External Tufted Cells: A Major Excitatory Element That Coordinates Glomerular Activity

Hayar, Abdallah; Karnup, Sergei; Ennis, Matthew; Shipley, Michael T.

doi:10.1523/jneurosci.1367-04.2004

Cited by 217 publications

(379 citation statements)

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“…Most of the spontaneous EPSCs in PG and SA cells occur in bursts and our previous results (Hayar et al 2004a) suggest that they originate at least in part from action potentialdependent propagation in ET cell dendrites. To test whether GABA B -Rs modulate ET-to-(PG or SA) cell dendrodendritic transmission, we first recorded spontaneous bursts of EPSCs in PG or SA cells (which responded disynaptically to olfactory nerve stimulation by a relatively long and variable latency; Hayar et al 2004a) in voltage-clamp mode at HP = −60 mV without addition of any blocker (Fig. 4).…”

Section: Baclofen Inhibits Spontaneous and Evoked Epscs In Jg Cellssupporting

confidence: 50%

“…To assess the postsynaptic effect of baclofen, we recorded ET cells in the presence of blockers of fast synaptic transmission, which included the non-N-methyl-D-aspartate (NMDA) receptor antagonist CNQX (10 μM), the NMDA receptor antagonist APV (50 μM), and the GABA A receptor antagonist gabazine (10 μM), which are referred to here as fast synaptic blockers. Under these conditions, any effect observed would most likely be attributable to direct activation of GABA B -Rs located on ET cells since the major synaptic inputs to ET cells have been blocked (Hayar and Ennis 2007;Hayar et al 2004aHayar et al ,b, 2005. ET cells can be readily identified in extracellular recordings because they exhibit spontaneous bursting that persists in the presence of synaptic blockers (Hayar and Ennis 2007;Hayar et al 2004aHayar et al ,b, 2005.…”

Section: Baclofen Modulates Spontaneous Bursting Of Et Cellsmentioning

confidence: 99%

“…Under these conditions, any effect observed would most likely be attributable to direct activation of GABA B -Rs located on ET cells since the major synaptic inputs to ET cells have been blocked (Hayar and Ennis 2007;Hayar et al 2004aHayar et al ,b, 2005. ET cells can be readily identified in extracellular recordings because they exhibit spontaneous bursting that persists in the presence of synaptic blockers (Hayar and Ennis 2007;Hayar et al 2004aHayar et al ,b, 2005. Other cells that stopped bursting during drug application were excluded from the analysis.…”

Section: Baclofen Modulates Spontaneous Bursting Of Et Cellsmentioning

confidence: 99%

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Activation of Postsynaptic GABA_BReceptors Modulates the Bursting Pattern and Synaptic Activity of Olfactory Bulb Juxtaglomerular Neurons

Karpuk

Hayar²

2008

Journal of Neurophysiology

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Olfactory bulb glomeruli are formed by a network of three major types of neurons collectively called juxtaglomerular (JG) cells, which include external tufted (ET), periglomerular (PG), and short axon (SA) cells. There is solid evidence that γ-aminobutyric acid (GABA) released from PG neurons presynaptically inhibits glutamate release from olfactory nerve terminals via activation of GABA B receptors (GABA B -Rs). However, it is still unclear whether ET cells have GABA B -Rs. We have investigated whether ET cells have functional postsynaptic GABA B -Rs using extracellular and whole cell recordings in olfactory bulb slices. In the presence of fast synaptic blockers (CNQX, APV, and gabazine), the GABA B -R agonist baclofen either completely inhibited the bursting or reduced the bursting frequency and increased the burst duration and the number of spikes/burst in ET cells. In the presence of fast synaptic blockers and tetrodotoxin, baclofen induced an outward current in ET cells, suggesting a direct postsynaptic effect. Baclofen reduced the frequency and amplitude of spontaneous EPSCs in PG and SA cells. In the presence of sodium and potassium channel blockers, baclofen reduced the frequency of miniature EPSCs, which were inhibited by the calcium channel blocker cadmium. All baclofen effects were reversed by application of the GABA B -R antagonist CGP55845. We suggest that activation of GABA B -Rs directly inhibits ET cell bursting and decreases excitatory dendrodendritic transmission from ET to PG and SA cells. Thus the postsynaptic GABA B -Rs on ET cells may play an important role in shaping the activation pattern of the glomeruli during olfactory coding.

