scholarly journals Age-dependent adrenergic actions in the main olfactory bulb that could underlie an olfactory-sensitive period

2012 ◽  
Vol 108 (7) ◽  
pp. 1999-2007 ◽  
Author(s):  
Sruthi Pandipati ◽  
Nathan E. Schoppa
Keyword(s):  
Olfactory Bulb ◽  
Neural Plasticity ◽  
Granule Cells ◽  
Gamma Oscillations ◽  
Sensitive Period ◽  
Loss Of Function ◽  
Main Olfactory Bulb ◽  
Cellular Mechanisms ◽  
Gamma Frequency ◽  
Age Dependent

Many sensory systems are endowed with mechanisms of neural plasticity that are restricted to a sensitive period in the young developing animal. In this study, we performed experiments in slices of the main olfactory bulb (OB) from rats to examine possible age-dependent cellular mechanisms of plasticity in the olfactory system. We focused on the neurotransmitter norepinephrine (NE), shown to be important in different forms of olfactory learning, examining whether two specific cellular effects of NE previously observed in rats less than P14 extended to older animals. These included an acute reduction in GABAergic synaptic transmission from granule cells (GCs) onto output mitral cells (MCs) and an enhancement in gamma frequency (30–70 Hz) oscillations that persists long after removal of NE. We found that NE failed to reduce GC-to-MC transmission or enhance gamma oscillations in older rats at P18–23. The loss of NE actions on both phenomena appeared to reflect an age-dependent loss of function of α2-adrenergic receptors. In addition, we found that NE induced an age-dependent enhancement of transient excitation in MCs, providing a mechanism to link the acute decrease in GC-to-MC inhibition to the long-term increase in gamma oscillations through increases in intracellular calcium. The age-dependent cellular mechanisms that we describe could underlie an olfactory-sensitive period in newborn rodents.

scholarly journals Granule cell excitability regulates gamma and beta oscillations in a model of the olfactory bulb dendrodendritic microcircuit

2016 ◽  
Vol 116 (2) ◽  
pp. 522-539 ◽  
Author(s):  
Bolesław L. Osinski ◽  
Leslie M. Kay
Keyword(s):  
Olfactory Bulb ◽  
Granule Cells ◽  
Field Potential ◽  
Gamma Oscillations ◽  
Causal Link ◽  
Beta Oscillations ◽  
Gamma Frequency ◽  
Voltage Dependent ◽  
Nmda Channels ◽  
Beta Frequency

Odors evoke gamma (40–100 Hz) and beta (20–30 Hz) oscillations in the local field potential (LFP) of the mammalian olfactory bulb (OB). Gamma (and possibly beta) oscillations arise from interactions in the dendrodendritic microcircuit between excitatory mitral cells (MCs) and inhibitory granule cells (GCs). When cortical descending inputs to the OB are blocked, beta oscillations are extinguished whereas gamma oscillations become larger. Much of this centrifugal input targets inhibitory interneurons in the GC layer and regulates the excitability of GCs, which suggests a causal link between the emergence of beta oscillations and GC excitability. We investigate the effect that GC excitability has on network oscillations in a computational model of the MC-GC dendrodendritic network with Ca2+-dependent graded inhibition. Results from our model suggest that when GC excitability is low, the graded inhibitory current mediated by NMDA channels and voltage-dependent Ca2+ channels (VDCCs) is also low, allowing MC populations to fire in the gamma frequency range. When GC excitability is increased, the activation of NMDA receptors and other VDCCs is also increased, allowing the slow decay time constants of these channels to sustain beta-frequency oscillations. Our model argues that Ca2+ flow through VDCCs alone could sustain beta oscillations and that the switch between gamma and beta oscillations can be triggered by an increase in the excitability state of a subpopulation of GCs.

scholarly journals Adrenergic Receptor-Mediated Disinhibition of Mitral Cells Triggers Long-Term Enhancement of Synchronized Oscillations in the Olfactory Bulb

2010 ◽  
Vol 104 (2) ◽  
pp. 665-674 ◽  
Author(s):  
Sruthi Pandipati ◽  
David H. Gire ◽  
Nathan E. Schoppa
Keyword(s):  
Olfactory Bulb ◽  
Granule Cells ◽  
Gamma Oscillations ◽  
Olfactory Learning ◽  
Inhibitory Synapses ◽  
Mitral Cells ◽  
Acute Effects ◽  
Long Term Effects ◽  
Gamma Frequency

