scholarly journals Circuit contributions to sensory-driven glutamatergic drive of olfactory bulb mitral and tufted cells during odorant inhalation

2021 ◽  
Author(s):  
Andrew K. Moran ◽  
Thomas P. Eiting ◽  
Matt Wachowiak
Keyword(s):  
Olfactory Bulb ◽  
Gabab Receptor ◽  
Glutamate Release ◽  
Excitatory Input ◽  
Slight Reduction ◽  
Receptor Antagonists ◽  
Glutamate Signaling ◽  
Inhibitory Circuits ◽  
Primary Determinant ◽  
Excitatory Drive

In the mammalian olfactory bulb (OB), mitral/tufted (MT) cells respond to odorant inhalation with diverse temporal patterns that are thought to encode odor information. Much of this diversity is already apparent at the level of glutamatergic input to MT cells, which receive direct, monosynaptic excitatory input from olfactory sensory neurons (OSNs) as well as multisynaptic excitatory drive via glutamatergic interneurons. Both pathways are also subject to modulation by inhibitory circuits in the glomerular layer of the OB. To understand the role of direct OSN input versus postsynaptic OB circuit mechanisms in shaping diverse dynamics of glutamatergic drive to MT cells, we imaged glutamate signaling onto MT cell dendrites in anesthetized mice while blocking multisynaptic excitatory drive with ionotropic glutamate receptor antagonists and blocking presynaptic modulation of glutamate release from OSNs with GABAB receptor antagonists. GABAB receptor blockade increased the magnitude of inhalation-linked glutamate transients onto MT cell apical dendrites without altering their inhalation-linked dynamics, confirming that presynaptic inhibition impacts the gain of OSN inputs to the OB. Surprisingly, blockade of multisynaptic excitation only modestly impacted glutamatergic input to MT cells, causing a slight reduction in the amplitude of inhalation-linked glutamate transients in response to low odorant concentrations and no change in the dynamics of each transient. Postsynaptic blockade also modestly impacted glutamate dynamics over a slower timescale, mainly by reducing adaptation of the glutamate response across multiple inhalations of odorant. These results suggest that direct glutamatergic input from OSNs provides the bulk of excitatory drive to MT cells, and that diversity in the dynamics of this input may be a primary determinant of the temporal diversity in MT cell responses that underlies odor representations at this stage.

Enhancement of Synaptic Excitation by GABAA Receptor Antagonists in Rat Embryonic Midbrain Culture

1998 ◽  
Vol 79 (2) ◽  
pp. 1113-1116 ◽  
Author(s):  
Jutta Rohrbacher ◽  
Katja Sauer ◽  
Andrea Lewen ◽  
Ulrich Misgeld
Keyword(s):  
Transmitter Release ◽  
Glutamate Release ◽  
Synaptic Activity ◽  
Aminobutyric Acid ◽  
Receptor Antagonists ◽  
Synaptic Excitation ◽  
Aspartate Receptor ◽  
Cell Recording ◽  
Per Se ◽  
Excitatory Drive

Rohrbacher, Jutta, Katja Sauer, Andrea Lewen, and Ulrich Misgeld. Enhancement of synaptic excitation by GABAA receptor antagonists in rat embryonic midbrain culture. J. Neurophysiol. 79: 1113–1116, 1998. Alterations of synaptic excitation induced by exposure to γ-aminobutyric acid-A (GABAA) receptor antagonists were investigated employing tight-seal whole cell recording from single neurons or pairs of neurons in rat embryonic midbrain culture. Application of GABAA receptor antagonists led to sustained depolarizations followed by synchronous paroxysmal depolarization shifts (PDSs). PDSs induced a transient increase in miniature excitatory postsynaptic currents in the presence as well as in the absence of a N-methyl-d-aspartate receptor antagonist. The increase in glutamate release supports the excitatory drive required to reinitiate PDSs from the quiescent interburst intervals. After washout of GABAA receptor antagonists, synaptic activity remained grouped, regardless of the presence or absence of PDS blockade by tetrodotoxin (TTX). Impediment of action potential-triggered transmitter release by Cd2+ or TTX also induced grouped activity. We conclude that changes in synaptic excitation are produced by the impaired GABAA inhibition per se and by the initiation of PDSs.

scholarly journals GABA and glutamate release affected by GABAB receptor antagonists with similar potency: no evidence for pharmacologically different presynaptic receptors

