Roles of D2Rs in dopaminergic and mushroom body neurons during larval olfactory learning.
(a) A schematic diagram shows the roles of D2R in dopaminergic neurons (DAN) and mushroom body neurons (MBN) in larval olfactory associative learning. During learning, olfactory stimuli (conditioned stimulus, CS) are received by olfactory sensory neurons (OSN) and transmitted to MBNs (green) via projection neurons (PN). Distinct gustatory stimuli (unconditioned stimulus, US) are received by gustatory sensory neurons (GSN) and transferred to different dopaminergic neurons. Aversive stimuli are sent to DAN-c1 (red) in the DL1 cluster which connects the lower peduncle compartment (LP, square in dash line), while appetitive stimuli are received by pPAM neurons (blue) innervating the medial lobe (ML). D2Rs (yellow square) are expressed in DAN-c1 and pPAM as autoreceptors, regulating dopamine release. Both D2R and dDA1 (magenta circle) are expressed in the MBNs. (b) A hypothetical curve showing the relationship between learning ability and cAMP level in the mushroom body. Insufficient cAMP (rutabaga mutant) cannot induce learning, while excessive cAMP (dunce mutant) also impairs learning. Only the appropriate level of cAMP regulated by the opposing actions of D1R (dDA1) and D2R leads to successful learning in wild type larvae (WT). Knockdown of D2R in DAN-c1 causes excessive dopamine release, elevating cAMP and resulting in impaired learning. D2R knockdown in MBNs relieves the inhibition effect of D2R, resulting in excessive intracellular cAMP and learning failure. (c-d) Potential molecular mechanisms underlying Drosophila olfactory learning in the square region shown in (a). (d) During aversive learning, olfactory stimuli induce depolarization of MBNs, which activates voltage-gated calcium channels and induces calcium influx. Gustatory stimuli, such as quinine, activates dopaminergic neurons and elevates dopamine (DA) release. D1 receptor (dDA1) activates adenylyl cyclase (AC) and elevates cAMP via Gαs, while D2 receptor (D2R) inhibits AC and suppresses cAMP via Gαi/o. In Drosophila, the coincidence detector rutabaga (AC) is activated by the existence of both calcium and Gαs, converging the olfactory and gustatory stimuli. cAMP activates the PKA signaling pathway, elevating the neuronal excitability. D1 and D2 receptors can also form heteromeric receptors and activate the PLC-PKC and CaMKII signaling pathways via Gαq. These pathways inhibit acetylcholine (ACh) release from MBNs to MB output neurons (MBON), which leads to avoidance of the learned odor. Abbreviations: AC, adenylyl cyclase; ACh, acetylcholine; ATP, adenosine triphosphate; CaM, calmodulin; CaMKII, Ca2+/calmodulin-dependent protein kinase II; cAMP, cyclic adenosine monophosphate; CS, conditioned stimulus; DA, dopamine; DAN, dopaminergic neurons; DL, dorsolateral; ER, endoplasmic reticulum; Gαi/o, Gi/o protein α subunit; Gαq, Gq protein α subunit; Gαs, Gs protein α subunit; GSN, gustatory sensory neurons; LP, lower peduncle; MBN, mushroom body neurons; MBON, mushroom body output neurons; ML, medial lobe; nAChR, nicotinic acetylcholine receptor; OSN, olfactory sensory neurons; PKA, protein kinase A; PKC, protein kinase C; PLC, phospholipase C; PN, projection neurons; pPAM, primary protocerebral anterior medial; RyR, ryanodine receptor; US, unconditioned stimulus; VGCC, voltage gated calcium channel.