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Real-time Analysis of Gut-brain Neural Communication: Cortex wide Calcium Dynamics in Response to Intestinal Glucose Stimulation
Published on: December 29, 2023
Glutamatergic inhibition in sensory neocortex
Charles C Lee1, S Murray Sherman
1Department of Neurobiology, University of Chicago, Chicago, IL 60637, USA. clee@bsd.uchicago.edu
Glutamate, typically excitatory, acts as an inhibitory neurotransmitter in the neocortex. This novel finding in layer 4 neurons reveals a new mechanism for refining brain activity and receptive fields.
Area of Science:
- Neuroscience
- Neurophysiology
Background:
- Glutamate is the primary excitatory neurotransmitter; gamma-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the mammalian brain.
- The role of glutamate in inhibition, particularly in the neocortex, is not well-established.
Purpose of the Study:
- To investigate the potential inhibitory role of glutamate in layer 4 of the neocortex.
- To elucidate the mechanisms underlying this novel inhibitory function.
Main Methods:
- Whole-cell recordings were performed on layer 4 neurons in mouse visual, auditory, and somatosensory cortical slices.
- Metabotropic glutamate receptor (mGluR) agonists and antagonists were used to probe receptor function.
- Electrical and photostimulation were employed to activate intracortical inputs.
Main Results:
- Metabotropic glutamate receptor (mGluR) agonists induced a significant, prolonged hyperpolarization in layer 4 neurons.
- This hyperpolarization was blocked by group II mGluR antagonists, indicating a specific receptor-mediated effect.
- The inhibitory response involved G-protein activity and GIRK channels, suggesting a K+ conductance mechanism.
- Stimulation of intracortical inputs to layer 4 also elicited a similar, mGluR-dependent hyperpolarization.
Conclusions:
- Glutamate can function as a postsynaptic inhibitory neurotransmitter in layer 4 of the neocortex via group II mGluRs.
- This inhibitory mechanism may refine cortical receptive fields and contribute to synaptic gain control during heightened neural activity.
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