Acetylcholine is an essential excitatory neurotransmitter in the central nervous system and undertakes a vital role in cognitive function. Consequently, there is ample evidence to suggest the involvement of both nicotinic and muscarinic acetylcholine receptors in the modulation of synaptic plasticity, which is believed to be the molecular correlate of learning and memory. In the hippocampus in particular, multiple subtypes of both nicotinic and muscarinic receptors are present at presynaptic and postsynaptic loci of both principal neurons and inhibitory interneurons, where they exert profound bi-directional influences on synaptic transmission. Further evidence points to a role for cholinergic activation in the induction and maintenance of synaptic plasticity, and key influences on hippocampal network oscillations. The present review examines these multiple roles of acetylcholine in hippocampal plasticity.
"). Activation of each type of nAChR in glutamatergic neurons enhances post-synaptic responses and cellular plasticity (Drever et al., 2011). Rodent studies have shown that α7 nAChRs on inhibitory GABAergic (gamma-aminobutyric acid) interneurons are essential for normal auditory gating (Alkondon et al., 2000), and also that reduced receptor expression deficits could be partially ameliorated by agonism of the receptor (Stevens et al., 1998). "
"Metab Brain Dis ChAT expression but did not show significant effect against AchE level. The diverse function of (M1) AchR and its occurrence in the hippocampus, suggests that (M1) AchR play a key role in learning and memory (Drever et al. 2011) and is known to transiently enhance long-term potentiation resulting in neurocognitive improvement (Anisuzzaman et al. 2013). Administration of selective (M1) AchR antagonists induces spatial memory deficit (Hunter and Roberts 1988). "
[Show abstract][Hide abstract] ABSTRACT: Diabetes mellitus is a chronic metabolic disorder and has been associated with cognitive dysfunction. In our earlier study, chronic Urtica dioica (UD) treatment significantly ameliorated diabetes induced associative and spatial memory deficit in mice. The present study was designed to explore the effect of UD leaves extract on muscarinic cholinergic system, which has long been known to be involved in cognition. Streptozotocin (STZ) (50 mg/kg, i.p., consecutively for 5 days) was used to induce diabetes followed by treatment with UD extract (50 mg/kg, oral) or rosiglitazone (5 mg/kg, oral) for 8 weeks. STZ-induced diabetic mice showed significant reduction in hippocampal muscarinic acetylcholine receptor-1 and choline acetyltransferase expressions. Chronic diabetes significantly up-regulated the protein expression of acetylcholinesterase associated with oxidative stress in hippocampus. Besides, STZ-induced diabetic mice showed hypolocomotion with up-regulation of muscarinic acetylcholine receptor-4 expression in striatum. Chronic UD treatment significantly attenuated the cholinergic dysfunction and oxidative stress in the hippocampus of diabetic mice. UD had no effect on locomotor activity and muscarinic acetylcholine receptor-4 expression in striatum. In conclusion, UD leaves extract has potential to reverse diabetes mediated alteration in muscarinic cholinergic system in hippocampus and thereby improve memory functions.
"Carbachol activates acetylcholine receptors leading to increased neuronal activity in hippocampus. It is well established that acetylcholine can induce hippocampal plasticity (Drever et al. 2011; Galey et al. 1994; Markevich et al. 1997; Fernández de Sevilla et al. 2008). Indeed, carbachol alone can induce lasting effects on the acetylcholine receptors (Auerbach and Segal 1994) and can facilitate hippocampal LTP (Auerbach and Segal 1996). "
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