ORCID Profile
0000-0002-6155-4950
Current Organisation
Australian National University
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Publisher: Informa UK Limited
Date: 09-2009
Publisher: Springer Science and Business Media LLC
Date: 06-03-2019
DOI: 10.1038/S41598-018-33000-1
Abstract: A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has been fixed in the paper.
Publisher: Cold Spring Harbor Laboratory
Date: 20-12-2019
DOI: 10.1101/2019.12.19.881896
Abstract: Transient Receptor Potential Ankyrin 1 (TRPA1) is a non-selective cation channel, which is broadly expressed throughout the body. Despite its expression in the mammalian cortex, little is known about the contribution of TRPA1 to cortical function. Here we investigate the role of TRPA1 in sensory information processing by performing electrophysiological recording and 2-photon calcium imaging from two sensory areas in mice: the primary vibrissal somatosensory cortex (vS1) and the primary visual cortex (V1). In vS1, local activation of TRPA1 by its agonist AITC significantly increased the spontaneous activity of cortical neurons, their evoked response to vibrissal stimulation, and their response range, consistent with a positive gain modulation. TRPA1 inhibition with HC-030031 reversed these modulations to below initial control gains. The gain modulations were absent in TRPA1 Knockout mice. In V1, TRPA1 activation increased the gain of direction and orientation selectivity similarly to the gain modulations observed in vS1 cortex. Linear decoding analysis of V1 population activity confirmed faster and more reliable encoding of visual signals in the presence of TRPA1 activation. Overall, our findings reveal a physiological role for TRPA1 in enhancing sensory signals in the mammalian cortex.
Publisher: Elsevier BV
Date: 04-2016
Publisher: Proceedings of the National Academy of Sciences
Date: 03-02-2014
Abstract: Acetaminophen overdose is the most common cause of acute liver failure and the leading cause of chronic liver damage requiring liver transplantation in developed countries. There are limited options for early treatment. Acetaminophen liver toxicity leads to the formation of reactive oxygen and nitrogen species which cause an increase in intracellular Ca 2+ and hepatocellular death. We show that acetaminophen-induced liver toxicity depends on Transient Receptor Potential Melanostatine 2 (TRPM2) cation channels in hepatocytes, which are activated in response to oxidative stress and are responsible for Ca 2+ overload. Lack of TRPM2 channels in hepatocytes or their pharmacological inhibition protects liver from acetaminophen toxicity. This provides evidence that TRPM2 may present a potential therapeutic target for treatment of oxidative-stress related liver diseases.
Publisher: Elsevier BV
Date: 09-2018
DOI: 10.1016/J.BBRC.2018.07.132
Abstract: Transient Receptor Potential Melastatin (TRPM) 2 is a non-selective Ca
Publisher: Springer Science and Business Media LLC
Date: 13-09-2017
DOI: 10.1038/S41598-017-11477-6
Abstract: Neuronal adaptation is a common feature observed at various stages of sensory processing. Here, we quantified the time course of adaptation in rat somatosensory cortex. Under urethane anesthesia, we juxta-cellularly recorded single neurons (n = 147) while applying a series of whisker deflections at various frequencies (2–32 Hz). For ~90% of neurons, the response per unit of time decreased with frequency. The degree of adaptation increased along the train of deflections and was strongest at the highest frequency. However, a subset of neurons showed facilitation producing higher responses to subsequent deflections. The response latency to consecutive deflections increased both for neurons that exhibited adaptation and for those that exhibited response facilitation. Histological reconstruction of neurons (n = 45) did not reveal a systematic relationship between adaptation profiles and cell types. In addition to the periodic stimuli, we applied a temporally irregular train of deflections with a mean frequency of 8 Hz. For 70% of neurons, the response to the irregular stimulus was greater than that of the 8 Hz regular. This increased response to irregular stimulation was positively correlated with the degree of adaptation. Altogether, our findings demonstrate high levels of ersity among cortical neurons, with a proportion of neurons showing facilitation at specific temporal intervals.
Publisher: IOP Publishing
Date: 12-04-2019
Publisher: Cold Spring Harbor Laboratory
Date: 07-06-2023
DOI: 10.1101/2023.06.06.543981
Abstract: An important function of the brain is to form accurate representations of the world around us. To optimise sensory representations based on the demands of the environment, activity of cortical neurons is regulated by neuromodulators such as Acetylcholine (ACh). As such, ACh is implicated in cognitive functions including attention, arousal and sleep cycles. However, it is not clear how specific ACh receptors shape the baseline activity of cortical neurons and their evoked response to sensory stimuli. Here, we investigate the role of a densely expressed muscarinic ACh receptor 1 (M1) in information processing in the mouse primary somatosensory cortex (vS1) and in the animal’s sensitivity in detecting vibrotactile stimuli. We show that M1 activation significantly enhances the evoked response of vS1 neurons and the reversal of this enhancement by blocking M1. In addition, we demonstrate that M1 activation results in faster and more reliable neuronal responses, which is manifested by a significant reduction in response latencies and the trial-to-trial variability in neuronal activity. At the population level, M1 activation reduces the network synchrony and thus enhances the capacity of vS1 neurons in conveying sensory information. Consistent with the neuronal findings, we show that M1 activation significantly improves performances in a vibrotactile detection task. Overall, the M1-mediated enhancement in sensory efficiency reflects a multiplicative gain modulation at the neuronal level, resembling the changes observed during high attention states.
Publisher: The Royal Society
Date: 04-2017
DOI: 10.1098/RSOB.160314
Abstract: TRPA1 is a non-selective cation channel involved in pain sensation and neurogenic inflammation. Although TRPA1 is well established in a number of organs including the nervous system, its presence and function in the mammalian cortex remains unclear. Here, we demonstrate the expression of TRPA1 in rodent somatosensory cortex through immunostaining and investigate its functional activation by whole-cell electrophysiology, Ca 2+ imaging and two-photon photoswitching. Application of TRPA1 agonist (AITC) and antagonist (HC-030031) produced significant modulation of activity in layer 5 (L5) pyramidal neurons in both rats and mice AITC increased intracellular Ca 2+ concentrations and depolarized neurons, and both effects were blocked by HC-030031. These modulations were absent in the TRPA1 knockout mice. Next, we used optovin, a reversible photoactive molecule, to activate TRPA1 in in idual L5 neurons of rat cortex. Optical control of activity was established by applying a tightly focused femtosecond-pulsed laser to optovin-loaded neurons. Light application depolarized neurons ( n = 17) with the maximal effect observed at λ = 720 nm. Involvement of TRPA1 was further confirmed by repeating the experiment in the presence of HC-030031, which diminished the light modulation. These results demonstrate the presence of TRPA1 in L5 pyramidal neurons and introduce a highly specific approach to further understand its functional significance.
Location: Iran (Islamic Republic of)
No related grants have been discovered for Ehsan Kheradpezhouh.