Abstract
Cholinergic neurons projecting from the nucleus basalis to the cerebral cortex are among those consistently rendered dysfunctional during the early stages of Alzheimer’s disease (1–3). These cholinergic neurons are implicated in the memory and cognitive disorders associated with the disease, based on pharmacological and pathological studies in humans and animals (4–6). Unfortunately, attempts to improve mental status by increasing brain cholinergic transmission have been only marginally successful because of at least four factors: 1) the multitransmitter basis of this disease, especially in its later stages; 2) our inability to diagnose the disease consistently in its earliest stages; 3) the lack of agents that selectively increase cholinergic transmission in brain pathways affected by Alzheimer’s disease; and 4) our lack of understanding about the long-term, trans-synaptic effects of cholinergic transmission that may modify the initial response to cholinergic agents. This chapter focuses on the fourth factor, with an emphasis on developing a neurochemical model for trans-synaptic changes associated with cholinergic transmission. Such a model would be particularly useful for characterizing the functional effects of agents purported to alter cholinergic transmission pre- or postsynaptically, e.g., trophic factors, receptor agonists and antagonists, as well as nootrophic drugs.
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Poulakos, J.J., Arendash, G.W., Millard, W.J., Sjak-Shie, N., Meyer, E.M. (1989). Cholinergic-Neuropeptide Y Interactions in the Rat Cerebral Cortex: Towards a Model for the Trans-Synaptic Effects of Cholinergic Transmission. In: Meyer, E.M., Simpkins, J.W., Yamamoto, J. (eds) Novel Approaches to the Treatment of Alzheimer’s Disease. Advances in Behavioral Biology, vol 36. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5727-8_23
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DOI: https://doi.org/10.1007/978-1-4684-5727-8_23
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