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Section: Baclofen Inhibits Spontaneous and Evoked Epscs In Jg Cellssupporting

confidence: 50%

Section: Baclofen Modulates Spontaneous Bursting Of Et Cellsmentioning

confidence: 99%

Section: Baclofen Modulates Spontaneous Bursting Of Et Cellsmentioning

confidence: 99%

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Activation of Postsynaptic GABA_BReceptors Modulates the Bursting Pattern and Synaptic Activity of Olfactory Bulb Juxtaglomerular Neurons

Karpuk

Hayar²

2008

Journal of Neurophysiology

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“…Dendritic tufts of ET cells arborize extensively inside glomeruli, where they receive monosynaptic glutamatergic input from olfactory nerve terminals (Hayar et al, 2004a). In slices, ET cells exhibit spontaneous burst firing driven by a persistent sodium current.…”

Section: Nih-pa Author Manuscriptmentioning

confidence: 99%

“…Identification of ET cells was based on a combination of morphological and physiological criteria established in previous studies (Pinching and Powell, 1971;Aungst et al, 2003;Hayar et al, 2004a). The ET cells tend to be distributed along the lower half of the glomeruli and their somata have larger diameters than periglomerular cells.…”

Section: Olfactory Nerve Stimulation Activates a Polyamine-sensitive mentioning

confidence: 99%

Calcium permeable AMPA receptors and autoreceptors in external tufted cells of rat olfactory bulb

Lowe

2007

Neuroscience

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Glomeruli are functional units of the olfactory bulb responsible for early processing of odor information encoded by single olfactory receptor genes. Glomerular neural circuitry includes numerous external tufted (ET) cells whose rhythmic burst firing may mediate synchronization of bulbar activity with the inhalation cycle. Bursting is entrained by glutamatergic input from olfactory nerve terminals, so specific properties of ionotropic glutamate receptors on ET cells are likely to be important determinants of olfactory processing. Particularly intriguing is recent evidence that α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors of juxta-glomerular neurons may permeate calcium. This could provide a novel pathway for regulating ET cell signaling. We tested the hypothesis that ET cells express functional calcium-permeable AMPA receptors. In rat olfactory bulb slices, excitatory postsynaptic currents (EPSCs) in ET cells were evoked by olfactory nerve shock, and by uncaging glutamate. We found attenuation of AMPA/kainate EPSCs by 1-naphthyl acetyl-spermine (NAS), an open-channel blocker specific for calcium permeable AMPA receptors. Cyclothiazide strongly potentiated EPSCs, indicating a major contribution from AMPA receptors. The current-voltage (I-V) relation of uncaging EPSCs showed weak inward rectification which was lost after > ~ 10 min of whole-cell dialysis, and was absent in NAS. In kainatestimulated slices, Co 2+ ions permeated cells of the glomerular layer. Large AMPA EPSCs were accompanied by fluorescence signals in fluo-4 loaded cells, suggesting calcium permeation. Depolarizing pulses evoked slow tail currents with pharmacology consistent with involvement of calcium permeable AMPA autoreceptors. Tail currents were abolished by Cd 2+ and NBQX, and were sensitive to NAS block. Glutamate autoreceptors were confirmed by uncaging intracellular calcium to evoke a large inward current. Our results provide evidence that calcium permeable AMPA receptors reside on ET cells, and are divided into at least two functionally distinct pools -postsynaptic receptors at olfactory nerve synaptic terminals, and autoreceptors sensitive to glutamate released from dendrodendritic synapses. Keywordsglutamate; glomerulus; dendrite; uncaging; fluorescence; rectification Olfaction begins with the binding of odorants to olfactory receptors which transduce sensory input into action potentials in axons of the olfactory nerve. Axons of cells expressing the same receptor gene converge to stereotypic glomeruli in the superficial layer of the olfactory bulb, forming a topographic neural map of receptor activation (Mombaerts et al., 1996). The olfactory nerve terminals make direct excitatory synapses on dendrites of bulb output neurons, Address correspondence to: Dr. Graeme Lowe, Monell Chemical Senses Center, 3500 Market St, Philadelphia, PA 19104-3308, phone: 215-573-5110, fax: 215-898-2084, email: loweg@monell.org. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for ...

