scholarly journals Serotonin modulates the population activity profile of olfactory bulb external tufted cells

2012 ◽  
Vol 107 (1) ◽  
pp. 473-483 ◽  
Author(s):  
Shaolin Liu ◽  
Jason L. Aungst ◽  
Adam C. Puche ◽  
Michael T. Shipley
Keyword(s):  
Olfactory Bulb ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Inhibitory Neurons ◽  
Raphe Nuclei ◽  
Population Activity ◽  
Odor Coding ◽  
Inward Current ◽  
Tufted Cells ◽  
Raphé Nuclei

Serotonergic neurons in the raphe nuclei constitute one of the most prominent neuromodulatory systems in the brain. Projections from the dorsal and median raphe nuclei provide dense serotonergic innervation of the glomeruli of olfactory bulb. Odor information is initially processed by glomeruli, thus serotonergic modulation of glomerular circuits impacts all subsequent odor coding in the olfactory system. The present study discloses that serotonin (5-HT) produces excitatory modulation of external tufted (ET) cells, a pivotal neuron in the operation of glomerular circuits. The modulation is due to a transient receptor potential (TRP) channel-mediated inward current induced by activation of 5-HT2A receptors. This current produces membrane depolarization and increased bursting frequency in ET cells. Interestingly, the magnitude of the inward current and increased bursting inversely correlate with ET cell spontaneous (intrinsic) bursting frequency: slower bursting ET cells are more strongly modulated than faster bursting cells. Serotonin thus differentially impacts ET cells such that the mean bursting frequency of the population is increased. This centrifugal modulation could impact odor processing by: 1) increasing ET cell excitatory drive on inhibitory neurons to increase presynaptic inhibition of olfactory sensory inputs and postsynaptic inhibition of mitral/tufted cells; and/or 2) coordinating ET cell bursting with exploratory sniffing frequencies (5–8 Hz) to facilitate odor coding.

scholarly journals Expression of transient receptor potential (TRP) channel mRNAs in the mouse olfactory bulb

2012 ◽  
Vol 524 (1) ◽  
pp. 49-54 ◽  
Author(s):  
Hong-Wei Dong ◽  
James C. Davis ◽  
ShengYuan Ding ◽  
Qiang Nai ◽  
Fu-Ming Zhou ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Trp Channel ◽  
Transient Receptor

scholarly journals Chemical Exposure-Induced Changes in the Expression of Neurotrophins and Their Receptors in the Main Olfactory System of Mice Lacking TRPM5-Expressing Microvillous Cells

2018 ◽  
Vol 19 (10) ◽  
pp. 2939 ◽  
Author(s):  
Abdullah AlMatrouk ◽  
Kayla Lemons ◽  
Tatsuya Ogura ◽  
Wangmei Luo ◽  
Chantel Wilson ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
Transient Receptor Potential ◽  
Wide Spectrum ◽  
Receptor Potential ◽  
Transient Receptor Potential Channel ◽  
Chemical Exposure ◽  
Environmental Chemicals ◽  
Signaling Proteins ◽  
Main Olfactory Epithelium ◽  
Gene Transcripts

Functional maintenance of the mammalian main olfactory epithelium (MOE) is challenging because of its direct exposure to a wide spectrum of environmental chemicals. We previously reported that transient receptor potential channel M5-expressing microvillous cells (TRPM5-MCs) in the MOE play an important role in olfactory maintenance. To investigate the underpinning mechanisms, we exposed transcription factor Skn-1a knockout (Skn-1a−/−) mice lacking TRPM5-MCs, and TRPM5-GFP mice to either vehicle (water) or a mixture of odorous chemicals and chitin for two weeks and analyzed the expression of olfactory signaling proteins using immunolabeling and neurotrophin (NT) and NT receptor (NTR) gene transcripts using real-time quantitative PCR. The chemical exposure did not significantly attenuate the immunolabeling of olfactory signaling proteins. Vehicle-exposed Skn-1a−/− and TRPM5-GFP mice expressed similar levels of NT and NTR gene transcripts in the MOE and olfactory bulb. Chemical exposure significantly increased MOE expression of p75NTR in Skn-1a−/− mice, while p75NTR expression was reduced in TRPM5-GFP mice, as compared to vehicle-exposed mice. Additionally, our RNA in situ hybridization analysis and immunolabeling confirmed MOE expression of most NTs and NTRs. Together, these results indicate that TRPM5-MCs and chemical exposure influence expression of some NTs and NTRs in the MOE and olfactory bulb (OB).

