ArticleCell reports2024
Distinctive physiology of molecularly identified medium spiny neurons in the macaque putamen.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Distinct electrophysiology and dopaminergic modulation of medium spiny neurons across divisions of the tail striatum and the dorsolateral striatum.Experimental physiology · 2026Article
- Multimodal characterization of variation in neuronal types in the mouse basal ganglia.bioRxiv : the preprint server for biology · 2026Article
- Conserved Kir channel mechanisms governing intrinsic excitability in human and rodent parvalbumin neurons.Communications biology · 2026Article
- Inter-individual variation of cellular and gene-expression properties of the human striatum.bioRxiv : the preprint server for biology · 2026Article
- Morphoelectric Diversity and Specialization of Neuronal Cell Types in the Primate Striatum.bioRxiv : the preprint server for biology · 2026Article
- Regulation of input excitability in human and mouse parvalbumin interneurons by Kir potassium channels.bioRxiv : the preprint server for biology · 2025Article
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22 authors.
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Abstract
The distinctive physiology of striatal medium spiny neurons (MSNs) underlies their ability to integrate sensory and motor input. In rodents, MSNs have a hyperpolarized resting potential and low input resistance. When activated, they have a delayed onset of spiking and regular spike rate. Here, we show that in the macaque putamen, latency to spike is reduced and spike rate adaptation is increased relative to mouse. We use whole-cell brain slice recordings and recover single-cell gene expression using Patch-seq to distinguish macaque MSN cell types. Species differences in the expression of ion channel genes including the calcium-activated chloride channel, ANO2, and an auxiliary subunit of the A-type potassium channel, DPP10, are correlated with species differences in spike rate adaptation and latency to the first spike, respectively. These surprising divergences in physiology better define the strengths and limitations of mouse models for understanding neuronal and circuit function in the primate basal ganglia.
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