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Michael T. Shipley - One of the best experts on this subject based on the ideXlab platform.
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two gabaergic intraglomerular circuits differentially regulate tonic and phasic presynaptic inhibition of Olfactory Nerve terminals
Journal of Neurophysiology, 2009Co-Authors: Zuoyi Shao, Adam C Puche, Emi Kiyokage, Gabor Szabo, Michael T. ShipleyAbstract:Olfactory Nerve axons terminate in Olfactory bulb glomeruli forming excitatory synapses onto the dendrites of mitral/tufted (M/T) and juxtaglomerular cells, including external tufted (ET) and periglomerular (PG) cells. PG cells are heterogeneous in neurochemical expression and synaptic organization. We used a line of mice expressing green fluorescent protein under the control of the glutamic acid decarboxylase 65-kDa gene (GAD65+) promoter to characterize a neurochemically identified subpopulation of PG cells by whole cell recording and subsequent morphological reconstruction. GAD65+ GABAergic PG cells form two functionally distinct populations: 33% are driven by monosynaptic Olfactory Nerve (ON) input (ON-driven PG cells), the remaining 67% receive their strongest drive from an ON→ET→PG circuit with no or weak monosynaptic ON input (ET-driven PG cells). In response to ON stimulation, ON-driven PG cells exhibit paired-pulse depression (PPD), which is partially reversed by GABAB receptor antagonists. The ON→ET→PG circuit exhibits phasic GABAB-R-independent PPD. ON input to both circuits is under tonic GABAB-R-dependent inhibition. We hypothesize that this tonic GABABR-dependent presynaptic inhibition of Olfactory Nerve terminals is due to autonomous bursting of ET cells in the ON→ET→PG circuit, which drives tonic spontaneous GABA release from ET-driven PG cells. Both circuits likely produce tonic and phasic postsynaptic inhibition of other intraglomerular targets. Thus Olfactory bulb glomeruli contain at least two functionally distinct GABAergic circuits that may play different roles in Olfactory coding.
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Evidence for GABAB-mediated inhibition of transmission from the Olfactory Nerve to mitral cells in the rat Olfactory bulb.
Brain Research Bulletin, 2003Co-Authors: W. T. Nickell, Michael M. Behbehani, Michael T. ShipleyAbstract:The GABAB agonist baclofen blocks transmission from the Olfactory Nerve to second order neurons in the frog Olfactory bulb, and GABAB receptors in the rat Olfactory bulb are selectively located in the glomerular layer. A reasonable hypothesis, therefore, is that inhibition in the glomerular layer is mediated, at least in part, by GABAB receptors. Here, we investigated the role of GABAB receptors in regulating the responses of mitral cells to activation of the Olfactory Nerve in the rat. Topical application of baclofen to the surface of the rat Olfactory bulb reduced the amplitude of field potentials evoked by Olfactory Nerve stimulation (orthodromic response). Baclofen reduced the orthodromic response in a dose-dependent manner but the drug had no effect on the field potential evoked by antidromic activation of mitral cell axons (antidromic response). Baclofen also reduced Olfactory Nerve-evoked responses of mitral cells in an Olfactory bulb slice preparation. The pharmacological specificity of the inhibition was confirmed by showing that the GABAB antagonist, CGP 55845A, blocked the inhibitory action of baclofen. These results suggest that transmission from Olfactory Nerve terminals to second order neurons is negatively regulated by periglomerular GABAergic interneurons; this inhibition is mediated, at least partially, by GABAB receptors.
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dopamine d2 receptor mediated presynaptic inhibition of Olfactory Nerve terminals
Journal of Neurophysiology, 2001Co-Authors: Matthew Ennis, Lee A. Zimmer, Fuming Zhou, Kelly J Ciombor, Vassiliki Aroniadouanderjaska, Abdallah Hayar, Emiliana Borrelli, Frank L Margolis, Michael T. ShipleyAbstract:Olfactory receptor neurons of the nasal epithelium project via the Olfactory Nerve (ON) to the glomeruli of the main Olfactory bulb, where they form glutamatergic synapses with the apical dendrites...
