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Cholinergic afferent stimulation induces axonal function plasticity in adult hippocampal granule cells.

Martinello K, Huang Z, Lujan R, Tran B, Watanabe M, Cooper EC, Brown DA, Shah MM - Neuron (2015)

Bottom Line: The effects of acetylcholine on axonal information processing, though, remain unknown.In support, immunohistochemistry revealed muscarinic M1 receptor, CaV3.2, and KV7.2/7.3 subunit localization in granule cell axons.Since alterations in axonal signaling affect neuronal firing patterns and neurotransmitter release, this is an unreported cellular mechanism by which acetylcholine might, at least partly, enhance cognitive processing.

View Article: PubMed Central - PubMed

Affiliation: UCL School of Pharmacy, University College London, London, WC1N 1AX, UK.

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Endogenous Acetylcholine Release Enhances Granule Cell Excitability by Lowering the Action Potential Threshold(Ai) Hippocampal slice preparation schematic and example image of granule cell. Scale bar, 50 μm.(Aii) Representative slow excitatory synaptic potentials before and after atropine (3 μM). The first burst is shown on an expanded timescale.(Bi and Ci) Typical traces obtained in response to 400 ms current steps before (control), immediately after stimulation (stim), and 25 min post-stimulation (25 min PS) in the absence and presence of atropine, respectively. The scale applies to all traces.(Bii and Cii) Mean action potential numbers (AP. No.) before and after cholinergic afferent stimulation with and without atropine.(Biii and Ciii) Typical action potentials and phase plane plots before, immediately after, or 25 min post-stimulation when atropine was absent or present.(Biv and Civ) Individual (open square) and mean (filled squares) spike threshold before and after stimulation without and with atropine.(Bv) The spike threshold change time course after stimulation in a subset of control neurons.(Bvi) Representative 50 Hz glutamatergic EPSP trains and alpha EPSPs before and after cholinergic stimulation. Also shown are the average spike numbers produced prior to and post cholinergic stimulation.(Bvii) Example records and average frequency of spontaneous action potentials before and after HF cholinergic stimulation is shown on the right. In all graphs, the numbers of observations are indicated in parenthesis and asterisks denote significant (p < 0.05) differences.
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fig1: Endogenous Acetylcholine Release Enhances Granule Cell Excitability by Lowering the Action Potential Threshold(Ai) Hippocampal slice preparation schematic and example image of granule cell. Scale bar, 50 μm.(Aii) Representative slow excitatory synaptic potentials before and after atropine (3 μM). The first burst is shown on an expanded timescale.(Bi and Ci) Typical traces obtained in response to 400 ms current steps before (control), immediately after stimulation (stim), and 25 min post-stimulation (25 min PS) in the absence and presence of atropine, respectively. The scale applies to all traces.(Bii and Cii) Mean action potential numbers (AP. No.) before and after cholinergic afferent stimulation with and without atropine.(Biii and Ciii) Typical action potentials and phase plane plots before, immediately after, or 25 min post-stimulation when atropine was absent or present.(Biv and Civ) Individual (open square) and mean (filled squares) spike threshold before and after stimulation without and with atropine.(Bv) The spike threshold change time course after stimulation in a subset of control neurons.(Bvi) Representative 50 Hz glutamatergic EPSP trains and alpha EPSPs before and after cholinergic stimulation. Also shown are the average spike numbers produced prior to and post cholinergic stimulation.(Bvii) Example records and average frequency of spontaneous action potentials before and after HF cholinergic stimulation is shown on the right. In all graphs, the numbers of observations are indicated in parenthesis and asterisks denote significant (p < 0.05) differences.

Mentions: To investigate how endogenous acetylcholine affects granule cell intrinsic activity, we made patch-clamp recordings from mature cells in brain slices before and after extracellular stimulation of afferents in the stratum moleculare (Figure 1A). These cells had input resistances (RN) of 297.94 ± 23.9 MΩ (n = 117) and complex dendritic trees (Figure 1A) as revealed by post hoc morphological analysis. Experiments were performed in the presence of glutamatergic and GABAergic ionotropic and metabotropic receptor inhibitors, unless otherwise stated.


