Feasibility and resolution limits of opto-magnetic imaging of neural network activity in brain slices using color centers in diamond

Neurons in the lateral septum (LS) integrate glutamatergic synaptic inputs, primarily from hippocampus, and send inhibitory projections to brain regions involved in reward and the generation of motivated behavior. Motivated learning and drugs of abuse have been shown to induce long-term changes in the strength of glutamatergic synapses in the LS, but the cellular mechanisms underlying long-term synaptic modification in the LS are poorly understood. Here we examined synaptic transmission and long-term depression (LTD) in brain slices prepared from male and female C57BL/6 mice. No sex differences were observed in whole-cell patch-clamp recordings of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPA-R) and N-methyl-D-aspartate receptor (NMDA-R) mediated currents. Low frequency stimulation of the fimbria fibre bundle (1 Hz 15 min) induced LTD of the LS field excitatory postsynaptic potential (fEPSP). Induction of LTD was blocked by the NMDA-R antagonist APV, but not the selective antagonist of GluN2B-containing NMDA-R ifenprodil. These results demonstrate the NMDA-R dependence of LTD in the LS. The LS is a sexually dimorphic structure and sex differences in glutamatergic transmission have been reported in vivo; our results suggest sex differences observed in vivo result from network activity rather than intrinsic differences in glutamatergic transmission.

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Understanding the Effects of General Anesthetics on Cortical Network Activity Using Ex Vivo Preparations

Anesthesiology ◽

10.1097/aln.0000000000002554 ◽

2019 ◽

Vol 130 (6) ◽

pp. 1049-1063 ◽

Cited By ~ 10

Author(s):

Logan J. Voss ◽

Paul S. García ◽

Harald Hentschke ◽

Matthew I. Banks

Keyword(s):

Molecular Mechanisms ◽

Ex Vivo ◽

Brain Slices ◽

Brain Regions ◽

Cortical Network ◽

Network Activity ◽

Common Mechanism ◽

General Anesthetics ◽

Neural Basis

Abstract General anesthetics have been used to ablate consciousness during surgery for more than 150 yr. Despite significant advances in our understanding of their molecular-level pharmacologic effects, comparatively little is known about how anesthetics alter brain dynamics to cause unconsciousness. Consequently, while anesthesia practice is now routine and safe, there are many vagaries that remain unexplained. In this paper, the authors review the evidence that cortical network activity is particularly sensitive to general anesthetics, and suggest that disruption to communication in, and/or among, cortical brain regions is a common mechanism of anesthesia that ultimately produces loss of consciousness. The authors review data from acute brain slices and organotypic cultures showing that anesthetics with differing molecular mechanisms of action share in common the ability to impair neurophysiologic communication. While many questions remain, together, ex vivo and in vivo investigations suggest that a unified understanding of both clinical anesthesia and the neural basis of consciousness is attainable.

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Beta and gamma synchronous oscillations in neural network activity in mice-induced by food deprivation

Neuroscience Letters ◽

10.1016/j.neulet.2019.134398 ◽

2019 ◽

Vol 709 ◽

pp. 134398

Author(s):

Nifareeda Samerphob ◽

Acharaporn Issuriya ◽

Dania Cheaha ◽

Surapong Chatpun ◽

Ole Jensen ◽

...

Keyword(s):

Neural Network ◽

Food Deprivation ◽

Network Activity ◽

Synchronous Oscillations

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Distribution of VTA Glutamate and Dopamine Terminals, and their Significance in CA1 Neural Network Activity

Neuroscience ◽

10.1016/j.neuroscience.2020.06.045 ◽

2020 ◽

Vol 446 ◽

pp. 171-198 ◽

Cited By ~ 2

Author(s):

Philip A. Adeniyi ◽

Amita Shrestha ◽

Olalekan M. Ogundele

Keyword(s):

Neural Network ◽

Network Activity

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Bursting as a source for predictability in biological neural network activity

Physica D Nonlinear Phenomena ◽

10.1016/s0167-2789(97)00131-0 ◽

1997 ◽

Vol 110 (3-4) ◽

pp. 323-331 ◽

Cited By ~ 23

Author(s):

L. Menendez de la Prida ◽

N. Stollenwerk ◽

J.V. Sanchez-Andres

Keyword(s):

Neural Network ◽

Network Activity ◽

Biological Neural Network

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Respiratory Neural Network: Activity and Connectivity

