ArticlePloS one2013
Contribution of dopamine d1/5 receptor modulation of post-spike/burst afterhyperpolarization to enhance neuronal excitability of layer v pyramidal neurons in prepubertal rat prefrontal cortex.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- In silico investigation of the puzzling dopamine effects on excitability and synaptic plasticity in hippocampal CA1 pyramidal neurons.Scientific reports · 2025Article
- Regulation of intrinsic excitability: Roles for learning and memory, aging and Alzheimer's disease, and genetic diversity.Neurobiology of learning and memory · 2019Review
- A Schizophrenia-Related Deletion Leads to KCNQ2-Dependent Abnormal Dopaminergic Modulation of Prefrontal Cortical Interneuron Activity.Cerebral cortex (New York, N.Y. : 1991) · 2018Article
- Layer- and Cell Type-Specific Modulation of Excitatory Neuronal Activity in the Neocortex.Frontiers in neuroanatomy · 2018Review
- Differential Expression of Dopamine D5 Receptors across Neuronal Subtypes in Macaque Frontal Eye Field.Frontiers in neural circuits · 2018Article
- Dopamine terminals from the ventral tegmental area gate intrinsic inhibition in the prefrontal cortex.Physiological reports · 2017Article
- Chronic cocaine disrupts mesocortical learning mechanisms.Brain research · 2015Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dopamine (DA) receptors in the prefrontal cortex (PFC) modulate both synaptic and intrinsic plasticity that may contribute to cognitive processing. However, the ionic basis underlying DA actions to enhance neuronal plasticity in PFC remains ill-defined. Using whole-cell patch-clamp recordings in layer V-VI pyramidal cells in prepubertal rat PFC, we showed that DA, via activation of D1/5, but not D2/3/4, receptors suppress a Ca(2+)-dependent, apamin-sensitive K(+) channel that mediates post-spike/burst afterhyperpolarization (AHP) to enhance neuronal excitability of PFC neurons. This inhibition is not dependent on HCN channels. The D1/5 receptor activation also enhanced an afterdepolarizing potential (ADP) that follows the AHP. Additional single-spike analyses revealed that DA or D1/5 receptor activation suppressed the apamin-sensitive post-spike mAHP, further contributing to the increase in evoked spike firing to enhance the neuronal excitability. Taken together, the D1/5 receptor modulates intrinsic mechanisms that amplify a long depolarizing input to sustain spike firing outputs in pyramidal PFC neurons.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.