Functional nicotinic ACh receptors on interneurones in the rat hippocampus

Jones, Susan; Yakel, Jerrel L.

doi:10.1111/j.1469-7793.1997.603bd.x

Cited by 250 publications

(231 citation statements)

References 20 publications

Supporting

Mentioning

204

Contrasting

Order By: Relevance

“…Depending on their electrophysiological and pharmacological properties they can be classified in at least three different receptor subtypes (Alkondon et al, 1993, Jones and Yakel, 1997, Buhler and Dunwiddie 2001. Based on results presented in this study, α2 containing nAChRs can be found in at least one subpopulation of GABAergic interneurons in cortical layer V and VI and hippocampal stratum oriens during postnatal development and in the adult.…”

Section: Expression Of Nachr α2 Mrna During Developmentmentioning

confidence: 66%

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

Son

Winzer‐Serhan

2006

Journal of Chemical Neuroanatomy

View full text Add to dashboard Cite

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.

show abstract

Section: Expression Of Nachr α2 Mrna During Developmentmentioning

confidence: 66%

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

Son

Winzer‐Serhan

2006

Journal of Chemical Neuroanatomy

View full text Add to dashboard Cite

show abstract

“…These findings suggest that activation of α7 receptors could influence GABA release in the hippocampus. Physiological studies in rat hippocampal slices have confirmed the presence of α7 receptors on interneurons in all layers of area CA1 (Alkondon et al, 1998;Buhler and Dunwiddie, 2001;Frazier et al, 1998b;Frazier et al, 1998a;Jones and Yakel, 1997;McQuiston and Madison, 1999) as well as GABA-mediated inhibition of CA1 pyramidal cells following activation of α7 receptors on CA1 interneurons (Alkondon and Albuquerque, 2001;Buhler and Dunwiddie, 2002;Ji and Dani, 2000). It seems reasonable to hypothesize that α7 receptors may also modulate GABA release from interneurons in hippocampal area CA3 given that α-BTX binding has been observed on CA3 interneuron subtypes (Freedman et al, 1993) that are known to make synaptic contact with CA3 pyramidal cells (Freund and Buzsaki, 1996).…”

Section: Altered Gaba Releasementioning

confidence: 93%

Altered hippocampal circuit function in C3H α7 null mutant heterozygous mice

et al. 2008

View full text Add to dashboard Cite

The α7 subtype of nicotinic receptor is highly expressed in the hippocampus where it is purported to modulate release of the inhibitory neurotransmitter γ-aminobutyric acid (GABA). The α7 receptormediated release of GABA is thought to contribute to hippocampal inhibition (gating) of response to repetitive auditory stimulation. This hypothesis is supported by observations of hippocampal auditory gating deficits in mouse strains with low levels of hippocampal α7 receptors compared to strains with high levels of hippocampal α7 receptors. The difficulty with comparisons between mouse strains, however, is that different strains have different genetic backgrounds. Thus, the observed interstrain differences in hippocampal auditory gating might result from factors other than interstrain variations in the density of hippocampal α7 receptors. To address this issue, hippocampal binding of the α7 receptor-selective antagonist α-bungarotoxin as well as hippocampal auditory gating characteristics were compared in C3H wild type and C3H α7 receptor null mutant heterozygous mice. The C3H α7 heterozygous mice exhibited significant reductions in hippocampal α7 receptors levels and abnormal hippocampal auditory gating compared to the C3H wild type mice. In addition, a general increase in CA3 pyramidal neuron responsivity was observed in the heterozygous mice compared to the wild type mice. These data suggest that decreasing hippocampal α7 receptor density results in a profound alteration in hippocampal circuit function.

show abstract

“…In addition, nAChRs can modulate GABAergic transmission in multiple brain areas, such as thalamus, cortex, hippocampus, and interpeduncular nucleus (Lena et al, 1993;Alkondon et al, 1997Alkondon et al, , 2000Lena and Changeux, 1997;Fisher et al, 1998;Radcliffe et al, 1999). Modulation of GABA neurons by nAChRs has been most extensively studied in the hippocampus, where GABAergic interneurons express multiple nAChR subtypes (Alkondon et al, 1997;Jones and Yakel, 1997;Frazier et al, 1998b;McQuiston and Madison, 1999;Ji and Dani, 2000). The physiologic impact of nAChR activation is critically dependent upon their localization.…”

Section: Nicotinic Modulation Of Gabaergic Transmission In the Vtamentioning

confidence: 99%

Cellular and synaptic mechanisms of nicotine addiction

2002

View full text Add to dashboard Cite

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.

show abstract

Functional nicotinic ACh receptors on interneurones in the rat hippocampus

Cited by 250 publications

References 20 publications

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

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

Altered hippocampal circuit function in C3H α7 null mutant heterozygous mice

Cellular and synaptic mechanisms of nicotine addiction

Contact Info

Product

Resources

About