo de Olavide, Spain
Synapses in the cerebral cortex constantly change and this dynamic property regulated by the action of neuromodulators such as dopamine (DA), is essential for reward learning and memory. DA modulates spike-timing-dependent plasticity (STDP), a cellular model of learning and memory, in juvenile rodent cortical neurons. However, it is unknown whether this neuromodulation also occurs at excitatory synapses of cortical neurons in mature adult mice or in humans. Cortical layer V pyramidal neurons were recorded with whole cell patch clamp electrophysiology and an extracellular stimulating electrode was used to induce STDP. DA was either bath-applied or optogenetically released in slices from mice. Classical STDP induction protocols triggered non-hebbian excitatory synaptic depression in the mouse or no plasticity at human cortical synapses. DA reverted long term synaptic depression to baseline in mouse via dopamine 2 type receptors or elicited long term synaptic potentiation in human cortical synapses. Furthermore, when DA was applied during an STDP protocol it depressed presynaptic inhibition in the mouse but not in the human cortex. Thus, DA modulates excitatory synaptic plasticity differently in human vs. mouse cortex. The data strengthens the importance of DA in gating cognition in humans, and may inform on therapeutic interventions to recover brain function from diseases.
These fibers were located by eYFP expression. Terminals were stimulated with blue light from a CoolLed PE-300ultra (Scientifica) (460 nm, ∼10 mW power).
Product Associated Features
The broad spectrum pE-300ultra offers TTL triggering, individual channel control and software integration. This makes it ideal for fast pulsing at differing durations and irradiance, such as in these optogenetic protocols.
Front. Cell Neurosci.
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