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norepinephrine increases rat mitral cell excitatory responses to weak Olfactory Nerve input via alpha 1 receptors in vitro
Neuroscience, 1999Co-Authors: Kelly J Ciombor, Matthew Ennis, Michael T. ShipleyAbstract:A rat Olfactory bulb in vitro slice preparation was used to investigate the actions of norepinephrine on spontaneous and afferent (Olfactory Nerve) evoked activity of mitral cells. Single Olfactory Nerve shocks elicited a characteristic mitral cell response consisting of distinct, early and late spiking components separated by a brief inhibitory epoch. Bath-applied norepinephrine (1 μM) increased the early spiking component elicited by perithreshold (79% increase, P 0.05), intensity Olfactory Nerve shocks. The facilitatory effect of norepinephrine was due to a reduction in the incidence of response failures to perithreshold intensity shocks. Norepinephrine also decreased the inhibitory epoch separating the early and late spiking components by 44% (P<0.05). By contrast, norepinephrine had no consistent effect on the spontaneous discharge rate of the mitral cells. The effects of norepinephrine were mimicked by the α1 receptor agonist phenylephrine (1 μM, P<0.001). Both norepinephrine and phenylephrine modulation of mitral cell responses were blocked by the α1 adrenergic antagonist WB-4101 (1 μM). These findings are consistent with observations that the main Olfactory bulb exhibits the highest density of α1 receptors in the brain. The α2 receptor agonist clonidine (100 nM) and the β receptor agonist isoproterenol (1 μM) had inconsistent effects on mitral cell spontaneous and Olfactory Nerve-evoked activity. These results indicate that norepinephrine increases mitral cell excitatory responses to weak but not strong Olfactory Nerve inputs in vitro via activation of α1 receptors. This is consistent with recent findings in vivo that synaptically released norepinephrine preferentially increases mitral cell excitatory responses to weak Olfactory Nerve inputs. Taken together, these results suggest that the release of norepinephrine in the Olfactory bulb may increase the sensitivity of mitral cells to weak odors. Olfactory cues evoke norepinephrine release in the main Olfactory bulb, and norepinephrine plays important roles in early Olfactory learning and reproductive/maternal behaviors. By increasing mitral cell responses to Olfactory Nerve input, norepinephrine may play a critical role in modulating Olfactory function, including formation and/or recall of specific Olfactory memories.
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Norepinephrine increases rat mitral cell excitatory responses to weak Olfactory Nerve input via alpha-1 receptors in vitro
Neuroscience, 1999Co-Authors: Kelly J Ciombor, Matthew Ennis, Michael T. ShipleyAbstract:A rat Olfactory bulb in vitro slice preparation was used to investigate the actions of norepinephrine on spontaneous and afferent (Olfactory Nerve) evoked activity of mitral cells. Single Olfactory Nerve shocks elicited a characteristic mitral cell response consisting of distinct, early and late spiking components separated by a brief inhibitory epoch. Bath-applied norepinephrine (1 μM) increased the early spiking component elicited by perithreshold (79% increase, P 0.05), intensity Olfactory Nerve shocks. The facilitatory effect of norepinephrine was due to a reduction in the incidence of response failures to perithreshold intensity shocks. Norepinephrine also decreased the inhibitory epoch separating the early and late spiking components by 44% (P
Takaki Miwa - One of the best experts on this subject based on the ideXlab platform.
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prognostic value of Olfactory Nerve damage measured with thallium based Olfactory imaging in patients with idiopathic Olfactory dysfunction
Scientific Reports, 2017Co-Authors: Hideaki Shiga, Junichi Taki, Koichi Okuda, Naoto Watanabe, Hisao Tonami, Hideaki Nakagawa, Seigo Kinuya, Takaki MiwaAbstract:Idiopathic Olfactory disorder is resistant to treatment, and the recovery time is long. This study investigated the prognostic value of the migration of nasally administered thallium-201 to the Olfactory bulb (thallium migration to the OB), a measure of Olfactory Nerve damage, in patients with idiopathic Olfactory disorders. Twenty-four patients with idiopathic Olfactory disorders were enrolled in the study (7 women and 17 men; aged 23–73 years). We retrospectively analyzed potential prognostic markers in subjects who underwent thallium-based Olfactory imaging with the nasal administration of thallium-201 before conventional treatment with the Japanese herbal medicine tokishakuyakusan and compared those data with the prognosis. Log-rank tests were performed to assess the relationship between thallium migration to the OB (<4.6% [low] vs. ≥4.6% [high]; data dichotomized at the optimal cutoff value) and the duration until recovery of the odor recognition threshold determined by a standard Olfactory function test (T&T olfactometry) after the treatment. Upon statistical analysis, we found that high thallium migration to the OB was significantly correlated with better prognosis in patients. Our results suggest that patients with intact Olfactory Nerve fibers could be selected using thallium-based imaging for the long-term follow-up of Olfactory dysfunction.
