α9: An acetylcholine receptor with novel pharmacological properties expressed in rat cochlear hair cells

Elgoyhen, Ana Belén; Johnson, D. S.; Boulter, Jim; Vetter, Douglas E.; Heinemann, Stephen F.

doi:10.1016/0092-8674(94)90555-x

Cited by 818 publications

(871 citation statements)

References 41 publications

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“…Pharmacologic and ligand-binding studies have demonstrated considerable diversity in neuronal nAChR subtypes. To date, 12 nAChR subunit genes have been identified, ␣2-␣10 and ␤2-␤4 (Heinemann et al, 1990;Sargent, 1993;Lindstrom, 1996;Elgoyhen et al, 1994Elgoyhen et al, , 2001). The contribution of specific subunits to cellular responses can be accomplished to a large degree with the use of selective agonists and antagonists.…”

Section: Nicotinic Receptors and Addictionmentioning

confidence: 99%

Cellular and synaptic mechanisms of nicotine addiction

2002

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ABSTRACT:The tragic health effects of nicotine addiction highlight the importance of investigating the cellular mechanisms of this complex behavioral phenomenon. The chain of cause and effect of nicotine addiction starts with the interaction of this tobacco alkaloid with nicotinic acetylcholine receptors (nAChRs). This interaction leads to activation of reward centers in the CNS, including the mesoaccumbens DA system, which ultimately leads to behavioral reinforcement and addiction. Recent findings from a number of laboratories have provided new insights into the biologic processes that contribute to nicotine self-administration.Examination of the nAChR subtypes expressed within the reward centers has identified potential roles for these receptors in normal physiology, as well as the effects of nicotine exposure. The high nicotine sensitivity of some nAChR subtypes leads to rapid activation followed in many cases by rapid desensitization. Assessing the relative importance of these molecular phenomena in the behavioral effects of nicotine presents an exciting challenge for future research efforts.

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Section: Nicotinic Receptors and Addictionmentioning

confidence: 99%

Cellular and synaptic mechanisms of nicotine addiction

2002

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“…MOC neurons reduce the effects of masking noise and protect the cochlea from damage due to acoustic overstimulation (reviewed by Guinan 1996) by altering the active mechanical properties of the outer hair cells in the cochlea (Housley and Ashmore 1991;Dallos et al 1997). Their effects are mediated via the release of acetylcholine, which activates a nicotinic receptor formed of α9 and α10 nicotinic receptor subunits (Elgoyhen et al 1994(Elgoyhen et al , 2001Sgard et al 2002).…”

Section: Introductionmentioning

confidence: 99%

“…1A) compensate for loss of MOC action peripherally so that behavioral measures are unchanged. These branches act via a receptor that has yet to be identified but is different from that of the periphery, since α9 nAChR is not present in the brain (Elgoyhen et al 1994).…”

Section: Introductionmentioning

confidence: 99%

Olivocochlear Neuron Central Anatomy Is Normal in α9 Knockout Mice

Brown

Vetter

2008

JARO

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Olivocochlear (OC) neurons were studied in a transgenic mouse with deletion of the α9 nicotinic acetylcholine receptor subunit. In this α9 knockout mouse, the peripheral effects of OC stimulation are lacking and the peripheral terminals of OC neurons under outer hair cells have abnormal morphology. To account for this mouse's apparently normal hearing, it has been proposed to have central compensation via collateral branches to the cochlear nucleus. We tested this idea by staining OC neurons for acetylcholinesterase and examining their morphology in knockout mice, wild-type mice of the same background strain, and CBA/CaJ mice. Knockout mice had normal OC systems in terms of numbers of OC neurons, dendritic patterns, and numbers of branches to the cochlear nucleus. The branch terminations were mainly to edge regions and to a lesser extent the core of the cochlear nucleus, and were similar among the strains in terms of the distribution and staining density. These data demonstrate that there are no obvious changes in the central morphology of the OC neurons in α9 knockout mice and make less attractive the idea that there is central compensation for deletion of the peripheral receptor in these mice.

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“…In the rat, a total of eight ligand binding α and three structural β subunits have been cloned, which in various combinations of α and β subunits, form distinct heteromeric or homomeric pentameric receptor subtypes (Couturier et al, 1990;Seguela et al, 1993, Sargent, 1993, Corringer et al, 2000. After cloning and characterization of the muscle type nAChR subunits (α1, β1, δ ,ε, γ ), the α2 was the first neuronal subunit to be cloned, sequenced and characterized (α2, Wada et al, 1988) followed by α3 (Boulter et al, 1986), α4 (Goldman et al, 1987), β2 , β3 , β4 (Isenberg andMeyer, 1989, Duvoisin et al, 1989), α5 (Boulter et al, 1990), α6, (Lamar et al, 1990), α7 (Seguela et al, 1993), α9 (Elgoyhen et al, 1994) and finally α 10 (Elgoyhen et al, 2001). …”

Section: Introductionmentioning

confidence: 99%

Postnatal expression of α2 nicotinic acetylcholine receptor subunit mRNA in developing cortex and hippocampus

Son

Winzer‐Serhan

2006

Journal of Chemical Neuroanatomy

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Nicotinic acetylcholine receptors (nAChRs) are pentameric ligand-gated cation channels composed of α and β subunits. nAChR subunit expression is highly regulated during development. Previous studies have revealed increased expression of α3, α5, α7, and β4 subunit mRNAs and α7 binding sites during hippocampal and cortical development. Here, we examined the expression of α2 subunit mRNA in rat cortex and hippocampus using highly sensitive radioactive in situ hybridization. α2 subunit mRNA expression was first detected at P3 in cortex and hippocampus. During postnatal development the distribution of α2 subunit mRNA expression was spatially similar to the one found in adult, exhibiting highly restricted expression in scattered cells mostly in cortical layer V and retrosplenial cortex, and in scattered cells in CA1/CA3 stratum oriens and CA3 stratum radiatum. However, the expression intensity and number of α2 positive cells strongly increased to reach peak levels in both cortex and hippocampus at P7 and decreased thereafter to moderate to low to levels. Double in situ hybridization revealed that most, but not all, α2 mRNA expression was located in nonpyramidal GAD-positive cortical and hippocampal interneurons. Thus, similar to other nAChR subunits, α2 mRNA expression is transiently upregulated during postnatal development and nAChRs containing α2 subunits could regulate GABAergic activity during a critical period of network formation.

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α9: An acetylcholine receptor with novel pharmacological properties expressed in rat cochlear hair cells

Cited by 818 publications

References 41 publications

Cellular and synaptic mechanisms of nicotine addiction

Cellular and synaptic mechanisms of nicotine addiction

Olivocochlear Neuron Central Anatomy Is Normal in α9 Knockout Mice

Postnatal expression of α2 nicotinic acetylcholine receptor subunit mRNA in developing cortex and hippocampus

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