Abstract 115: Reduction of Trpv1 Activity in Aortic Baroreceptor Neurons in Diabetic Neuropathy: Role of Brain-derived Neurotrophic Factor

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Yingying Tan ◽  
Qi Zhang
Keyword(s):  
Diabetic Neuropathy ◽  
Transient Receptor Potential ◽  
Kinase Inhibitor ◽  
Receptor Potential ◽  
Diabetic Rats ◽  
Control Group ◽  
Transient Receptor Potential Vanilloid ◽  
Peak Current Density ◽  
Inward Current ◽  
Pre Treatment

It has been well documented that diabetes mellitus is associated with cardiovascular autonomic neuropathy including dysfunction of arterial baroreflex. The mechanisms underlying diabetes-induced baroreflex dysfunction remain poorly understood. Here we investigated the function and expression of transient receptor potential vanilloid 1 (TRPV1) in aortic baroreceptor (AB) neurons isolated from streptozotocin-induced diabetic rats between 4 and 8 weeks after onset of diabetes. AB neurons in nodose ganglion were retrograde-labeled by a transported fluorescent dye, Dil. Using the whole-cell patch clamp, we found that the inward current activated by the application of capsaicin (1 μM) was significantly smaller in AB neurons from diabetic rats compared with controls. The mean peak current density of capsaicin-induced currents was 145.7 ± 24.7 pA/pF (n = 16) in diabetic neurons and 269.3 ± 31.8 pA/pF (n =15) in controls, respectively. The duration of inward current was decreased 51% in diabetic rats compared with the control group. These evoked currents were completely blocked by the capsaicin antagonist capsazepine. In addition, capsaicin-induced desensitization of TRPV1 was up-regulated, whereas TRPV1 re-sensitization was down-regulated in AB neurons from diabetic rats. Immunofluorescence staining studies demonstrated that the percentage of TRPV1-positive neurons was 50.2 ± 5.0% in control rats and 38.2 ± 1.9% in diabetic rats, respectively. This reduction in TRPV1-positive neurons in AB neurons in diabetic rats was significant (n = 11, P < 0.01). In addition, the reductions in TRPV1 currents and positive neurons s in diabetic rats were normalized by pre-treatment with anti-BDNF antibody or K252a, a TrkB tyrosine kinase inhibitor. Furthermore, incubation with BDNF caused a large reduction in TRPV1 currents in AB neurons from control rats, and the number of AB neurons with BDNF immunoreactivity was greater in diabetic than control rats. These results suggest that reduced expression and function of TRPV1 are involved in the attenuation of baroreceptor neuron excitability, and increased BDNF activity in these neurons likely contributes to the reduction in TRPV1 function through TrkB receptor stimulation in diabetic neuropathy.

Thermal sensitivity of isolated vagal pulmonary sensory neurons: role of transient receptor potential vanilloid receptors

2006 ◽  
Vol 291 (3) ◽  
pp. R541-R550 ◽  
Author(s):  
Dan Ni ◽  
Qihai Gu ◽  
Hong-Zhen Hu ◽  
Na Gao ◽  
Michael X. Zhu ◽  
...  
Keyword(s):  
Sensory Neurons ◽  
Transient Receptor Potential ◽  
Thermal Sensitivity ◽  
Receptor Potential ◽  
Ruthenium Red ◽  
Transient Receptor Potential Vanilloid ◽  
Temperature Sensitive ◽  
Inward Current ◽  
Transient Receptor ◽  
Increasing Temperature

