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Li, K.-L.

Publications and source records attributed to Li, K.-L..

3 recordsLinked to original sources

Refinement of Nucleus Accumbens Neuronal Dynamics During Cocaine Self-Administration Training

Drug addiction is an acquired motivational-behavioral state that begins with drug taking, which is comprised of a series of phases, including initial acquisition, stabilization, habituation, and maintenance. In rodent models of cocaine self-administration, the forebrain region nucleus accumbens (NAc) has been critically implicated in the acquisition-maintenance process of drug taking and seeking behaviors. However, it remains unknown how NAc neurons shift their activity patterns in response to these phasic transitions during cocaine taking. To examine this, we used GCaMP6m-based in vivo Ca2+ imaging to monitor activities of principal medium spiny neurons (MSNs) in the NAc across eleven days of cocaine self-administration. Behaviorally, mice exhibited progressive stabilization of operant responding and locomotion across 11 days of cocaine self-administration. During the early training days, we detected a portion of NAc neurons--a potential neuronal ensemble--that exhibited increased activities temporally contingent to the lever-press for cocaine. The number of NAc neurons exhibiting contingent activity increased progressively over the first three training days and then decreased gradually during the later training days, exhibiting expansion-refinement dynamics that may correspond to the acquisition and subsequent stabilization/maintenance of cocaine self-administration. Using a neuron-tracking technique, we found that the lever-press-contingent NAc ensemble exhibited substantial compositional dynamics, with neurons dropping into and out across training days. These activity features of lever-press-contingent neurons may represent key circuit dynamics of the NAc that transition the acquisition toward the maintenance of cocaine-taking behavior.

neuroscience↗

Deconstructing the common anteroposterior organisation of adult bilaterian guts

A through-gut is one of the major features of bilaterians. Comparative work among bilaterians has identified common molecular mechanisms during early gut patterning, but the primordial gut later often undergoes different degrees of reorganization in each lineage to form a fully differentiated adult gut with specializations along its anteroposterior (AP) axis. Yet, how the conserved embryonic gut AP pattern relates to the adult guts in diverse bilaterians after metamorphosis is still poorly understood. To unravel the molecular subdivisions of adult guts, we investigated the gut through transcriptomic analyses of five phylogenetically informative species, an annelid, a sea urchin, a hemichordate, a cephalochordate, and a vertebrate. We identified bipartite transcriptional programs defining the AP functional subdivisions. Patterning systems composed of Hox, Parahox, and, surprisingly, other transcription factors (TFs) known to be involved in gut formation in sea urchin larvae are maintained in these adult tissues. Using unbiased analyses, we identified five conserved TF modules corresponding to the AP compartments of the guts that are elaborated or shifted in different species. Our study inferred conserved and modified adult AP patterning modules along bilaterian guts enabling the reconstruction of ancestral bilaterian features with profound implications for the evolution of the bilaterian body plan.

developmental biology↗

Cocaine triggers glial-mediated synaptogenesis

Synaptogenesis is essential in forming new neurocircuits during development, and this is mediated in part by astrocyte-released thrombospondins (TSPs) and activation of their neuronal receptor, 2{delta}-1. Here, we show that this developmental synaptogenic mechanism is utilized during cocaine experience to induce spinogenesis and the generation of AMPA receptor-silent glutamatergic synapses in the adult nucleus accumbens (NAc). Specifically, cocaine administration activates NAc astrocytes, and preventing this activation blocks cocaine-induced generation of silent synapses. Furthermore, knockout of TSP2, or pharmacological inhibition or viral-mediated knockdown of 2{delta}-1, prevents cocaine-induced generation of silent synapses. Moreover, disrupting TSP2-2{delta}-1-mediated spinogenesis and silent synapse generation in the NAc occludes cue-induced cocaine seeking after withdrawal from cocaine self-administration and cue-induced reinstatement of cocaine seeking after drug extinction. These results establish that silent synapses are generated by an astrocyte-mediated synaptogenic mechanism in response to cocaine experience and embed critical cue-associated memory traces that promote cocaine relapse.

neuroscience↗