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Clinical diagnosis of the Olfactory Nerve transport function
Yakugaku Zasshi-journal of The Pharmaceutical Society of Japan, 2012Co-Authors: Hideaki Shiga, Junpei Yamamoto, Takaki MiwaAbstract:Nasal administration of macromolecular drugs (peptides, nanoparticles) has a possibility to enable a drug delivery system beyond the blood brain barrier via Olfactory Nerve transport. Basic research on nasal drug delivery to the brain has been well studied. However, evaluation of the Olfactory Nerve transport function in patients with Olfactory disorders has yet to be done, although such an evaluation is important in selecting candidates for clinical trials. Current Olfactory function tests are useful for the analysis of Olfactory thresholds in olfaction-impaired patients. However, the usefulness of using the increase in Olfactory thresholds in patients as an index for evaluating Olfactory Nerve damage has not been confirmed because of the difficulty in directly evaluating the viability of the peripheral Olfactory Nerves. Nasally administered thallium-201 migrates to the Olfactory bulb, as has been shown in healthy volunteers. Furthermore, transection of Olfactory Nerve fibers in mice significantly decreases migration of nasally administered thallium-201 to the Olfactory bulb. The migration of thallium-201 to the Olfactory bulb is reduced in patients with impaired olfaction due to head trauma, upper respiratory tract infections, and chronic rhinosinusitis, relative to the values in healthy volunteers. Nasally administrating thallium-201 followed by single photon emission computed tomography, X-ray computed tomography and magnetic resonance imaging might be useful in choosing candidates for clinical trials of nasal drug delivery methods to the brain.
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Use of thallium transport to visualize functional Olfactory Nerve regeneration in vivo
Rhinology, 2009Co-Authors: Hideaki Shiga, Ryohei Amano, Kohshin Washiyama, Mitsuru Furukawa, Kyoko Hirota, Takaki MiwaAbstract:Objective: To image Olfactory Nerve regeneration in vivo using a high-resolution gamma camera and radiography after nasal administration of thallium-201 (olfacto-scintigraphy). Methods: Six Wistar rats were trained to avoid the smell of cycloheximide as a test of Olfactory function. The Olfactory Nerve fibers of 3 rats were then carefully transected bilaterally with a Teflon knife, avoiding damage to the Olfactory bulbs. The remaining 3 rats underwent sham operations and were used as controls. Steel wires were implanted in the left Olfactory bulb of each rat for locating the bulbs with plain X-rays. The rats were assessed 2, 14, 28, and 42 d after the Olfactory Nerve transection or sham operation for their ability to detect odours and for transport of 201 Tl to the Olfactory bulb area 8 h after nasal administration of 201 Tl. Results: Both transport of 201 Tl to the Olfactory bulb area (p < 0.04) and ability to detect odours (p < 0.04) significantly increased with a time course after Olfactory Nerve transection. Conclusion: 201 Tl transport to the Olfactory bulb may be useful to visually assess Olfactory ability in vivo. We plan to test olfacto-scintigraphy clinically by nasal administration of 201 Tl in patients with posttraumatic Olfactory loss.
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Odor Detection Ability and Thallium-201 Transport in the Olfactory Nerve of Traumatic Olfactory-Impaired Mice
Chemical Senses, 2008Co-Authors: Hideaki Shiga, Yayoi Kinoshita, Toshiaki Tsukatani, Ryohei Amano, Daisuke Ogawa, Kohshin Washiyama, Mitsuru Furukawa, Kyoko Hirota, Takaki MiwaAbstract:Although Olfactory Nerve damage is a contributing factor in the diagnosis of posttraumatic Olfactory loss, at present, there are no methods to directly assess injury to these Nerves. We have shown that following Olfactory Nerve injury in mice, thallium-201 ( 201 Tl) transport from the nasal cavity to the Olfactory bulb decreases. To determine if Olfactory function after Nerve injury could be assessed with nasal administration of 201 Tl, we measured the correlation between odor detection ability (ODA) and the rate of transport of 201 Tl in Olfactory Nerves. Both ODA and 201 Tl transport were measured after bilateral Olfactory Nerve transection for a 4-week period. Cycloheximide solution was used for ODA against tap water. 201 Tl transport was measured as the ratio of radioactivity in the nasal cavity and Olfactory bulb with gamma spectrometry. There was a significant correlation between ODA and the rate of 201 Tl transport in the Olfactory Nerve. These findings suggest that Olfactory function after Nerve injury can be objectively evaluated with the nasal administration of 201 Tl.