Norepinephrine (NE) is widely implicated in various forms of associative olfactory learning in rodents, including early learning preference in neonates. Here we used patch-clamp recordings in rat olfactory bulb slices to assess cellular actions of NE, examining both acute, short-term effects of NE as well as the relationship between these acute effects and long-term cellular changes that could underlie learning. Our focus for long-term effects was on synchronized gamma frequency (30–70 Hz) oscillations, shown in prior studies to be enhanced for up to an hour after brief exposure of a bulb slice to NE and neuronal stimulation. In terms of acute effects, we found that a dominant action of NE was to reduce inhibitory GABAergic transmission from granule cells (GCs) to output mitral cells (MCs). This disinhibition was also induced by clonidine, an agonist specific for α2 adrenergic receptors (ARs). Acute NE-induced disinhibition of MCs appeared to be linked to long-term enhancement of gamma oscillations, based, first, on the fact that clonidine, but not agonists specific for other AR subtypes, mimicked NE's long-term actions. In addition, the α2 AR-specific antagonist yohimbine blocked the long-term enhancement of the oscillations due to NE. Last, brief exposure of the slice to the GABAA receptor antagonist gabazine, to block inhibitory synapses directly, also induced the long-term changes. Acute disinhibition is a plausible permissive effect of NE leading to olfactory learning, because, when combined with exposure to a specific odor, it should lead to neuron-specific increases in intracellular calcium of the type generally associated with long-term synaptic modifications.

scholarly journals Transient Activity Induces a Long-Lasting Increase in the Excitability of Olfactory Bulb Interneurons

2008 ◽  
Vol 99 (1) ◽  
pp. 187-199 ◽  
Author(s):  
Tsuyoshi Inoue ◽  
Ben W. Strowbridge
Keyword(s):  
Olfactory Bulb ◽  
Granule Cells ◽  
Receptor Activation ◽  
Brain Regions ◽  
Persistent Activity ◽  
Cellular Mechanisms ◽  
Calcium Dependent ◽  
Transient Activity ◽  
Olfactory Bulb Slices ◽  
Processing And Storage

Little is known about the cellular mechanisms that underlie the processing and storage of sensory in the mammalian olfactory system. Here we show that persistent spiking, an activity pattern associated with working memory in other brain regions, can be evoked in the olfactory bulb by stimuli that mimic physiological patterns of synaptic input. We find that brief discharges trigger persistent activity in individual interneurons that receive slow, subthreshold oscillatory input in acute rat olfactory bulb slices. A 2- to 5-Hz oscillatory input, which resembles the synaptic drive that the olfactory bulb receives during sniffing, is required to maintain persistent firing. Persistent activity depends on muscarinic receptor activation and results from interactions between calcium-dependent afterdepolarizations and low-threshold Ca spikes in granule cells. Computer simulations suggest that intrinsically generated persistent activity in granule cells can evoke correlated spiking in reciprocally connected mitral cells. The interaction between the intrinsic currents present in reciprocally connected olfactory bulb neurons constitutes a novel mechanism for synchronized firing in subpopulations of neurons during olfactory processing.

Presynaptic Muscarinic Receptors Enhance Glutamate Release at the Mitral/Tufted to Granule Cell Dendrodendritic Synapse in the Rat Main Olfactory Bulb

2009 ◽  
Vol 101 (4) ◽  
pp. 2052-2061 ◽  
Author(s):  
Ambarish S. Ghatpande ◽  
Alan Gelperin
Keyword(s):  
Olfactory Bulb ◽  
Granule Cell ◽  
Basal Forebrain ◽  
Granule Cells ◽  
Calcium Influx ◽  
Glutamate Release ◽  
Gaba Release ◽  
Cellular Mechanisms ◽  
Tufted Cells

The mammalian olfactory bulb receives multiple modulatory inputs, including a cholinergic input from the basal forebrain. Understanding the functional roles played by the cholinergic input requires an understanding of the cellular mechanisms it modulates. In an in vitro olfactory bulb slice preparation we demonstrate cholinergic muscarinic modulation of glutamate release onto granule cells that results in γ-aminobutyric acid (GABA) release onto mitral/tufted cells. We demonstrate that the broad-spectrum cholinergic agonist carbachol triggers glutamate release from mitral/tufted cells that activates both AMPA and NMDA receptors on granule cells. Activation of the granule cell glutamate receptors leads to calcium influx through voltage-gated calcium channels, resulting in spike-independent, asynchronous GABA release at reciprocal dendrodendritic synapses that granule cells form with mitral/tufted cells. This cholinergic modulation of glutamate release persists through much of postnatal bulbar development, suggesting a functional role for cholinergic inputs from the basal forebrain in bulbar processing of olfactory inputs and possibly in postnatal development of the olfactory bulb.

scholarly journals Paradoxically sparse chemosensory tuning in broadly-integrating external granule cells in the mouse accessory olfactory bulb

2019 ◽  
Author(s):  
Xingjian Zhang ◽  
Julian P. Meeks
Keyword(s):  
Patch Clamp ◽  
Olfactory Bulb ◽  
Olfactory System ◽  
Granule Cells ◽  
Ex Vivo ◽  
Accessory Olfactory Bulb ◽  
Main Olfactory Bulb ◽  
Patch Clamp Electrophysiology ◽  
Accessory Olfactory System ◽  
Critical Circuit