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Olfactory Bulb: Synaptic Organisation

Lowe

2013

Encyclopedia of Life Sciences

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Odour information is encoded by sensory neurons expressing a large family of ∼10 2 –10 3 distinct olfactory receptors, and is mapped to an equally numerous population of glomeruli in the olfactory bulb. Each glomerulus is a modular circuit composed of a variety of local interneurons and bulb output neurons that receive primary afferent signals encoded by a single olfactory receptor. Incoming signals are filtered by inhibition from periglomerular cells and amplified by mutual excitation of mitral and tufted cells. Odour codes are further transformed by lateral inhibition between glomeruli mediated by short axon and granule cells that communicate through specialised dendrodendritic reciprocal synapses. These network mechanisms interact with a diversity of cell biophysical properties to shape spiking patterns of bulb output neurons. Synaptic processing in the bulb is also dynamically regulated by feedback from olfactory cortex, centrifugal modulation from basal forebrain nuclei and plasticity of local circuits sustained by adult neurogenesis. Key Concepts: Odour information is mapped to discrete glomeruli in the olfactory bulb that receive sensory inputs encoded by different olfactory receptors. Sensory neuron terminals in glomeruli release the excitatory transmitter glutamate, under control of presynaptic inhibition by dopamine and GABA receptors. Glomeruli contain multiple excitatory and inhibitory circuits for coordinating odour‐evoked spike activity of bulb output neurons, the mitral and tufted cells. Most olfactory bulb circuits include dendrodendritic reciprocal synapses with closely linked glutamatergic excitatory and GABAergic inhibitory transmission. Mitral and tufted cell responses are triggered and amplified by dendrodendritic excitation of glomerular dendritic tufts, and are controlled by periglomerular cell inhibition. Glomeruli are connected by pervasive short‐ and long‐range networks of inhibitory superficial short axon cells. Granule cells form complex webs of lateral inhibitory connections between mitral and tufted cells of different glomeruli. Synaptic inhibition in the bulb is coordinated by networks of deep short axon cells that inhibit periglomerular and granule cells. Synaptic inhibition in the bulb is strongly influenced by centrifugal inputs from olfactory cortex and subcortical modulatory centres.

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External Tufted Cells: A Major Excitatory Element That Coordinates Glomerular Activity

Cited by 217 publications

References 54 publications

Activation of Postsynaptic GABA_BReceptors Modulates the Bursting Pattern and Synaptic Activity of Olfactory Bulb Juxtaglomerular Neurons

Activation of Postsynaptic GABA_BReceptors Modulates the Bursting Pattern and Synaptic Activity of Olfactory Bulb Juxtaglomerular Neurons

Calcium permeable AMPA receptors and autoreceptors in external tufted cells of rat olfactory bulb

Olfactory Bulb: Synaptic Organisation

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External Tufted Cells: A Major Excitatory Element That Coordinates Glomerular Activity

Cited by 217 publications

References 54 publications

Activation of Postsynaptic GABABReceptors Modulates the Bursting Pattern and Synaptic Activity of Olfactory Bulb Juxtaglomerular Neurons

Activation of Postsynaptic GABABReceptors Modulates the Bursting Pattern and Synaptic Activity of Olfactory Bulb Juxtaglomerular Neurons

Calcium permeable AMPA receptors and autoreceptors in external tufted cells of rat olfactory bulb

Olfactory Bulb: Synaptic Organisation

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Activation of Postsynaptic GABA_BReceptors Modulates the Bursting Pattern and Synaptic Activity of Olfactory Bulb Juxtaglomerular Neurons

Activation of Postsynaptic GABA_BReceptors Modulates the Bursting Pattern and Synaptic Activity of Olfactory Bulb Juxtaglomerular Neurons