Advances in Dynamics, Patterns, Cognition - Nonlinear Systems and Complexity ◽

10.1007/978-3-319-53673-6_14 ◽

2017 ◽

pp. 227-242

Author(s):

Laurence Mangin ◽

Maurice Courbage

Keyword(s):

Neural Network ◽

Network Activity

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Dopaminergic Modulation of Local Network Activity in Rat Prefrontal Cortex

Journal of Neurophysiology ◽

10.1152/jn.00898.2006 ◽

2007 ◽

Vol 97 (6) ◽

pp. 4120-4128 ◽

Cited By ~ 31

Author(s):

Susanta Bandyopadhyay ◽

John J. Hablitz

Keyword(s):

Prefrontal Cortex ◽

Synaptic Transmission ◽

Receptor Agonist ◽

Neuronal Networks ◽

Brain Slices ◽

Pyramidal Cells ◽

Network Activity ◽

Lateral Spread ◽

Local Network ◽

Evoked Activity

Dopamine modulates prefrontal cortex excitability in complex ways. Dopamine's net effect on local neuronal networks is therefore difficult to predict based on studies on pharmacologically isolated excitatory or inhibitory connections. In the present work, we have studied the effects of dopamine on evoked activity in acute rat brain slices when both excitation and inhibition are intact. Whole cell recordings from layer II/III pyramidal cells under conditions of normal synaptic transmission showed that bath-applied dopamine (30 μM) increased the outward inhibitory component of composite postsynaptic currents, whereas inward excitatory currents were not significantly affected. Optical imaging with the voltage-sensitive dye N-(3-(triethylammonium)propyl)-4-(4-(p-diethylaminophenyl)buta-dienyl)pyridinium dibromide revealed that bath application of dopamine significantly decreased the amplitude, duration, and lateral spread of activity in local cortical networks. This effect of dopamine was observed both with single and train (5 at 20 Hz) stimuli. The effect was mimicked by the D1-like receptor agonist R(+)-6-chloro-7,8-dihydroxy-1-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine hydrobromide (1 μM) and was blocked by R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine hydrochloride (10 μM), a selective antagonist for D1-like receptors. The D2-like receptor agonist quinpirole (10 μM) had no significant effect on evoked dye signals. Our results suggest that dopamine's effect on inhibition dominates over that on excitation under conditions of normal synaptic transmission. Such neuromodulation by dopamine may be important for maintenance of stability in local neuronal networks in the prefrontal cortex.

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A Metabolic Mechanism for Anaesthetic Suppression of Cortical Synaptic Function in Mouse Brain Slices—A Pilot Investigation

International Journal of Molecular Sciences ◽

10.3390/ijms21134703 ◽

2020 ◽

Vol 21 (13) ◽

pp. 4703

Author(s):

Logan J. Voss ◽

Jamie W. Sleigh

Keyword(s):

Brain Slices ◽

Inhibitory Effect ◽

Temporal Sequence ◽

Synaptic Function ◽

Network Activity ◽

Tissue Oxygen ◽

Pilot Investigation ◽

Metabolic Mechanism ◽

Mitochondrial Complex I Inhibitor ◽

Measurable Change

Regulation of synaptically located ionotropic receptors is thought to be the main mechanism by which anaesthetics cause unconsciousness. An alternative explanation, which has received much less attention, is that of primary anaesthetic disruption of brain metabolism via suppression of mitochondrial proteins. In this pilot study in mouse cortical slices, we investigated the effect of disrupting cellular metabolism on tissue oxygen handling and cortical population seizure-like event (SLE) activity, using the mitochondrial complex I inhibitor rotenone, and compared this to the effects of the general anaesthetics sevoflurane, propofol and ketamine. Rotenone caused an increase in tissue oxygen (98 mmHg to 157 mmHg (p < 0.01)) before any measurable change in SLE activity. Thereafter, tissue oxygen continued to increase and was accompanied by a significant and prolonged reduction in SLE root mean square (RMS) activity (baseline RMS of 1.7 to 0.7 µV, p < 0.001) and SLE frequency (baseline 4.2 to 0.4 events/min, p = 0.001). This temporal sequence of effects was replicated by all three anaesthetic drugs. In conclusion, anaesthetics with differing synaptic receptor mechanisms all effect changes in tissue oxygen handling and cortical network activity, consistent with a common inhibitory effect on mitochondrial function. The temporal sequence suggests that the observed synaptic depression—as seen in anaesthesia—may be secondary to a reduction in cellular metabolic capacity.

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