Relationship of opioid receptors with GABAergic neurons in the rat inferior colliculus

Tongjaroenbuangam, Walaiporn; Jongkamonwiwat, Nopporn; Phansuwan‐Pujito, Pansiri; Casalotti, Stefano O.; Forge, Andrew; Dodson, H.C.; Govitrapong, Piyarat

doi:10.1111/j.1460-9568.2006.05098.x

Cited by 20 publications

(14 citation statements)

References 42 publications

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“…In addition to the 5-HT1B receptor, several other types of neuromodulatory receptor are capable of altering GABAergic transmission in the IC (Ma et al 2002;Tongjaroenbungam et al 2004;Yigit et al 2003), or have anatomical associations with GABAergic neurons (Kalyuzhny et al 2000;Peruzzi and Dut 2004;Tongjaroenbuangam et al 2006). These studies underscore that the 5-HT1B receptor is one of multiple neurochemical mechanisms likely to regulate inhibition within the IC, although these other mechanisms have not been explored in terms of their regulation of frequency responsiveness.…”

Section: Evidence That the 5-ht1b Receptor Regulates Inhibitionmentioning

confidence: 89%

Serotonin 1B Receptor Modulates Frequency Response Curves and Spectral Integration in the Inferior Colliculus by Reducing GABAergic Inhibition

Hurley

Tracy²,

Bohorquez³

2008

Journal of Neurophysiology

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Hurley LM, Tracy JA, Bohorquez A. Serotonin 1B receptor modulates frequency response curves and spectral integration in the inferior colliculus by reducing GABAergic inhibition. J Neurophysiol 100: 1656 -1667, 2008. First published July 16, 2008 doi:10.1152/jn.90536.2008. The selectivity of sensory neurons for stimuli is often shaped by a balance between excitatory and inhibitory inputs, making this balance an effective target for regulation. In the inferior colliculus (IC), an auditory midbrain nucleus, the amplitude and selectivity of frequency response curves are altered by the neuromodulator serotonin, but the changes in excitatoryinhibitory balance that mediate this plasticity are not well understood. Previous findings suggest that the presynaptic 5-HT1B receptor may act to decrease the release of GABA onto IC neurons. Here, in vivo extracellular recording and iontophoresis of the selective 5-HT1B agonist CP93129 were used to characterize inhibition within and surrounding frequency response curves using two-tone protocols to indirectly measure inhibition as a decrease in spikes relative to an excitatory tone alone. The 5-HT1B agonist attenuated such two-tone spike reduction in a varied pattern among neurons, suggesting that the function of 5-HT1B modulation also varies. The hypothesis that the 5-HT1B receptor reduces inhibition was tested by comparing the effects of CP93129 and the GABA A antagonists bicuculline and gabazine in the same neurons. The effects of GABA A antagonists on spike count, tuning bandwidth, twotone ratio, and temporal response characteristics mimicked those of CP93129 across the neuron population. GABA A antagonists also blocked or reduced the facilitation of evoked responses by CP93129. These results are all consistent with the reduction of GABA A -mediated inhibition by 5-HT1B receptors in the IC, resulting in an increase in the level of evoked responses in some neurons, and a decrease in spectral selectivity in others. I N T R O D U C T I O NNeuromodulatory signals such as serotonin are broadly released in the brain in response to changes in internal state (Trulson andJacobs 1979, 1981) but transform the response properties of sensory neurons in highly specific ways (Hurley et al. 2004;Mooney et al. 1996;Xiang and Prince 2003). This specificity is achieved through the targeting of classes of neurons by a variety of receptor types that may alter intrinsic neuron properties or target presynaptic neurons and alter the release of neurotransmitter (Hoyer et al. 1994(Hoyer et al. , 2002. One consequence of these effects is that serotonin can alter the balance of different types of inputs within sensory regions. For example, serotonin may alter the balance between ascending versus descending projections (Mooney et al. 1996) or the balance between within-versus between-layer communication in the cortex (Xiang and Prince 2003).In the inferior colliculus (IC), an auditory midbrain nucleus, serotonin modifies a number of response properties, including both spectral and temporal aspects of ev...

