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  • Knockouts reveal overlapping functions of M(2) and M(4) muscarinic receptors and evidence for a local glutamatergic circuit within the laterodorsal tegmental nucleus.

Knockouts reveal overlapping functions of M(2) and M(4) muscarinic receptors and evidence for a local glutamatergic circuit within the laterodorsal tegmental nucleus.

Journal of neurophysiology (2012-09-08)
Kristi A Kohlmeier, Masaru Ishibashi, Jürgen Wess, Martha E Bickford, Christopher S Leonard
ABSTRACT

Cholinergic neurons in the laterodorsal tegmental (LDT) and peduncolopontine tegmental (PPT) nuclei regulate reward, arousal, and sensory gating via major projections to midbrain dopamine regions, the thalamus, and pontine targets. Muscarinic acetylcholine receptors (mAChRs) on LDT neurons produce a membrane hyperpolarization and inhibit spike-evoked Ca(2+) transients. Pharmacological studies suggest M(2) mAChRs are involved, but the role of these and other localized mAChRs (M(1-)-M(4)) has not been definitively tested. To identify the underlying receptors and to circumvent the limited receptor selectivity of available mAChR ligands, we used light- and electron-immunomicroscopy and whole cell recording with Ca(2+) imaging in brain slices from knockout mice constitutively lacking either M(2), M(4), or both mAChRs. Immunomicroscopy findings support a role for M(2) mAChRs, since cholinergic and noncholinergic LDT and pedunculopontine tegmental neurons contain M(2)-specific immunoreactivity. However, whole cell recording revealed that the presence of either M(2) or M(4) mAChRs was sufficient, and that the presence of at least one of these receptors was required for these carbachol actions. Moreover, in the absence of M(2) and M(4) mAChRs, carbachol elicited both direct excitation and barrages of spontaneous excitatory postsynaptic potentials (sEPSPs) in cholinergic LDT neurons mediated by M(1) and/or M(3) mAChRs. Focal carbachol application to surgically reduced slices suggest that local glutamatergic neurons are a source of these sEPSPs. Finally, neither direct nor indirect excitation were knockout artifacts, since each was detected in wild-type slices, although sEPSP barrages were delayed, suggesting M(2) and M(4) receptors normally delay excitation of glutamatergic inputs. Collectively, our findings indicate that multiple mAChRs coordinate cholinergic outflow from the LDT in an unexpectedly complex manner. An intriguing possibility is that a local circuit transforms LDT muscarinic inputs from a negative feedback signal for transient inputs into positive feedback for persistent inputs to facilitate different firing patterns across behavioral states.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Anti-Muscarinic Acetylcholine Receptor m2 Antibody, clone M2-2-B3, clone M2-2-B3, Chemicon®, from rat
Sigma-Aldrich
Anti-Muscarinic Acetylcholine Receptor m4 Antibody, clone 17F10.2, purified antibody, clone 17F10.2, Chemicon®
Sigma-Aldrich
Monoclonal Anti-Nitric Oxide Synthase, Brain (1-181) antibody produced in mouse, clone NOS-B1, ascites fluid
Sigma-Aldrich
Anti-Muscarinic Acetylcholine Receptor (M1) antibody produced in rabbit, affinity isolated antibody, lyophilized powder
Sigma-Aldrich
Anti-Nitric Oxide Synthase, Brain (1409-1429) antibody produced in rabbit, IgG fraction of antiserum, buffered aqueous solution
Sigma-Aldrich
Anti-Choline Acetyltransferase Antibody, Chemicon®, from goat