Renshaw cells, nicotinic receptors

Despite the widespread presence of neuronal nicotinic receptors, for a long time their only known physiological role in the CNS was in mediating the excitation of Renshaw cells by motoneuron axon collaterals (201). The situation has now changed, particularly with respect to the demonstration of a synaptic role, especially for a7-like receptors. 

Receptor Types. In many areas of the CNS, the most represented type of hetero-meric nicotinic receptor is likely to be a4/32 or q 4j82 these receptors correspond to high affinity binding sites for [ H]nicotine. This is likely to be the synaptic receptor on Renshaw cells, which are immunopositiveforthe a4and /32, but not the a 7 subunit, in agreement with the insensitivity of their synaptic responses to methyllycaconitine (202). 

ACETYLCHOLINE In most regions of the CNS, the effects of ACh, assessed either by iontophoresis or by radioligand-binding assays, appear to be generated by interaction with a mixture of nicotinic and muscarinic receptors. Several presumptive chohnergic pathways have been proposed in addition to that of the motoneuron-Renshaw cell. Eight major clusters of ACh neurons and their pathways have been characterized. 

Acetylcholine Approximately 5% of brain neurons have receptors for ACh. Most CNS responses to ACh are mediated by a large family of G protein-coupled muscarinic M receptors that lead to slow excitation when activated. The ionic mechanism of slow excitation involves a decrease in membrane permeability to potassium. Of the nicotinic receptors present in the CNS (they are less common than muscarinic receptors), those on the Renshaw cells activated by motor axon collaterals in the spinal cord are the best-characterized. Drugs affecting the activity of cholinergic systems in the brain include the acetylcholinesterase inhibitors used in Alzheimer s disease (eg, tacrine) and the muscarinic blocking agents used in parkinsonism (eg, benztropine). 

Nicotinic receptors on the Renshaw cell are activated by the release of ACh from motoneuron collaterals. This results in the release of glycine, which, via interaction with its receptors on the motoneuron, causes membrane hyperpolarization—an example of feedback inhibition. The receptors were so-named because of their activation by nicotine. The answer is (D). 

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