A recent study has demonstrated that increasing the intrathoracic temperature from 36°C to 41°C induced a distinct stimulatory and sensitizing effect on vagal pulmonary C-fiber afferents in anesthetized rats ( J Physiol 565: 295–308, 2005). We postulated that these responses are mediated through a direct activation of the temperature-sensitive transient receptor potential vanilloid (TRPV) receptors by hyperthermia. To test this hypothesis, we studied the effect of increasing temperature on pulmonary sensory neurons that were isolated from adult rat nodose/jugular ganglion and identified by retrograde labeling, using the whole cell perforated patch-clamping technique. Our results showed that increasing temperature from 23°C (or 35°C) to 41°C in a ramp pattern evoked an inward current, which began to emerge after exceeding a threshold of ∼34.4°C and then increased sharply in amplitude as the temperature was further increased, reaching a peak current of 173 ± 27 pA ( n = 75) at 41°C. The temperature coefficient, Q10, was 29.5 ± 6.4 over the range of 35–41°C. The peak inward current was only partially blocked by pretreatment with capsazepine (Δ I = 48.1 ± 4.7%, n = 11) or AMG 9810 (Δ I = 59.2 ± 7.8%, n = 8), selective antagonists of the TRPV1 channel, but almost completely abolished (Δ I = 96.3 ± 2.3%) by ruthenium red, an effective blocker of TRPV1–4 channels. Furthermore, positive expressions of TRPV1–4 transcripts and proteins in these neurons were demonstrated by RT-PCR and immunohistochemistry experiments, respectively. On the basis of these results, we conclude that increasing temperature within the normal physiological range can exert a direct stimulatory effect on pulmonary sensory neurons, and this effect is mediated through the activation of TRPV1, as well as other subtypes of TRPV channels.

scholarly journals L-type calcium channels and MAP kinase contribute to thyrotropin-releasing hormone-induced depolarization in thalamic paraventricular nucleus neurons

2016 ◽  
Vol 310 (11) ◽  
pp. R1120-R1127 ◽  
Author(s):  
Miloslav Kolaj ◽  
Li Zhang ◽  
Leo P. Renaud
Keyword(s):  
Transient Receptor Potential ◽  
Cannabinoid Receptor ◽  
Ryanodine Receptors ◽  
Critical Role ◽  
Receptor Potential ◽  
Thyrotropin Releasing Hormone ◽  
Induced Response ◽  
Inward Current ◽  
Releasing Hormone ◽  
Intracellular Ca

In rat paraventricular thalamic nucleus (PVT) neurons, activation of thyrotropin-releasing hormone (TRH) receptors enhances neuronal excitability via concurrent decrease in a G protein-coupled inwardly rectifying K (GIRK)-like conductance and opening of a cannabinoid receptor-sensitive transient receptor potential canonical (TRPC)-like conductance. Here, we investigated the calcium (Ca2+) contribution to the components of this TRH-induced response. TRH-induced membrane depolarization was reduced in the presence of intracellular BAPTA, also in media containing nominally zero [Ca2+]o, suggesting a critical role for both intracellular Ca2+ release and Ca2+ influx. TRH-induced inward current was unchanged by T-type Ca2+ channel blockade, but was decreased by blockade of high-voltage-activated Ca2+ channels (HVACCs). Both the pharmacologically isolated GIRK-like and the TRPC-like components of the TRH-induced response were decreased by nifedipine and increased by BayK8644, implying Ca2+ influx via L-type Ca2+ channels. Only the TRPC-like conductance was reduced by either thapsigargin or dantrolene, suggesting a role for ryanodine receptors and Ca2+-induced Ca2+ release in this component of the TRH-induced response. In pituitary and other cell lines, TRH stimulates MAPK. In PVT neurons, only the GIRK-like component of the TRH-induced current was selectively decreased in the presence of PD98059, a MAPK inhibitor. Collectively, the data imply that TRH-induced depolarization and inward current in PVT neurons involve both a dependency on extracellular Ca2+ influx via opening of L-type Ca2+ channels, a sensitivity of a TRPC-like component to intracellular Ca2+ release via ryanodine channels, and a modulation by MAPK of a GIRK-like conductance component.