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Thallium Transport and the Evaluation of Olfactory Nerve Connectivity between the Nasal Cavity and Olfactory Bulb
Chemical Senses, 2007Co-Authors: Yayoi Kinoshita, Toshiaki Tsukatani, Ryohei Amano, Daisuke Ogawa, Hideaki Shiga, Kohshin Washiyama, Mitsuru Furukawa, Takaki MiwaAbstract:Little is known regarding how alkali metal ions are transported in the Olfactory Nerve following their intranasal administration. In this study, we show that an alkali metal ion, thallium is transported in the Olfactory Nerve fibers to the Olfactory bulb in mice. The Olfactory Nerve fibers of mice were transected on both sides of the body under anesthesia. A double tracer solution (thallium-201, (201)Tl; manganese-54, (54)Mn) was administered into the nasal cavity the following day. Radioactivity in the Olfactory bulb and nasal turbinate was analyzed with gamma spectrometry. Auto radiographic images were obtained from coronal slices of frozen heads of mice administered with (201)Tl or (54)Mn. The transection of the Olfactory Nerve fibers was confirmed with a neuronal tracer. The transport of intranasal administered (201)Tl/(54)Mn to the Olfactory bulb was significantly reduced by the transection of Olfactory Nerve fibers. The Olfactory Nerve transection also significantly inhibited the accumulation of fluoro-ruby in the Olfactory bulb. Findings indicate that thallium is transported by the Olfactory Nerve fibers to the Olfactory bulb in mice. The assessment of thallium transport following head injury may provide a new diagnostic method for the evaluation of Olfactory Nerve injury.
Hideaki Shiga - One of the best experts on this subject based on the ideXlab platform.
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prognostic value of Olfactory Nerve damage measured with thallium based Olfactory imaging in patients with idiopathic Olfactory dysfunction
Scientific Reports, 2017Co-Authors: Hideaki Shiga, Junichi Taki, Koichi Okuda, Naoto Watanabe, Hisao Tonami, Hideaki Nakagawa, Seigo Kinuya, Takaki MiwaAbstract:Idiopathic Olfactory disorder is resistant to treatment, and the recovery time is long. This study investigated the prognostic value of the migration of nasally administered thallium-201 to the Olfactory bulb (thallium migration to the OB), a measure of Olfactory Nerve damage, in patients with idiopathic Olfactory disorders. Twenty-four patients with idiopathic Olfactory disorders were enrolled in the study (7 women and 17 men; aged 23–73 years). We retrospectively analyzed potential prognostic markers in subjects who underwent thallium-based Olfactory imaging with the nasal administration of thallium-201 before conventional treatment with the Japanese herbal medicine tokishakuyakusan and compared those data with the prognosis. Log-rank tests were performed to assess the relationship between thallium migration to the OB (<4.6% [low] vs. ≥4.6% [high]; data dichotomized at the optimal cutoff value) and the duration until recovery of the odor recognition threshold determined by a standard Olfactory function test (T&T olfactometry) after the treatment. Upon statistical analysis, we found that high thallium migration to the OB was significantly correlated with better prognosis in patients. Our results suggest that patients with intact Olfactory Nerve fibers could be selected using thallium-based imaging for the long-term follow-up of Olfactory dysfunction.