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Section: Evidence That the 5-ht1b Receptor Regulates Inhibitionmentioning

confidence: 89%

Serotonin 1B Receptor Modulates Frequency Response Curves and Spectral Integration in the Inferior Colliculus by Reducing GABAergic Inhibition

Hurley

Tracy²,

Bohorquez³

2008

Journal of Neurophysiology

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“…Intense sounds are not only perceived as painfully loud (Ades et al, 1959), but can also induce pain sensations in around the external ear (otalgia; Dominguez et al, 2006; Hebert et al, 2013; Henry et al, 2014; Kaltenbach et al, 2000; Knipper et al, 2013; McFerran and Baguley, 2007; Norena, 2011; Pienkowski et al, 2014; Tyler et al, 2014a; Van Campen et al, 1999; Westcott et al, 2013). Pain transmitting neuropeptides and receptors are present in the CN and auditory nerve (Aguilar et al, 2004; Bauer et al, 2007b; Jongkamonwiwat et al, 2003; Nguyen et al, 2014; Phansuwan-Pujito et al, 2003; Tongjaroenbuangam et al, 2006), raising the possibility that loud sounds may trigger the perception of pain through these signaling pathways.…”

Section: Introductionmentioning

confidence: 99%

Noise-induced hearing loss: Neuropathic pain via Ntrk1 signaling

Manohar

Dahar

Adler

et al. 2016

Molecular and Cellular Neuroscience

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Severe noise-induced damage to the inner ear leads to auditory nerve fiber degeneration thereby reducing the neural input to the cochlear nucleus (CN). Paradoxically, this leads to a significant increase in spontaneous activity in the CN which has been linked to tinnitus, hyperacusis and ear pain. The biological mechanisms that lead to an increased spontaneous activity are largely unknown, but could arise from changes in glutamatergic or GABAergic neurotransmission or neuroinflammation. To test this hypothesis, we unilaterally exposed rats for 2 h to a 126 dB SPL narrow band noise centered at 12 kHz. Hearing loss measured by auditory brainstem responses exceeded 55 dB from 6 to 32 kHz. The mRNA from the exposed CN was harvested at 14 or 28 days post-exposure and qRT-PCR analysis was performed on 168 genes involved in neural inflammation, neuropathic pain and glutamatergic or GABAergic neurotransmission. Expression levels of mRNA of Slc17a6 and Gabrg3, involved in excitation and inhibition respectively, were significantly increased at 28 days post-exposure, suggesting a possible role in the CN spontaneous hyperactivity associated with tinnitus and hyperacusis. In the pain and inflammatory array, noise exposure up-regulated mRNA expression levels of four pain/inflammatory genes, Tlr2, Oprd1, Kcnq3 and Ntrk1 and decreased mRNA expression levels of two more genes, Ccl12 and Il1β. Pain/inflammatory gene expression changes via Ntrk1 signaling may induce sterile inflammation, neuropathic pain, microglial activation and migration of nerve fibers from the trigeminal nerve and cuneate and vestibular nuclei into the CN. These changes could contribute to somatic tinnitus, hyperacusis and otalgia.

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“…MOR, KOR and DOR receptors were found in disc-shaped and stellate cells of the inferior colliculus with MOR and GABA receptors co-localized in the central nucleus, dorsal cortex and external cortex of the inferior colliculus. BEND and GABA neurons were in close proximity to each other (1126). MOR is extensively co-localized with parvalbumin, but not somatostatin, in the hippocampal dentate gyrus (299).…”

Section: B-i Mu Agonists and Receptors-immunohistochemical Labelingmentioning

confidence: 90%

Endogenous opiates and behavior: 2009

Bodnar

2010

Peptides

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Relationship of opioid receptors with GABAergic neurons in the rat inferior colliculus

Cited by 20 publications

References 42 publications

Serotonin 1B Receptor Modulates Frequency Response Curves and Spectral Integration in the Inferior Colliculus by Reducing GABAergic Inhibition

Serotonin 1B Receptor Modulates Frequency Response Curves and Spectral Integration in the Inferior Colliculus by Reducing GABAergic Inhibition

Noise-induced hearing loss: Neuropathic pain via Ntrk1 signaling

Endogenous opiates and behavior: 2009

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