AbstractThe accessory olfactory bulb (AOB) is a critical circuit in the mouse accessory olfactory system (AOS), but AOB processing is poorly understood compared to the main olfactory bulb (MOB). We used 2-photon GCaMP6f Ca2+ imaging in an ex vivo preparation to study the chemosensory tuning of AOB external granule cells (EGCs), an interneuron population hypothesized to broadly integrate from mitral cells (MCs). We measured MC and EGC tuning to natural chemosignal blends and monomolecular ligands, finding that EGC tuning was far sparser than MC tuning. Simultaneous patch-clamp electrophysiology and Ca2+ imaging indicated that this was only partially explained by lower GCaMP6f-to-spiking ratios in EGCs compared to MCs. Ex vivo patch-clamp recordings revealed that EGC subthreshold responsivity was broad, but monomolecular ligand responses were insufficient to elicit spiking. These results indicate that EGC spiking is selectively engaged by chemosensory blends, suggesting different roles for EGCs than analogous interneurons in the MOB.

Dopaminergic neuromodulation of synaptic transmission between mitral and granule cells in the teleost olfactory bulb

2012 ◽  
Vol 107 (5) ◽  
pp. 1313-1324 ◽  
Author(s):  
Takafumi Kawai ◽  
Hideki Abe ◽  
Yoshitaka Oka
Keyword(s):  
Olfactory Bulb ◽  
Synaptic Transmission ◽  
Granule Cells ◽  
Glutamate Release ◽  
Field Potential ◽  
Olfactory Nerve ◽  
Oscillatory Activity ◽  
Cellular Mechanisms ◽  
Olfactory Information

A growing body of evidence suggests that teleosts are important models for the study of neural processing of olfactory information, and the functional role of dopamine (DA), which is a potent neuromodulator endogenous to the mammalian olfactory bulb, has been one of the strongest focuses in this field. However, the cellular mechanisms of dopaminergic neuromodulation in olfactory bulbar neural circuits have not been fully understood. We investigated such mechanisms by using the goldfish, which offers several advantages for analyzing olfactory information processing by electrophysiological methods. First, we found in the olfactory bulb that numerous cell bodies of the dopaminergic neurons are mainly distributed in the mitral cell layer and extend fine processes to the glomerular layer. Next, we made in vitro field potential recordings and showed that synaptic transmissions from mitral to granule cells were suppressed by DA application. DA also increased the paired-pulse ratio, suggesting that the suppression of synaptic transmission is caused by a decrease in presynaptic glutamate release from the mitral cells. Furthermore, DA significantly suppressed the oscillatory activity of the olfactory bulb in response to olfactory stimuli. Although DA suppresses the synaptic inputs from the olfactory nerve to the olfactory bulbar neurons in mammals, this phenomenon was not observed in the goldfish. These findings indicate that suppression of the mitral to granule cell synaptic transmission in the reciprocal synapses plays an important role in the negative regulation of olfactory responsiveness in the goldfish olfactory bulb.

scholarly journals α-Synuclein aggregation in the olfactory bulb induces olfactory deficits by perturbing granule cells and granular–mitral synaptic transmission

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Fengjiao Chen ◽  
Wei Liu ◽  
Penglai Liu ◽  
Zhen Wang ◽  
You Zhou ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
Neural Circuit ◽  
Granule Cells ◽  
Gamma Oscillations ◽  
Olfactory Dysfunction ◽  
Synaptic Function ◽  
Neural Mechanisms ◽  
Motor Symptom ◽  
High Gamma

AbstractOlfactory dysfunction is an early pre-motor symptom of Parkinson’s disease (PD) but the neural mechanisms underlying this dysfunction remain largely unknown. Aggregation of α-synuclein is observed in the olfactory bulb (OB) during the early stages of PD, indicating a relationship between α-synuclein pathology and hyposmia. Here we investigate whether and how α-synuclein aggregates modulate neural activity in the OB at the single-cell and synaptic levels. We induced α-synuclein aggregation specifically in the OB via overexpression of double-mutant human α-synuclein by an adeno-associated viral (AAV) vector. We found that α-synuclein aggregation in the OB decreased the ability of mice to detect odors and to perceive attractive odors. The spontaneous activity and odor-evoked firing rates of single mitral/tufted cells (M/Ts) were increased by α-synuclein aggregates with the amplitude of odor-evoked high-gamma oscillations increased. Furthermore, the decreased activity in granule cells (GCs) and impaired inhibitory synaptic function were responsible for the observed hyperactivity of M/Ts induced by α-synuclein aggregates. These results provide direct evidences of the role of α-synuclein aggregates on PD-related olfactory dysfunction and reveal the neural circuit mechanisms by which olfaction is modulated by α-synuclein pathology.

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