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Clinical diagnosis of the Olfactory Nerve transport function
Yakugaku Zasshi-journal of The Pharmaceutical Society of Japan, 2012Co-Authors: Hideaki Shiga, Junpei Yamamoto, Takaki MiwaAbstract:Nasal administration of macromolecular drugs (peptides, nanoparticles) has a possibility to enable a drug delivery system beyond the blood brain barrier via Olfactory Nerve transport. Basic research on nasal drug delivery to the brain has been well studied. However, evaluation of the Olfactory Nerve transport function in patients with Olfactory disorders has yet to be done, although such an evaluation is important in selecting candidates for clinical trials. Current Olfactory function tests are useful for the analysis of Olfactory thresholds in olfaction-impaired patients. However, the usefulness of using the increase in Olfactory thresholds in patients as an index for evaluating Olfactory Nerve damage has not been confirmed because of the difficulty in directly evaluating the viability of the peripheral Olfactory Nerves. Nasally administered thallium-201 migrates to the Olfactory bulb, as has been shown in healthy volunteers. Furthermore, transection of Olfactory Nerve fibers in mice significantly decreases migration of nasally administered thallium-201 to the Olfactory bulb. The migration of thallium-201 to the Olfactory bulb is reduced in patients with impaired olfaction due to head trauma, upper respiratory tract infections, and chronic rhinosinusitis, relative to the values in healthy volunteers. Nasally administrating thallium-201 followed by single photon emission computed tomography, X-ray computed tomography and magnetic resonance imaging might be useful in choosing candidates for clinical trials of nasal drug delivery methods to the brain.
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Use of thallium transport to visualize functional Olfactory Nerve regeneration in vivo
Rhinology, 2009Co-Authors: Hideaki Shiga, Ryohei Amano, Kohshin Washiyama, Mitsuru Furukawa, Kyoko Hirota, Takaki MiwaAbstract:Objective: To image Olfactory Nerve regeneration in vivo using a high-resolution gamma camera and radiography after nasal administration of thallium-201 (olfacto-scintigraphy). Methods: Six Wistar rats were trained to avoid the smell of cycloheximide as a test of Olfactory function. The Olfactory Nerve fibers of 3 rats were then carefully transected bilaterally with a Teflon knife, avoiding damage to the Olfactory bulbs. The remaining 3 rats underwent sham operations and were used as controls. Steel wires were implanted in the left Olfactory bulb of each rat for locating the bulbs with plain X-rays. The rats were assessed 2, 14, 28, and 42 d after the Olfactory Nerve transection or sham operation for their ability to detect odours and for transport of 201 Tl to the Olfactory bulb area 8 h after nasal administration of 201 Tl. Results: Both transport of 201 Tl to the Olfactory bulb area (p < 0.04) and ability to detect odours (p < 0.04) significantly increased with a time course after Olfactory Nerve transection. Conclusion: 201 Tl transport to the Olfactory bulb may be useful to visually assess Olfactory ability in vivo. We plan to test olfacto-scintigraphy clinically by nasal administration of 201 Tl in patients with posttraumatic Olfactory loss.
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Odor Detection Ability and Thallium-201 Transport in the Olfactory Nerve of Traumatic Olfactory-Impaired Mice
Chemical Senses, 2008Co-Authors: Hideaki Shiga, Yayoi Kinoshita, Toshiaki Tsukatani, Ryohei Amano, Daisuke Ogawa, Kohshin Washiyama, Mitsuru Furukawa, Kyoko Hirota, Takaki MiwaAbstract:Although Olfactory Nerve damage is a contributing factor in the diagnosis of posttraumatic Olfactory loss, at present, there are no methods to directly assess injury to these Nerves. We have shown that following Olfactory Nerve injury in mice, thallium-201 ( 201 Tl) transport from the nasal cavity to the Olfactory bulb decreases. To determine if Olfactory function after Nerve injury could be assessed with nasal administration of 201 Tl, we measured the correlation between odor detection ability (ODA) and the rate of transport of 201 Tl in Olfactory Nerves. Both ODA and 201 Tl transport were measured after bilateral Olfactory Nerve transection for a 4-week period. Cycloheximide solution was used for ODA against tap water. 201 Tl transport was measured as the ratio of radioactivity in the nasal cavity and Olfactory bulb with gamma spectrometry. There was a significant correlation between ODA and the rate of 201 Tl transport in the Olfactory Nerve. These findings suggest that Olfactory function after Nerve injury can be objectively evaluated with the nasal administration of 201 Tl.
