D2 dopamine receptors recruit a GABA component for their attenuation of excitatory synaptic transmission in the adult rat prefrontal cortex.

@article{citeulike:2712823, abstract = {The dopamine modulation of neuronal excitability in the prefrontal cortex (PFC) changes during critical late periods of postnatal development. In particular, D2 receptors activate fast-spiking interneurons after, and not before, adolescence. To test the functional impact of this change, we investigated the effects of dopamine agonists on PFC excitatory synaptic transmission with whole-cell recordings from deep-layer pyramidal neurons in brain slices obtained from prepubertal [postnatal day (PD) 28-35] and postpubertal (PD>51) rats. Electrical stimulation of superficial layers elicited a fast AMPA/kainate excitatory postsynaptic potential (EPSP). In the adult PFC, the D2 agonist quinpirole decreased EPSP amplitude, an effect that lasted for at least 25 min after drug washout and was blocked by the D2 antagonist eticlopride. The late component of this effect was blocked by the GABA-A antagonist picrotoxin without affecting the early inhibition. Quinpirole also decreased EPSP amplitude in deep-layer pyramidal neurons from prepubertal rats, but this response was not affected by picrotoxin. A D1 agonist, on the other hand, did not affect the pyramidal neuron EPSP. These results indicate that D2, not D1, receptors attenuate local excitatory synaptic transmission in the adult PFC, and this effect of D2 involves a recruitment of local GABAergic activity.}, address = {Center for Neuropharmacology and Neuroscience, Albany Medical College (MC-136), Albany, New York 12208, USA.}, author = {Tseng, K. Y. and O'Donnell, P. }, citeulike-article-id = {2712823}, doi = {10.1002/syn.20432}, issn = {0887-4476}, journal = {Synapse (New York, N.Y.)}, keywords = {dopamine, inhibition, pfc}, month = {October}, number = {10}, pages = {843--850}, posted-at = {2008-04-24 13:10:44}, priority = {2}, title = {D2 dopamine receptors recruit a GABA component for their attenuation of excitatory synaptic transmission in the adult rat prefrontal cortex.}, url = {http://dx.doi.org/10.1002/syn.20432}, volume = {61}, year = {2007} }

TY - JOUR ID - citeulike:2712823 L3 - citeulike-article-id:2712823 TI - D2 dopamine receptors recruit a GABA component for their attenuation of excitatory synaptic transmission in the adult rat prefrontal cortex. JF - Synapse (New York, N.Y.) VL - 61 IS - 10 SP - 843 EP - 850 AD - Center for Neuropharmacology and Neuroscience, Albany Medical College (MC-136), Albany, New York 12208, USA. SN - 0887-4476 N2 - The dopamine modulation of neuronal excitability in the prefrontal cortex (PFC) changes during critical late periods of postnatal development. In particular, D2 receptors activate fast-spiking interneurons after, and not before, adolescence. To test the functional impact of this change, we investigated the effects of dopamine agonists on PFC excitatory synaptic transmission with whole-cell recordings from deep-layer pyramidal neurons in brain slices obtained from prepubertal [postnatal day (PD) 28-35] and postpubertal (PD>51) rats. Electrical stimulation of superficial layers elicited a fast AMPA/kainate excitatory postsynaptic potential (EPSP). In the adult PFC, the D2 agonist quinpirole decreased EPSP amplitude, an effect that lasted for at least 25 min after drug washout and was blocked by the D2 antagonist eticlopride. The late component of this effect was blocked by the GABA-A antagonist picrotoxin without affecting the early inhibition. Quinpirole also decreased EPSP amplitude in deep-layer pyramidal neurons from prepubertal rats, but this response was not affected by picrotoxin. A D1 agonist, on the other hand, did not affect the pyramidal neuron EPSP. These results indicate that D2, not D1, receptors attenuate local excitatory synaptic transmission in the adult PFC, and this effect of D2 involves a recruitment of local GABAergic activity. KW - dopamine KW - inhibition KW - pfc AU - Tseng, KY AU - O'Donnell, P PY - 2007/10// UR - http://dx.doi.org/10.1002/syn.20432 ER -