Detailed mapping of behavior reveals the formation of prelimbic neural ensembles across operant learning

Zhang, Yan; Denman, Alexander J.; Liang, Bo; Werner, Craig T.; Beacher, Nicholas J.; Chen, Rong; Li, Yun; Shaham, Yavin; Barbera, Giovanni; Lin, Da-Ting

doi:10.1016/j.neuron.2021.11.022

Cited by 21 publications

(17 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This suggests that learned experiences may be consolidated in the cortex concomitantly with hippocampal processing, rather than initially stored in the hippocampus and subsequently moved to the cortex. Additionally, PL ensembles are highly specific to behavior soon after experience and adapt over the learning process (Zhang et al, 2021 ). However, it is currently unknown how early in the learning process Fos-expressing PL ensembles become behaviorally relevant in cocaine seeking.…”

Section: Introductionmentioning

confidence: 99%

Prelimbic Ensembles Mediate Cocaine Seeking After Behavioral Acquisition and Once Rats Are Well-Trained

Sortman

Gobin

Rakela

et al. 2022

Front. Behav. Neurosci.

View full text Add to dashboard Cite

Substance use disorder (SUD) is a chronic relapsing condition characterized by continued use of drugs despite negative consequences. SUD is thought to involve disordered learning and memory wherein drug-paired cues gain increased salience, and ultimately drive craving and relapse. These types of associations are thought to be encoded within sparsely distributed sets of neurons, called neuronal ensembles, that drive encoded behaviors through synchronous activity of the participant neurons. We have previously found that Fos-expressing neuronal ensembles within the prefrontal cortex are required for well-trained cocaine seeking. However, less is known about how quickly cortical neuronal ensembles form during the initiation of cocaine seeking behavior. Here, we seek to further elucidate the role of Fos-expressing neuronal ensembles within the prelimbic cortex (PL) after the initial acquisition of cocaine self-administration (SA), or, after 10 days of additional SA training (well-trained). We trained Fos-LacZ transgenic rats to lever press for cocaine under an FR1 schedule of reinforcement. Once rats met acquisition criteria for cocaine self-administration, we ablated Fos-expressing neuronal ensembles in the PL using the Daun02 inactivation method, either 1 or 10 days after the rats met the acquisition criteria. Targeted ablation of Fos-expressing neuronal ensembles in the PL attenuated active lever pressing both 1 day and 10 days after rats acquired cocaine self-administration. Together, this suggests that Fos-expressing neuronal ensembles rapidly form in the PL and continue to mediate maintained cocaine seeking behavior.

show abstract

Section: Introductionmentioning

confidence: 99%

Prelimbic Ensembles Mediate Cocaine Seeking After Behavioral Acquisition and Once Rats Are Well-Trained

Sortman

Gobin

Rakela

et al. 2022

Front. Behav. Neurosci.

View full text Add to dashboard Cite

show abstract

“…We then implanted a 1-mm diameter gradient index (GRIN) lens into the PFC of these KO and CTRL mice. Via a custom-built miniscope recording system ( Barbera et al, 2016 ; Liang et al, 2018 ; Zhang et al, 2021 ), we performed in vivo calcium imaging during a 20-minute social behavior test containing two stages (10-minute each), namely, habituation (H) and sociability (SB). We found that KO mice exhibited normal sociability, like that of CTRL mice ( Fig.…”

Section: Resultsmentioning

confidence: 99%

“…All miniscopes used for the experiment were custom-built by Dr. Da-Ting Lin’s group at NIDA IRP ( Barbera et al, 2016 ; Liang et al, 2018 ; Zhang et al, 2021 ). After 4 weeks of GRIN lens implantation, a miniscope base was permanently mounted on the mouse skull.…”

Section: Methodsmentioning

confidence: 99%

Aberrant neural activity in prefrontal pyramidal neurons lacking TDP-43 precedes neuron loss

Liang

Thapa

Zhang³

et al. 2022

Progress in Neurobiology

Self Cite

View full text Add to dashboard Cite

“…Modern in vivo imaging techniques can be harnessed to study how these different biological markers contribute to schizophrenia in animal models. For example, mouse models displaying schizophrenia-like behavior can be imaged with miniaturized microscopes (miniscopes) (87)(88)(89)(90)(91)(92)(93) to examine longitudinal changes in activity of excitatory and inhibitory neurons in brain regions implicated in schizophrenia. Simultaneous optogenetic manipulations of circuitry are also possible using miniscopes (94,95) to explore how in vivo manipulation of circuitry impacts behavior using animal models for schizophrenia.…”

Section: Discussionmentioning

confidence: 99%

Dysbindin-1, BDNF, and GABAergic Transmission in Schizophrenia

et al. 2022

Self Cite

View full text Add to dashboard Cite

Schizophrenia is a psychiatric disorder characterized by hallucinations, anhedonia, disordered thinking, and cognitive impairments. Both genetic and environmental factors contribute to schizophrenia. Dysbindin-1 (DTNBP1) and brain-derived neurotrophic factor (BDNF) are both genetic factors associated with schizophrenia. Mice lacking Dtnbp1 showed behavioral deficits similar to human patients suffering from schizophrenia. DTNBP1 plays important functions in synapse formation and maintenance, receptor trafficking, and neurotransmitter release. DTNBP1 is co-assembled with 7 other proteins into a large protein complex, known as the biogenesis of lysosome-related organelles complex-1 (BLOC-1). Large dense-core vesicles (LDCVs) are involved in the secretion of hormones and neuropeptides, including BDNF. BDNF plays important roles in neuronal development, survival, and synaptic plasticity. BDNF is also critical in maintaining GABAergic inhibitory transmission in the brain. Two studies independently showed that DTNBP1 mediated activity-dependent BDNF secretion to maintain inhibitory transmission. Imbalance of excitatory and inhibitory neural activities is thought to contribute to schizophrenia. In this mini-review, we will discuss a potential pathogenetic mechanism for schizophrenia involving DTNBP1, BDNF, and inhibitory transmission. We will also discuss how these processes are interrelated and associated with a higher risk of schizophrenia development.

show abstract

Detailed mapping of behavior reveals the formation of prelimbic neural ensembles across operant learning

Cited by 21 publications

References 45 publications

Prelimbic Ensembles Mediate Cocaine Seeking After Behavioral Acquisition and Once Rats Are Well-Trained

Prelimbic Ensembles Mediate Cocaine Seeking After Behavioral Acquisition and Once Rats Are Well-Trained

Aberrant neural activity in prefrontal pyramidal neurons lacking TDP-43 precedes neuron loss

Dysbindin-1, BDNF, and GABAergic Transmission in Schizophrenia

Contact Info

Product

Resources

About