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Thallium Transport and the Evaluation of Olfactory Nerve Connectivity between the Nasal Cavity and Olfactory Bulb
Chemical Senses, 2007Co-Authors: Yayoi Kinoshita, Toshiaki Tsukatani, Ryohei Amano, Daisuke Ogawa, Hideaki Shiga, Kohshin Washiyama, Mitsuru Furukawa, Takaki MiwaAbstract:Little is known regarding how alkali metal ions are transported in the Olfactory Nerve following their intranasal administration. In this study, we show that an alkali metal ion, thallium is transported in the Olfactory Nerve fibers to the Olfactory bulb in mice. The Olfactory Nerve fibers of mice were transected on both sides of the body under anesthesia. A double tracer solution (thallium-201, (201)Tl; manganese-54, (54)Mn) was administered into the nasal cavity the following day. Radioactivity in the Olfactory bulb and nasal turbinate was analyzed with gamma spectrometry. Auto radiographic images were obtained from coronal slices of frozen heads of mice administered with (201)Tl or (54)Mn. The transection of the Olfactory Nerve fibers was confirmed with a neuronal tracer. The transport of intranasal administered (201)Tl/(54)Mn to the Olfactory bulb was significantly reduced by the transection of Olfactory Nerve fibers. The Olfactory Nerve transection also significantly inhibited the accumulation of fluoro-ruby in the Olfactory bulb. Findings indicate that thallium is transported by the Olfactory Nerve fibers to the Olfactory bulb in mice. The assessment of thallium transport following head injury may provide a new diagnostic method for the evaluation of Olfactory Nerve injury.
Matthew Ennis - One of the best experts on this subject based on the ideXlab platform.
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dopamine d2 receptor mediated presynaptic inhibition of Olfactory Nerve terminals
Journal of Neurophysiology, 2001Co-Authors: Matthew Ennis, Lee A. Zimmer, Fuming Zhou, Kelly J Ciombor, Vassiliki Aroniadouanderjaska, Abdallah Hayar, Emiliana Borrelli, Frank L Margolis, Michael T. ShipleyAbstract:Olfactory receptor neurons of the nasal epithelium project via the Olfactory Nerve (ON) to the glomeruli of the main Olfactory bulb, where they form glutamatergic synapses with the apical dendrites...
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norepinephrine increases rat mitral cell excitatory responses to weak Olfactory Nerve input via alpha 1 receptors in vitro
Neuroscience, 1999Co-Authors: Kelly J Ciombor, Matthew Ennis, Michael T. ShipleyAbstract:A rat Olfactory bulb in vitro slice preparation was used to investigate the actions of norepinephrine on spontaneous and afferent (Olfactory Nerve) evoked activity of mitral cells. Single Olfactory Nerve shocks elicited a characteristic mitral cell response consisting of distinct, early and late spiking components separated by a brief inhibitory epoch. Bath-applied norepinephrine (1 μM) increased the early spiking component elicited by perithreshold (79% increase, P 0.05), intensity Olfactory Nerve shocks. The facilitatory effect of norepinephrine was due to a reduction in the incidence of response failures to perithreshold intensity shocks. Norepinephrine also decreased the inhibitory epoch separating the early and late spiking components by 44% (P<0.05). By contrast, norepinephrine had no consistent effect on the spontaneous discharge rate of the mitral cells. The effects of norepinephrine were mimicked by the α1 receptor agonist phenylephrine (1 μM, P<0.001). Both norepinephrine and phenylephrine modulation of mitral cell responses were blocked by the α1 adrenergic antagonist WB-4101 (1 μM). These findings are consistent with observations that the main Olfactory bulb exhibits the highest density of α1 receptors in the brain. The α2 receptor agonist clonidine (100 nM) and the β receptor agonist isoproterenol (1 μM) had inconsistent effects on mitral cell spontaneous and Olfactory Nerve-evoked activity. These results indicate that norepinephrine increases mitral cell excitatory responses to weak but not strong Olfactory Nerve inputs in vitro via activation of α1 receptors. This is consistent with recent findings in vivo that synaptically released norepinephrine preferentially increases mitral cell excitatory responses to weak Olfactory Nerve inputs. Taken together, these results suggest that the release of norepinephrine in the Olfactory bulb may increase the sensitivity of mitral cells to weak odors. Olfactory cues evoke norepinephrine release in the main Olfactory bulb, and norepinephrine plays important roles in early Olfactory learning and reproductive/maternal behaviors. By increasing mitral cell responses to Olfactory Nerve input, norepinephrine may play a critical role in modulating Olfactory function, including formation and/or recall of specific Olfactory memories.