Cholinergic afferent stimulation induces axonal function plasticity in adult hippocampal granule cells.

Martinello K, Huang Z, Lujan R, Tran B, Watanabe M, Cooper EC, Brown DA, Shah MM - Neuron (2015)

Endogenous Acetylcholine Release Enhances Granule Cell Excitability by Lowering the Action Potential Threshold(Ai) Hippocampal slice preparation schematic and example image of granule cell. Scale bar, 50 μm.(Aii) Representative slow excitatory synaptic potentials before and after atropine (3 μM). The first burst is shown on an expanded timescale.(Bi and Ci) Typical traces obtained in response to 400 ms current steps before (control), immediately after stimulation (stim), and 25 min post-stimulation (25 min PS) in the absence and presence of atropine, respectively. The scale applies to all traces.(Bii and Cii) Mean action potential numbers (AP. No.) before and after cholinergic afferent stimulation with and without atropine.(Biii and Ciii) Typical action potentials and phase plane plots before, immediately after, or 25 min post-stimulation when atropine was absent or present.(Biv and Civ) Individual (open square) and mean (filled squares) spike threshold before and after stimulation without and with atropine.(Bv) The spike threshold change time course after stimulation in a subset of control neurons.(Bvi) Representative 50 Hz glutamatergic EPSP trains and alpha EPSPs before and after cholinergic stimulation. Also shown are the average spike numbers produced prior to and post cholinergic stimulation.(Bvii) Example records and average frequency of spontaneous action potentials before and after HF cholinergic stimulation is shown on the right. In all graphs, the numbers of observations are indicated in parenthesis and asterisks denote significant (p < 0.05) differences.
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

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Show All Figures
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fig1: Endogenous Acetylcholine Release Enhances Granule Cell Excitability by Lowering the Action Potential Threshold(Ai) Hippocampal slice preparation schematic and example image of granule cell. Scale bar, 50 μm.(Aii) Representative slow excitatory synaptic potentials before and after atropine (3 μM). The first burst is shown on an expanded timescale.(Bi and Ci) Typical traces obtained in response to 400 ms current steps before (control), immediately after stimulation (stim), and 25 min post-stimulation (25 min PS) in the absence and presence of atropine, respectively. The scale applies to all traces.(Bii and Cii) Mean action potential numbers (AP. No.) before and after cholinergic afferent stimulation with and without atropine.(Biii and Ciii) Typical action potentials and phase plane plots before, immediately after, or 25 min post-stimulation when atropine was absent or present.(Biv and Civ) Individual (open square) and mean (filled squares) spike threshold before and after stimulation without and with atropine.(Bv) The spike threshold change time course after stimulation in a subset of control neurons.(Bvi) Representative 50 Hz glutamatergic EPSP trains and alpha EPSPs before and after cholinergic stimulation. Also shown are the average spike numbers produced prior to and post cholinergic stimulation.(Bvii) Example records and average frequency of spontaneous action potentials before and after HF cholinergic stimulation is shown on the right. In all graphs, the numbers of observations are indicated in parenthesis and asterisks denote significant (p < 0.05) differences.
Mentions: To investigate how endogenous acetylcholine affects granule cell intrinsic activity, we made patch-clamp recordings from mature cells in brain slices before and after extracellular stimulation of afferents in the stratum moleculare (Figure 1A). These cells had input resistances (RN) of 297.94 ± 23.9 MΩ (n = 117) and complex dendritic trees (Figure 1A) as revealed by post hoc morphological analysis. Experiments were performed in the presence of glutamatergic and GABAergic ionotropic and metabotropic receptor inhibitors, unless otherwise stated.

Bottom Line: The effects of acetylcholine on axonal information processing, though, remain unknown.In support, immunohistochemistry revealed muscarinic M1 receptor, CaV3.2, and KV7.2/7.3 subunit localization in granule cell axons.Since alterations in axonal signaling affect neuronal firing patterns and neurotransmitter release, this is an unreported cellular mechanism by which acetylcholine might, at least partly, enhance cognitive processing.

View Article: PubMed Central - PubMed

Affiliation: UCL School of Pharmacy, University College London, London, WC1N 1AX, UK.

Show MeSH
Related in: MedlinePlus