1994 ◽  
Vol 113 (4) ◽  
pp. 1515-1521 ◽  
Author(s):  
Peter C. Waldmeier ◽  
Peter Wicki ◽  
Jean-Jacques Feldtrauer ◽  
Stuart J. Mickel ◽  
Helmut Bittiger ◽  
...  
Keyword(s):  
Gabab Receptor ◽  
Glutamate Release ◽  
Presynaptic Receptors ◽  
Receptor Antagonists ◽  
Gabab Receptor Antagonists

Opponent vesicular transporters regulate the strength of glutamatergic neurotransmission in a C. elegans sensory circuit

2021 ◽  
Author(s):  
Jung-Hwan Choi ◽  
Lauren Bayer Horowitz ◽  
Niels Ringstad
Keyword(s):  
Synaptic Vesicles ◽  
Glutamate Release ◽  
Glutamate Transporter ◽  
Synaptic Function ◽  
Functional Coupling ◽  
Glutamate Signaling ◽  
C Elegans ◽  
Vesicular Transporters ◽  
Chemical Synapses

At chemical synapses, neurotransmitters are packaged into synaptic vesicles that release their contents in response to depolarization. Despite its central role in synaptic function, regulation of the machinery that loads vesicles with neurotransmitters remains poorly understood. We find that synaptic glutamate signaling in a C. elegans chemosensory circuit is regulated by antagonistic interactions between the canonical vesicular glutamate transporter EAT-4/VGLUT and another vesicular transporter, VST-1. Loss of VST-1 strongly potentiates glutamate release from chemosensory BAG neurons and disrupts chemotaxis behavior. Analysis of the circuitry downstream of BAG neurons shows that excess glutamate release disrupts behavior by inappropriately recruiting RIA interneurons to the BAG-associated chemotaxis circuit. Our data indicate that in vivo the strength of glutamatergic synapses is controlled by regulation of neurotransmitter packaging into synaptic vesicles via functional coupling of VGLUT and VST-1.

scholarly journals Massive normalization of olfactory bulb output in mice with a 'monoclonal nose'

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Benjamin Roland ◽  
Rebecca Jordan ◽  
Dara L Sosulski ◽  
Assunta Diodato ◽  
Izumi Fukunaga ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
Transgenic Mice ◽  
Neural Correlates ◽  
Mitral Cell ◽  
Inhibitory Circuits ◽  
Cell Responses ◽  
Mechanistic Basis ◽  
Signal Normalization ◽  
Whole Cell Recordings

Perturbations in neural circuits can provide mechanistic understanding of the neural correlates of behavior. In M71 transgenic mice with a “monoclonal nose”, glomerular input patterns in the olfactory bulb are massively perturbed and olfactory behaviors are altered. To gain insights into how olfactory circuits can process such degraded inputs we characterized odor-evoked responses of olfactory bulb mitral cells and interneurons. Surprisingly, calcium imaging experiments reveal that mitral cell responses in M71 transgenic mice are largely normal, highlighting a remarkable capacity of olfactory circuits to normalize sensory input. In vivo whole cell recordings suggest that feedforward inhibition from olfactory bulb periglomerular cells can mediate this signal normalization. Together, our results identify inhibitory circuits in the olfactory bulb as a mechanistic basis for many of the behavioral phenotypes of mice with a “monoclonal nose” and highlight how substantially degraded odor input can be transformed to yield meaningful olfactory bulb output.

scholarly journals Opponent vesicular transporters regulate the strength of glutamatergic neurotransmission in a C. elegans sensory circuit

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jung-Hwan Choi ◽  
Lauren Bayer Horowitz ◽  
Niels Ringstad
Keyword(s):  
Synaptic Vesicles ◽  
Glutamate Release ◽  
Glutamate Transporter ◽  
Synaptic Function ◽  
Functional Coupling ◽  
Glutamate Signaling ◽  
C Elegans ◽  
Vesicular Transporters ◽  
Chemical Synapses