scholarly journals Activation of raphe nuclei triggers rapid and distinct effects on parallel olfactory bulb output channels

2016 ◽  
Vol 19 (2) ◽  
pp. 271-282 ◽  
Author(s):  
Vikrant Kapoor ◽  
Allison C Provost ◽  
Prateek Agarwal ◽  
Venkatesh N Murthy
Keyword(s):  
Olfactory Bulb ◽  
Raphe Nuclei ◽  
Raphé Nuclei

scholarly journals Characterization of acid signaling in rat vagal pulmonary sensory neurons

2006 ◽  
Vol 291 (1) ◽  
pp. L58-L65 ◽  
Author(s):  
Qihai Gu ◽  
Lu-Yuan Lee
Keyword(s):  
Sensory Neurons ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Low Ph ◽  
Receptor Subtype ◽  
Transient Receptor Potential Vanilloid ◽  
Inward Current ◽  
Transient Component ◽  
Current Voltage Curve ◽  
Transient Receptor

Local tissue acidosis frequently occurs in airway inflammatory and ischemic conditions. The effect of physiological/pathophysiological-relevant low pH (7.0–5.5) on isolated rat vagal pulmonary sensory neurons was investigated using whole cell perforated patch-clamp recordings. In voltage-clamp recordings, vagal pulmonary sensory neurons exhibited distinct pH sensitivities and different phenotypes of inward current in responding to acidic challenge. The current evoked by lowering the pH of extracellular solution to 7.0 consisted of only a transient, rapidly inactivating component with small amplitude. The amplitude of this transient current increased when the proton concentration was elevated. In addition, a slow, sustained inward current began to emerge when pH was reduced to <6.5. The current-voltage curve indicated that the transient component of acid-evoked current was carried predominantly by Na+. This transient component was dose-dependently inhibited by amiloride, a common blocker of acid-sensing ion channels (ASICs), whereas the sustained component was significantly attenuated by capsazepine, a selective antagonist of transient receptor potential vanilloid receptor subtype-1 (TRPV1). The two components of acid-evoked current also displayed distinct recovery kinetics from desensitization. Furthermore, in current-clamp recordings, transient extracellular acidification depolarized the membrane potential and generated action potentials in these isolated neurons. In summary, our results have demonstrated that low pH can stimulate rat vagal pulmonary sensory neurons through the activation of both ASICs and TRPV1. The relative roles of these two current species depend on the range of pH and vary between neurons.

A hyperpolarization- and acid-activated nonselective cation current in Xenopus oocytes

2000 ◽  
Vol 279 (5) ◽  
pp. C1401-C1413 ◽  
Author(s):  
Akinori Kuruma ◽  
Yoshiyuki Hirayama ◽  
H. Criss Hartzell
Keyword(s):  
Heterologous Expression ◽  
Xenopus Oocytes ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Voltage Sensitivity ◽  
Inward Current ◽  
Cation Current ◽  
Nonselective Cation Current ◽  
Transient Receptor ◽  
A Current

Heterologous expression of a variety of membrane proteins in Xenopus oocytes sometimes results in the appearance of a hyperpolarization-activated inward current. The nature of this current remains incompletely understood. Some investigators have suggested that this current is a Cl current, whereas others have identified it as a nonselective cation current. The purpose of this investigation was to characterize this current in more detail. The hyperpolarization-activated inward current ( I IN) present in native oocytes was composed of a current carried at least partly by Ca and Mg under physiological ionic conditions plus a Ca-activated Cl current. The Ca-activated Cl current was blocked by chelation of cytosolic Ca with 1,2-bis(2-aminophenoxy)ethane- N,N,N′,N′-tetraacetic acid. When Cl currents were blocked, the cation current could be carried by Ca, Mg, or Co, but not appreciably by Ba, Mn, or Cd. I IN was stimulated by intracellular acidification. The properties of I IN were quite different from those of the store-operated Ca current. Heterologous expression of transient receptor potential-like gene product (TRPL), one of the members of the transient receptor potential family of putative store-operated Ca channels, apparently resulted in alteration of the voltage sensitivity of the endogenous I IN.

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