Presynaptic D₁Dopamine Receptors in Primate Prefrontal Cortex: Target-Specific Expression in the Glutamatergic Synapse

Dopaminergic Regulation of Inhibitory and Excitatory Transmission in the Basolateral Amygdala–Prefrontal Cortical Pathway

“…This indicates that prolonged increases in DA receptor tone moderately attenuate the excitatory impact that BLA inputs exert over mPFC neural activity. Although the mechanisms by which D 1 receptors suppress BLAevoked firing are unclear, there is evidence to suggest that this effect may be mediated by DA acting on presynaptic glutamate terminals of BLA axons (Paspalas and Goldman-Rakic, 2005). …”

D1-Like Dopamine Receptor Activation Modulates GABAergic Inhibition But Not Electrical Coupling between Neocortical Fast-Spiking Interneurons

“…Therefore, the use of dopamine or a nonspecific agonist in these experiments would activate both types of receptors, perhaps resulting in the physiological effects from activation of one receptor type canceling out those caused by agonism of the other (Trantham-Davidson et al, 2004). Parvalbumin-containing fast-spiking interneurons are particularly sensitive to D 1 -like receptor activation compared with calbindin-expressing, low-thresholdspiking cells, reflecting the preferential expression of this receptor in the former (Le Moine and Gaspar, 1998;Muly et al, 1998;Gorelova et al, 2002;Paspalas and Goldman-Rakic, 2005;Kroner et al, 2007). The proportion of PV-immunoreactive neurons that express the D 1 receptor is particularly high (Ͼ60%) in the infragranular layers.…”

“…We found that application of a D 1 -like agonist reduced IPSCs by approximately one-third. D 1 receptors are present on both presynaptic and postsynaptic compartments of FS cells (Muly et al, 1998;Paspalas and Goldman-Rakic, 2005), so it is conceivable that the D 1 -like receptor-mediated depression of IPSCs could have a presynaptic site of action, a postsynaptic mechanism, or a combination of both. Our finding that SKF81297 increased the coefficient of variation of IPSC amplitudes suggests that activation of presynaptic D 1 -like receptors affected the release of GABA and reduced the amplitude of GABAergic postsynaptic events.…”

Repeated Amphetamine Exposure Disrupts Dopaminergic Modulation of Amygdala–Prefrontal Circuitry and Cognitive/Emotional Functioning

“…Findings from in vitro studies suggest that these effects are likely mediated by presynaptic and postsynaptic actions of DA. D 1 receptor activity suppresses pyramidal cell excitability and evoked EPSCs, reducing postsynaptic Na ϩ currents via PKA-dependent mechanisms (Peterson et al, 2006), and may also attenuate BLA inputs presynaptically (Gao et al, 2001;Seamans et al, 2001b;Paspalas and Goldman-Rakic, 2005). Conversely, activation of D 2 /D 4 receptors can attenuate evoked IPSCs by reducing GABA release from local interneurons and desensitizing postsynaptic GABA receptors localized on mPFC pyramidal cells (Seamans et al, 2001a;Wang et al, 2002;Trantham-Davidson et al, 2004;Kroener and Lavin, 2010).…”