English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Cholinergic signaling coupled to sensory-driven neuronal depolarization is essential for modulating lasting changes in deep-layer neural excitability and experience-dependent plasticity in the primary auditory cortex. However, the underlying cellular mechanism(s) associated with coincident cholinergic receptor activation and neuronal depolarization of deep-layer cortical neurons remains unknown. Using in vitro whole cell patch-clamp recordings targeted to neurons ( n = 151) in isolated brain slices containing the primary auditory cortex (AI), we investigated the effects of cholinergic receptor activation and neuronal depolarization on the electrophysiological properties of AI layer 5 intrinsic-bursting and regular-spiking neurons. Bath application of carbachol (5 µM; cholinergic receptor agonist) paired with suprathreshold intracellular depolarization led to persistent activity in these neurons. Persistent activity may involve similar cellular mechanisms and be generated intrinsically in both intrinsic-bursting and regular-spiking neurons given that it 1) persisted under the blockade of ionotropic glutamatergic (kynurenic acid, 2 mM) and GABAergic receptors (picrotoxin, 100 µM), 2) was fully blocked by both atropine (10 µM; nonselective muscarinic antagonist) and flufenamic acid [100 µM; nonspecific Ca 2+ -sensitive cationic channel (CAN) blocker], and 3) was sensitive to the voltage-gated Ca 2+  channel blocker nifedipine (50 µM) and Ca 2+ -free artificial cerebrospinal fluid. Together, our results support a model through which coincident activation of AI layer 5 neuron muscarinic receptors and suprathreshold activation can lead to sustained changes in layer 5 excitability, providing new insight into the possible role of a calcium-CAN-dependent cholinergic mechanism of AI cortical plasticity. These findings also indicate that distinct streams of auditory processing in layer 5 intrinsic-bursting and regular-spiking neurons may run in parallel during learning-induced auditory plasticity.    NEW &amp; NOTEWORTHY Cholinergic signaling coupled to sensory-driven neuronal depolarization is essential for modulating lasting changes in experience-dependent plasticity in the primary auditory cortex. Cholinergic activation together with cellular depolarization can lead to persistent activity in both intrinsic-bursting and regular-spiking layer 5 pyramidal neurons. A similar mechanism involving muscarinic acetylcholine receptor, voltage-gated Ca 2+  channel, and possible Ca 2+ -sensitive nonspecific cationic channel activation provides new insight into our understanding of the cellular mechanisms that govern learning-induced auditory cortical and subcortical plasticity.

Muscarinic acetylcholine receptor-dependent persistent activity of layer 5 intrinsic-bursting and regular-spiking neurons in primary auditory cortex