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Increased polyphosphoinositide responsiveness in the cerebral cortex induced by cholinergic denervation
1Department of Biochemistry, Charing Cross and Westminster Medical School, London, England.
Journal of Neurochemistry
|May 1, 1988
Summary
Lesioning the nucleus basalis causes cholinergic neuron loss and impaired cortical function. However, spared axon sprouting leads to functional recovery of muscarinic acetylcholine receptors within 150 days.
Area of Science:
- Neuroscience
- Neurobiology
- Cellular Neuroscience
Background:
- The nucleus basalis in the basal forebrain projects cholinergic neurons to the cortex.
- Lesions here cause degeneration of these neurons, impacting cortical cholinergic function.
Purpose of the Study:
- To investigate the recovery of cortical muscarinic acetylcholine receptor response after denervation.
- To understand the mechanisms underlying functional recovery following neuronal loss.
Main Methods:
- Rat models with nucleus basalis lesions were used.
- Acetylcholinesterase activity and muscarinic acetylcholine receptor number were assessed.
- Polyphosphoinositide response assay using [3H]inositol was performed on cortical tissue slices.
Main Results:
- Lesions initially decreased cholinergic parameters.
- A significant increase in carbachol-stimulated [3H]inositol monophosphate ([3H]IP1) production was observed 5 days post-lesion.
- This enhanced response, indicating increased receptor sensitivity, attenuated by 2 weeks but recovery occurred by 150 days.
Conclusions:
- Cortical cholinergic denervation leads to a transient hypersensitivity of muscarinic receptors.
- Spared axon sprouting and re-establishment of synapses likely mediate functional recovery.
- The polyphosphoinositide response is a valuable index for assessing receptor integrity post-lesion.