ABSTRACTDepolarisation of distal axons is necessary for somatic action potentials to be translated into axonal neurotransmitter release. Here, we show that activation of striatal cholinergic interneurons (ChIs) and nicotinic receptors (nAChRs) on mouse DA axons transiently prevents the release of dopamine (DA) by subsequent stimuli for ~100 ms. Previous studies have shown that nAChRs on DA axons can drive ectopic action potentials in DA axons to trigger DA release. We demonstrate ex vivo that a lower level of activation of ChIs is needed to suppress DA release than to trigger it, an effect that is not due to DA depletion, but to restricted re-activation of DA axons. This axonal brake on DA output is stronger and more persistent in dorsal than ventral striatum.  In vivo, we reveal a predominant depression of DA release by endogenous acetylcholine, as antagonism of nAChRs in dorsal striatum conversely elevated tonic DA detected with optic-fibre photometry of GRABDA2m sensor and promoted conditioned place-preference. Our findings reveal that ChIs acting via nAChRs limit activation of DA axons by subsequent DA neuron activity, uncoupling DA axons from ascending action potentials and generating a dynamic inverse scaling of DA release according to ChI activity. FILE DESCRIPTIONSThis repository contains the following files:Key Resources Table (.xlsx) - Table containing details on key resources (antibodies, mouse lines, virus strains, and software), and the persistent identifiers for protocols and code used and generated in this study. Source Data Folder (.zip):_README_Source_Data (.txt) with detailed information about each dataset.Individual tabular datasets corresponding to panels shown in the Main Figures 1 to 5 (.csv).Excel spreadsheet containing all tabular datasets plotted in Main Figures 1 to 5 (.xlsx)Supplementary Data Folder (.zip):_README_Supplementary_Data (.txt) with detailed information about each dataset.Individual tabular datasets corresponding to panels shown in the Supplementary Figures 1 to 6 (.csv).Excel spreadsheet containing all tabular datasets plotted in Supplementary Figures 1 to 6  (.xlsx)

ABSTRACTDepolarisation of distal axons is necessary for somatic action potentials to be translated into axonal neurotransmitter release. Here, we show that activation of striatal cholinergic interneurons (ChIs) and nicotinic receptors (nAChRs) on mouse DA axons transiently prevents the release of dopamine (DA) by subsequent stimuli for ~100 ms. Previous studies have shown that nAChRs on DA axons can drive ectopic action potentials in DA axons to trigger DA release. We demonstrate ex vivo that a lower level of activation of ChIs is needed to suppress DA release than to trigger it, an effect that is not due to DA depletion, but to restricted re-activation of DA axons. This axonal brake on DA output is stronger and more persistent in dorsal than ventral striatum.  In vivo, we reveal a predominant depression of DA release by endogenous acetylcholine, as antagonism of nAChRs in dorsal striatum conversely elevated tonic DA detected with optic-fibre photometry of GRABDA2m sensor and promoted conditioned place-preference. Our findings reveal that ChIs acting via nAChRs limit activation of DA axons by subsequent DA neuron activity, uncoupling DA axons from ascending action potentials and generating a dynamic inverse scaling of DA release according to ChI activity. FILE DESCRIPTIONSThis repository contains the following files:Key Resources Table (.xlsx) - Table containing details on key resources (antibodies, mouse lines, virus strains, and software), and the persistent identifiers for protocols and code used and generated in this study. Source Data Folder (.zip):_README_Source_Data (.txt) with detailed information about each dataset.Individual tabular datasets corresponding to panels shown in the Main Figures 1 to 5 (.csv).Excel spreadsheet containing all tabular datasets plotted in Main Figures 1 to 5 (.xlsx)Supplementary Data Folder (.zip):_README_Supplementary_Data (.txt) with detailed information about each dataset.Individual tabular datasets corresponding to panels shown in the Supplementary Figures 1 to 6 (.csv).Excel spreadsheet containing all tabular datasets plotted in Supplementary Figures 1 to 6  (.xlsx)