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Norepinephrine increases rat mitral cell excitatory responses to weak Olfactory Nerve input via alpha-1 receptors in vitro
Neuroscience, 1999Co-Authors: Kelly J Ciombor, Matthew Ennis, Michael T. ShipleyAbstract:A rat Olfactory bulb in vitro slice preparation was used to investigate the actions of norepinephrine on spontaneous and afferent (Olfactory Nerve) evoked activity of mitral cells. Single Olfactory Nerve shocks elicited a characteristic mitral cell response consisting of distinct, early and late spiking components separated by a brief inhibitory epoch. Bath-applied norepinephrine (1 μM) increased the early spiking component elicited by perithreshold (79% increase, P 0.05), intensity Olfactory Nerve shocks. The facilitatory effect of norepinephrine was due to a reduction in the incidence of response failures to perithreshold intensity shocks. Norepinephrine also decreased the inhibitory epoch separating the early and late spiking components by 44% (P
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glomerular synaptic responses to Olfactory Nerve input in rat Olfactory bulb slices
Neuroscience, 1997Co-Authors: Vassiliki Aroniadouanderjaska, Matthew Ennis, Michael T. ShipleyAbstract:Abstract In Olfactory bulb slices from young rats, the field potential evoked in the glomerular layer by stimulation in the Olfactory Nerve layer consisted of two negative components: an early component (N1) which was blocked by bath application of the kainate/amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 μ M), and a late, prolonged component (N2; duration ≥350 msec) which was unaffected by CNQX, was enhanced by reduction of Mg 2+ in the medium, and was blocked by the N -methyl- d -aspartate receptor antagonist dl -2-amino-5-phosphonovalerate (50 μ M). A comparison of the glomerular field potentials before and after knife cuts that isolated the glomerular layer from the deeper layers of the Olfactory bulb indicated that both N1 and N2 were produced by currents generated, for the most part, within the glomeruli. A laminar analysis of the field potential profiles evoked by Olfactory Nerve stimulation in standard medium, or in the presence of CNQX, showed that N1 and N2 reversed polarity in the external plexiform and mitral cell layers, suggesting that both components reflected synaptic responses in the distal, apical dendrites of mitral/tufted cells. Simultaneous field potential recordings in the glomerular layer and intracellular recordings in the mitral cell layer showed that: (i) N1 is associated with a brief, short-latency spiking activity of mitral cells, and (ii) N2 is associated with prolonged mitral cell spiking, since N2 and the late cell firing had similar time-courses, and both were blocked by bath applied dl -2-amino-5-phosphonovalerate. Application of the GABA A receptor antagonist bicuculline methiodide (10 μ M) to standard medium selectively enhanced N2. The enhanced N2 was significantly reduced by dl -2-amino-5-phosphonovalerate. Strychnine, an antagonist of glycine receptors, had similar effects to those of bicuculline, but only at high concentrations that have been previously shown to block GABA A receptors; at low concentrations strychnine had no effect. The effects of all drugs tested were reversible. In the rat Olfactory bulb, activation of the Olfactory Nerve evokes a kainate/AMPA receptor-mediated response in the distal, apical dendrites of mitral/tufted cells, followed by a slow N -methyl- d -aspartate receptor-mediated response which triggers prolonged discharge of mitral cells. GABA A receptor-mediated inhibition appears to suppress, preferentially, this N -methyl- d -aspartate receptor-mediated component. The presence of prolonged N -methyl- d -aspartate receptor-mediated postsynaptic activity at the primary synapses of the Olfactory system may play a key role in Olfactory processing by facilitating synaptic integration and plasticity.
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activation of locus coeruleus enhances the responses of Olfactory bulb mitral cells to weak Olfactory Nerve input
The Journal of Neuroscience, 1996Co-Authors: Maorong Jiang, Lee A. Zimmer, Matthew Ennis, Edwin R Griff, Michael T. ShipleyAbstract:The main Olfactory bulb (MOB) receives a dense projection from the pontine nucleus locus coeruleus (LC), the largest collection of norepinephrine (NE)-containing cells in the brain. LC is the sole source of NE innervation of MOB. Previous studies of the actions of exogenously applied NE on mitral cells, the principal output neurons of MOB, are contradictory. The effect of synaptically released NE on mitral cell activity is not known, nor is the influence of NE on responses of mitral cells to Olfactory Nerve inputs. The goal of the present study was to assess the influence of LC activation on spontaneous and Olfactory Nerve-evoked activity of mitral cells. In methoxyflurane-anesthetized rats, intracoerulear microinfusions of acetylcholine (ACh) (200 mm; 90–120 nl) evoked a four- to fivefold increase in LC neuronal discharge, and a transient EEG desynchronization and decrease in mitral cell discharge. LC activation increased excitatory responses of mitral cells evoked by weak (i.e., perithreshold) nasal epithelium shocks (1.0 Hz) in 17/18 cells (mean increase = 67%). The discharge rate of mitral cells at the time that epithelium-evoked responses were increased did not differ significantly from pre-LC activation baseline values. Thus, changes in mitral baseline activity do not account for the increased response to epithelium stimulation. These findings suggest that increased activity in LC–NE projections to MOB may enhance detection of relatively weak odors.
