scholarly journals Cortical ChAT+ neurons co-transmit acetylcholine and GABA in a target- and brain-region specific manner

2020 ◽  
Author(s):  
Adam J Granger ◽  
Wengang Wang ◽  
Keiramarie Robertson ◽  
Mahmoud El-Rifai ◽  
Andrea Zanello ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Synaptic Connectivity ◽  
Local Source ◽  
Inhibitory Interneurons ◽  
Target Neuron ◽  
Specific Manner ◽  
Release Of Acetylcholine ◽  
Differential Transmission ◽  
Sparse Population ◽  
Postsynaptic Target

AbstractThe cerebral cortex contains neurons that express choline acetyltransferase (ChAT) and are a potential local source of acetylcholine. However, the neurotransmitters released by cortical ChAT+ neurons and their synaptic connectivity are unknown. We show that the nearly all cortical ChAT+ neurons are specialized VIP+ interneurons that release GABA strongly onto other inhibitory interneurons and acetylcholine sparsely onto layer 1 interneurons and other VIP+/ChAT+ interneurons. This differential transmission of ACh and GABA based on the postsynaptic target neuron is reflected in VIP+/ChAT+ interneuron pre-synaptic terminals, as quantitative molecular analysis shows that only a subset of these are specialized to release acetylcholine. In addition, we identify a separate, sparse population of non-VIP ChAT+ neurons in the medial prefrontal cortex with a distinct developmental origin that robustly release acetylcholine in layer 1. These results demonstrate both cortex-region heterogeneity in cortical ChAT+ interneurons and target-specific co-release of acetylcholine and GABA.

scholarly journals Cortical ChAT+ neurons co-transmit acetylcholine and GABA in a target- and brain-region-specific manner

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Adam J Granger ◽  
Wengang Wang ◽  
Keiramarie Robertson ◽  
Mahmoud El-Rifai ◽  
Andrea F Zanello ◽  
...  
Keyword(s):  
Synaptic Connectivity ◽  
Local Source ◽  
Inhibitory Interneurons ◽  
Target Neuron ◽  
Mouse Cerebral Cortex ◽  
Specific Manner ◽  
Release Of Acetylcholine ◽  
Differential Transmission ◽  
Sparse Population ◽  
Postsynaptic Target

The mouse cerebral cortex contains neurons that express choline acetyltransferase (ChAT) and are a potential local source of acetylcholine. However, the neurotransmitters released by cortical ChAT+ neurons and their synaptic connectivity are unknown. We show that the nearly all cortical ChAT+ neurons in mice are specialized VIP+ interneurons that release GABA strongly onto other inhibitory interneurons and acetylcholine sparsely onto layer 1 interneurons and other VIP+/ChAT+ interneurons. This differential transmission of ACh and GABA based on the postsynaptic target neuron is reflected in VIP+/ChAT+ interneuron pre-synaptic terminals, as quantitative molecular analysis shows that only a subset of these are specialized to release acetylcholine. In addition, we identify a separate, sparse population of non-VIP ChAT+ neurons in the medial prefrontal cortex with a distinct developmental origin that robustly release acetylcholine in layer 1. These results demonstrate both cortex-region heterogeneity in cortical ChAT+ interneurons and target-specific co-release of acetylcholine and GABA.

scholarly journals Diversity and Function of Somatostatin-Expressing Interneurons in the Cerebral Cortex

2019 ◽  
Vol 20 (12) ◽  
pp. 2952 ◽  
Author(s):  
Therese Riedemann
Keyword(s):  
Major Depressive Disorder ◽  
Cerebral Cortex ◽  
Depressive Disorder ◽  
Neurological Disorders ◽  
Synaptic Connectivity ◽  
Inhibitory Interneurons ◽  
Cortical Circuits ◽  
Major Depressive ◽  
Neuron Population ◽  
And Function

Inhibitory interneurons make up around 10–20% of the total neuron population in the cerebral cortex. A hallmark of inhibitory interneurons is their remarkable diversity in terms of morphology, synaptic connectivity, electrophysiological and neurochemical properties. It is generally understood that there are three distinct and non-overlapping interneuron classes in the mouse neocortex, namely, parvalbumin-expressing, 5-HT3A receptor-expressing and somatostatin-expressing interneuron classes. Each class is, in turn, composed of a multitude of subclasses, resulting in a growing number of interneuron classes and subclasses. In this review, I will focus on the diversity of somatostatin-expressing interneurons (SOM+ INs) in the cerebral cortex and elucidate their function in cortical circuits. I will then discuss pathological consequences of a malfunctioning of SOM+ INs in neurological disorders such as major depressive disorder, and present future avenues in SOM research and brain pathologies.

scholarly journals Excitatory Projection Neuron Subtypes Control the Distribution of Local Inhibitory Interneurons in the Cerebral Cortex

Neuron ◽  
2011 ◽  
Vol 69 (4) ◽  
pp. 763-779 ◽  
Author(s):  
Simona Lodato ◽  
Caroline Rouaux ◽  
Kathleen B. Quast ◽  
Chanati Jantrachotechatchawan ◽  
Michèle Studer ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Projection Neuron ◽  
Inhibitory Interneurons ◽  
Excitatory Projection

Effect of Lithium Ions on the Release of Acetylcholine from the Cerebral Cortex

Nature ◽  
1971 ◽  
Vol 230 (5296) ◽  
pp. 587-588 ◽  
Author(s):  
M. BJEGOVIĆ ◽  
M. RANDIĆ
Keyword(s):  
Cerebral Cortex ◽  
Lithium Ions ◽  
Release Of Acetylcholine

scholarly journals PlexinA4-Semaphorin3A mediated crosstalk between main cortical interneuron classes is required for superficial interneurons lamination

2020 ◽  
Author(s):  
Greta Limoni ◽  
Mathieu Niquille ◽  
Sahana Murthy ◽  
Denis Jabaudon ◽  
Alexandre Dayer
Keyword(s):  
Cerebral Cortex ◽  
Serotonin Receptor ◽  
Deep Layer ◽  
Cortical Plate ◽  
Inhibitory Interneurons ◽  
Cell Type ◽  
Cortical Layers ◽  
Cortical Interneuron ◽  
Cell Type Specific ◽  
Genetic Deletion

SummaryIn the mammalian cerebral cortex, the developmental events governing the allocation of different classes of inhibitory interneurons (INs) into distinct cortical layers are poorly understood. Here we report that the guidance receptor PlexinA4 (PLXNA4) is upregulated in serotonin receptor 3a-expressing (HTR3A+) cortical INs (hINs) as they invade the cortical plate and that it regulates their laminar allocation to superficial cortical layers. We find that the PLXNA4 ligand Semaphorin3A (SEMA3A) acts as a chemorepulsive factor on hINs migrating into the nascent cortex and demonstrate that SEMA3A specifically controls their laminar positioning through PLXNA4. We identify that deep layer INs constitute a major source of SEMA3A in the developing cortex and demonstrate that cell-type specific genetic deletion of SEMA3A in these INs specifically affects the laminar allocation of hINs. These data demonstrate that in the neocortex, deep layer INs control the laminar allocation of hINs into superficial layers.

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