ABSTRACTDepolarisation of distal axons is necessary for somatic action potentials to be translated into axonal neurotransmitter release. Here, we show that activation of striatal cholinergic interneurons (ChIs) and nicotinic receptors (nAChRs) on mouse DA axons transiently prevents the release of dopamine (DA) by subsequent stimuli for ~100 ms. Previous studies have shown that nAChRs on DA axons can drive ectopic action potentials in DA axons to trigger DA release. We demonstrate ex vivo that a lower level of activation of ChIs is needed to suppress DA release than to trigger it, an effect that is not due to DA depletion, but to restricted re-activation of DA axons. This axonal brake on DA output is stronger and more persistent in dorsal than ventral striatum.  In vivo, we reveal a predominant depression of DA release by endogenous acetylcholine, as antagonism of nAChRs in dorsal striatum conversely elevated tonic DA detected with optic-fibre photometry of GRABDA2m sensor and promoted conditioned place-preference. Our findings reveal that ChIs acting via nAChRs limit activation of DA axons by subsequent DA neuron activity, uncoupling DA axons from ascending action potentials and generating a dynamic inverse scaling of DA release according to ChI activity. FILE DESCRIPTIONSThis repository contains the following files:Key Resources Table (.xlsx) - Table containing details on key resources (antibodies, mouse lines, virus strains, and software), and the persistent identifiers for protocols and code used and generated in this study. Source Data Folder (.zip):_README_Source_Data (.txt) with detailed information about each dataset.Individual tabular datasets corresponding to each panel shown in the Main Figures 1 to 6 (.csv).Excel spreadsheet containing all tabular datasets plotted in Main Figures 1 to 6 (.xlsx)Supplementary Data Folder (.zip):_README_Supplementary_Data (.txt) with detailed information about each dataset.Individual tabular datasets corresponding to each panel shown in the Supplementary Figures (.csv).Excel spreadsheet containing all tabular datasets plotted in Supplementary Figures  (.xlsx)

Using fMRI experiments, Zhang et al. found that activation of two canonical language areas in sentence comprehension reflects the working memory of social semantics rather than general semantic and/or syntactic processing. Here we shared the data that support our fingdings.

AbstractMolecules –– the elementary units of substances –– are commonly considered the units of processing in olfaction, giving rise to undifferentiated odor objects invariant to environmental variations. By selectively perturbing the processing of chemical substructures with adaptation, “the psychologist's microelectrode”, the current study provides psychophysical and neuroimaging evidence (n = 350) that argues otherwise. We show that two perceptually distinct odorants sharing part of their structural features become significantly less discernable following adaptation to a third odorant containing their non-shared structural features, in manners independent of olfactory intensity, valence, quality, or general olfactory adaptation. The effect is accompanied by reorganizations of ensemble activity patterns in the posterior piriform cortex that parallel subjective odor quality changes, in addition to substructure-based neural adaptations in the anterior piriform cortex and amygdala. These findings demonstrate that central representations of odor quality and the perceptual outcome embed submolecular structural information and are malleable by recent olfactory encounters.Usage NotesThe ‘preprocessed images.zip’ file stores fMRI data that were preprocessed using the standard procedure in SPM12(http://www.fil.ion.ucl.ac.uk/spm). EPI images were corrected for slice timing differences and geometric distortion due to susceptibility artefacts (using participants’ field maps), spatially realigned to the first volume of the first session (first baseline run on Day 1) and unwarped to reduce movement related variance, and smoothed by a Gaussian kernel with 6-mm full width at half maximum to increase signal-to-noise ratio.The ‘clean data.zip’ file stores fMRI data that the no interest effects (motion regressors and low-frequency drift) were subtracted out from the preprocessed functional data with AFNI programs 3dDeconvolve and 3dSynthesize (https://afni.nimh.nih.gov/).The ‘OdorDetectionTask.zip’ file stores the task scripts used in the fMRI scanner.The ‘ROI.zip’ file stores the masks of region of interest used in analysis.The ‘Results.zip’ file stores all results.