Patrick Gourmelon - One of the best experts on this subject based on the ideXlab platform.
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Intranasal exposure to uranium results in direct transfer to the brain along Olfactory Nerve bundles
Neuropathology and Applied Neurobiology, 2014Co-Authors: Chrystelle Ibanez, Olivia Delissen, Philippe Lestaevel, Isabelle Dublineau, David Suhard, Christine Tessier, Patrick GourmelonAbstract:Aims Uranium Olfactory uptake after intranasal exposure raises some concerns for people potentially exposed to airborne radionuclide contamination as the brain could be a direct target for these contaminants. A model of nasal instillation was used to elucidate the transport mechanisms of uranium to the brain and to map its localization. Methods Increasing concentrations of depleted uranium containing solutions were instilled in the nasal cavity of adult male rats. Uranium concentrations were measured using inductively coupled plasma-mass spectrometry (ICP-MS) 4h after instillation. Olfactory neuroepithelium cytoarchitecture was studied using immunohistochemistry experiments. Secondary ion mass spectrometry (SIMS) microscopy was performed to localize uranium in the Olfactory system. Results ICP-MS analyses showed a frontal accumulation of uranium in the Olfactory bulbs associated with a smaller increase in more caudal brain regions (frontal cortex, hippocampus and cerebellum). Uranium concentrations in the Olfactory bulbs do not reach a saturation point. Olfactory Nerve bundle integrity is not affected by uranium as revealed by immunohistochemistry. SIMS microscopy allowed us to show that uranium localization is mainly restricted to the Olfactory neuroepithelium and around Olfactory Nerve bundles. It is subsequently detected in the Olfactory Nerve layer of the Olfactory bulb. Discussion These results suggest the existence of a transcellular passage from the mucosa to the perineural space around axon bundles. Uranium bypasses the blood brain barrier and is conveyed to the brain via the cerebrospinal fluid along the Olfactory Nerve. Future studies might need to integrate this new contamination route to assess uranium neurotoxicity after nasal exposure. © 2013 British Neuropathological Society.
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Intranasal exposure to uranium results in direct transfer to the brain along Olfactory Nerve bundles
Neuropathology and Applied Neurobiology, 2014Co-Authors: Chrystelle Ibanez, Olivia Delissen, Philippe Lestaevel, Isabelle Dublineau, David Suhard, Christine Tessier, Patrick GourmelonAbstract:Aims Uranium Olfactory uptake after intranasal exposure raises some concerns for people potentially exposed to airborne radionuclide contamination as the brain could be a direct target for these contaminants. A model of nasal instillation was used to elucidate the transport mechanisms of uranium to the brain and to map its localization. Methods Increasing concentrations of depleted uranium containing solutions were instilled in the nasal cavity of adult male rats. Uranium concentrations were measured using inductively coupled plasma-mass spectrometry (ICP-MS) 4 h after instillation. Olfactory neuroepithelium cytoarchitecture was studied using immunohistochemistry experiments. Secondary ion mass spectrometry (SIMS) microscopy was performed to localize uranium in the Olfactory system. Results ICP-MS analyses showed a frontal accumulation of uranium in the Olfactory bulbs associated with a smaller increase in more caudal brain regions (frontal cortex, hippocampus and cerebellum). Uranium concentrations in the Olfactory bulbs do not reach a saturation point. Olfactory Nerve bundle integrity is not affected by uranium as revealed by immunohistochemistry. SIMS microscopy allowed us to show that uranium localization is mainly restricted to the Olfactory neuroepithelium and around Olfactory Nerve bundles. It is subsequently detected in the Olfactory Nerve layer of the Olfactory bulb. Discussion These results suggest the existence of a transcellular passage from the mucosa to the perineural space around axon bundles. Uranium bypasses the blood brain barrier and is conveyed to the brain via the cerebrospinal fluid along the Olfactory Nerve. Future studies might need to integrate this new contamination route to assess uranium neurotoxicity after nasal exposure.
