Jingda Qiao,Shengxi Yang,Hongyan Geng,Wing-Ho Yung,Ya Ke
Summary Aversive olfactory conditioning in Drosophila is a valuable model for elucidating the mechanism of associative learning . Much effort has centered around the role of neuroplasticity at the mushroom body (MB)-mushroom body output neuron (MBON) synapses in mapping odors to specific behaviors . By electrophysiological recordings from MB neurons, we discovered a form of input-timing-dependent plasticity at the incoming synapses from projection neurons that controls the efficacy of aversive olfactory memory formation. Importantly, this plasticity is facilitated by the neural activity of PPL1, the neuronal cluster that also modulates MB-MBON connections at the output stage of MB. Unlike the MB-MBON synapses that probably utilize dopamine D1-like receptors, this neuroplasticity is dependent on D2-like receptors that are expressed mainly by γ Kenyon cells noticeably in their somato-dendritic region. The D2-like receptors recruit voltage-gated calcium channels , leading to calcium influx in the soma and dendrites of γ neurons. Together, our results reveal a previously unrecognized synaptic component of the MB circuit architecture that not only could increase the salience of a conditioning odor but also couples the process of memory encoding and valency mapping to drive-associative learning.
In vivo administration of dopamine (DA) receptor (DR)-related drugs modulate gastric pepsinogen secretion. However, DRs on gastric pepsinogen-secreting chief cells and DA D2 receptor (D2R) on somatostatin-secreting D cells were subsequently acquired. In this study, we aimed to further investigate the local effect of DA on gastric pepsinogen secretion through DRs expressed on chief cells or potential D2Rs expressed on D cells. To elucidate the modulation of DRs in gastric pepsinogen secretion, immunofluorescence staining, ex vivo incubation of gastric mucosa isolated from normal and D2R−/− mice were conducted, accompanied by measurements of pepsinogen or somatostatin levels using biochemical assays or enzyme-linked immunosorbent assays. D1R, D2R, and D5R-immunoreactivity (IR) were observed on chief cells in mouse gastric mucosa. D2R-IR was widely distributed on D cells from the corpus to the antrum. Ex vivo incubation results showed that DA and the D1-like receptor agonist SKF38393 increased pepsinogen secretion, which was blocked by the D1-like receptor antagonist SCH23390. However, D2-like receptor agonist quinpirole also significantly increased pepsinogen secretion, and D2-like receptor antagonist sulpiride blocked the promotion of DA. Besides, D2-like receptors exerted an inhibitory effect on somatostatin secretion, in contrast to their effect on pepsinogen secretion. Furthermore, D2R−/− mice showed much lower basal pepsinogen secretion but significantly increased somatostatin release and an increased number of D cells in gastric mucosa. Only SKF38393, not quinpirole, increased pepsinogen secretion in D2R−/− mice. DA promotes gastric pepsinogen secretion directly through D1-like receptors on chief cells and indirectly through D2R-mediated suppression of somatostatin release.
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