AbstractAt chemical synapses, neurotransmitters are packaged into synaptic vesicles that release their contents in response to depolarization. Despite its central role in synaptic function, regulation of the machinery that loads vesicles with neurotransmitters remains poorly understood. We find that synaptic glutamate signaling in a C. elegans chemosensory circuit is regulated by antagonistic interactions between the canonical vesicular glutamate transporter EAT-4/VGLUT and another vesicular transporter, VST-1. Loss of VST-1 strongly potentiates glutamate release from chemosensory BAG neurons and disrupts chemotaxis behavior. Analysis of the circuitry downstream of BAG neurons shows that excess glutamate release disrupts behavior by inappropriately recruiting RIA interneurons to the BAG-associated chemotaxis circuit. Our data indicate that in vivo the strength of glutamatergic synapses is controlled by regulation of neurotransmitter packaging into synaptic vesicles via functional coupling of VGLUT and VST-1.

scholarly journals The dominant functional nicotinic receptor in progenitor cells in the rostral migratory stream is the α3β4 subtype

2013 ◽  
Vol 109 (3) ◽  
pp. 867-872 ◽  
Author(s):  
Geeta Sharma
Keyword(s):  
Olfactory Bulb ◽  
Perceptual Learning ◽  
Progenitor Cells ◽  
Glutamate Release ◽  
Brain Regions ◽  
Odor Discrimination ◽  
Rostral Migratory Stream ◽  
Receptor Expression ◽  
Granule Cell Layer ◽  
Migratory Stream

Addition of newly generated neurons into mature neural circuits in the adult CNS responds to changes in neurotransmitter levels and is tightly coupled to the activity of specific brain regions. This postnatal neurogenesis contributes to plasticity of the olfactory bulb and hippocampus and is thought to play a role in learning and memory, context and odor discrimination, as well as perceptual learning. While acetylcholine plays an important role in odor discrimination and perceptual learning, its role in adult neurogenesis in the olfactory bulb has not been elucidated. In this study, I have examined the functional expression of nAChRs in progenitor cells of the rostral migratory stream (RMS) in the adult olfactory bulb of mice. I show that most of these cells in the RMS exhibit large nAChR-mediated calcium transients upon application of acetylcholine (ACh). Unlike in the hippocampus, the predominant functional nAChRs on progenitor cells are of α3β4 subtype. Interestingly, functional receptor expression is lost once progenitor cells mature, and are incorporated into the granule cell layer. Instead, nAChRs are now expressed on some presynaptic terminals and modulate glutamate release onto granule cells. My results imply that ACh is a part of the permissive niche and likely plays a role in development of progenitor cells.

Arterial chemoreceptor input to respiratory hypoglossal motoneurons

1990 ◽  
Vol 69 (2) ◽  
pp. 700-709 ◽  
Author(s):  
S. W. Mifflin
Keyword(s):  
Membrane Potential ◽  
Upper Airway ◽  
Excitatory Input ◽  
Airway Patency ◽  
Hypoglossal Motoneurons ◽  
End Tidal ◽  
Carotid Body Chemoreceptors ◽  
Excitatory Drive ◽  
Arterial Chemoreceptor

To better understand the role of the arterial chemoreceptors in the regulation of upper airway patency at the level of the oropharynx, intracellular recordings were obtained from inspiratory hypoglossal motoneurons (IHMs), and the responses to selective activation of the carotid body chemoreceptors were examined. In pentobarbital-anesthetized, vagotomized, paralyzed, and artificially ventilated cats, chemoreceptor activation enhanced the inspiratory depolarization of membrane potential in 32 of 36 IHMs. This was manifested as an increase in either the amplitude (n = 13) or duration (n = 3) or an increase in both amplitude and duration (n = 16) of the inspiratory membrane potential depolarization. The amplitude and duration of the inspiratory membrane potential depolarization increased 98 +/- 15% (n = 29) and 78 +/- 13% (n = 19), respectively. Similar patterns of enhanced activity (increased duration and/or amplitude of membrane depolarization) were observed in five expiratory hypoglossal motoneurons (EHMs) after chemoreceptor activation. In 16 of the 32 IHMs, chemoreceptor activation also evoked changes in IHM membrane potential during expiration: enhanced post-inspiratory discharge (n = 6), expiratory depolarization/discharge (n = 6), and tonic depolarization/discharge, which persisted for several respiratory cycles (n = 4). The arterial chemoreceptors provide a powerful excitatory input to IHMs during both inspiration and expiration. This excitatory drive to IHMs and EHMs will aid in the maintenance of upper airway patency throughout the respiratory cycle during increases in end-tidal CO2.

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