The role of cholinergic system in neuronal plasticity: Focus on visual cortex and muscarinic receptors

Institute of Neuroscience (C.N.R.), 56100 Pisa, Italy.
Archives italiennes de biologie (Impact Factor: 1.49). 10/2008; 146(3-4):165-88. DOI: 10.4449/aib.v146i3.767
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Available from: Luciano Domenici, Apr 01, 2014
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    • "A more intriguing possibility concerns the roles in neural plasticity and memory formation played by ACh and theta, either of which has been separately implicated in many early studies. Particularly, cholinergic transmission permits and promotes hippocampal LTP formation (Jerusalinsky et al., 1997; Segal and Auerbach, 1997; Leung et al., 2003; Doralp and Leung, 2008), and permits the reorganization of cortical sensory representation (Kilgard and Merzenich, 1998; Sachdev et al., 1998; Conner et al., 2005; Origlia et al., 2008) as well as associated behavioral memory (Bakin and Weinberger, 1996). Temporally-specific activation of cholinergic nuclei was shown to be effective in inducing such plastic changes too (Bakin and Weinberger, 1996), while temporally-mismatched activation interferes with specific memory (Winters et al., 2007). "
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    ABSTRACT: Both acetylcholine (ACh) and theta oscillations are important for learning and memory, but the dynamic interaction between these two processes remains unclear. Recent advances in amperometry techniques have revealed phasic ACh releases in vivo. However, it is unknown whether phasic ACh release co-occurs with theta oscillations. We investigated this issue in the CA1 region of urethane-anesthetized male rats using amperometric and electrophysiological recordings. We found that ACh release was highly correlated with the appearance of both spontaneous and induced theta oscillations. Moreover, the maximal ACh release was observed around or slightly above the pyramidal layer. Interestingly, such release lagged behind theta initiation by 25-60 s. The slow ACh release profile was matched by the slow firing rate increase of a subset of medial-septal low-firing-rate neurons. Together, these results establish, for the first time, the in vivo coupling between phasic ACh release and theta oscillations on spatiotemporal scales much finer than previously known. These findings also suggest that phasic ACh is not required for theta initiation and may instead operate synergistically with theta oscillations to promote neural plasticity in the service of learning and memory.
    The Journal of Neuroscience : The Official Journal of the Society for Neuroscience 10/2010; 30(40):13431-40. DOI:10.1523/JNEUROSCI.1144-10.2010 · 6.34 Impact Factor
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    ABSTRACT: Acetylcholine (ACh) contributes to learning processes by modulating cortical plasticity in terms of intensity of neuronal activity and selectivity properties of cortical neurons. However, it is not known if ACh induces long term effects within the primary visual cortex (V1) that could sustain visual learning mechanisms. In the present study we analyzed visual evoked potentials (VEPs) in V1 of rats during a 4-8 h period after coupling visual stimulation to an intracortical injection of ACh analog carbachol or stimulation of basal forebrain. To clarify the action of ACh on VEP activity in V1, we individually pre-injected muscarinic (scopolamine), nicotinic (mecamylamine), alpha7 (methyllycaconitine), and NMDA (CPP) receptor antagonists before carbachol infusion. Stimulation of the cholinergic system paired with visual stimulation significantly increased VEP amplitude (56%) during a 6 h period. Pre-treatment with scopolamine, mecamylamine and CPP completely abolished this long-term enhancement, while alpha7 inhibition induced an instant increase of VEP amplitude. This suggests a role of ACh in facilitating visual stimuli responsiveness through mechanisms comparable to LTP which involve nicotinic and muscarinic receptors with an interaction of NMDA transmission in the visual cortex.
    PLoS ONE 02/2009; 4(6):e5995. DOI:10.1371/journal.pone.0005995 · 3.23 Impact Factor
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    ABSTRACT: Age-related differences in the regional recruitment of prefrontal cortex (PFC) during cognitive tasks suggests that aging is associated with functional reorganization. Cholinergic enhancement with physostigmine reduces activity in the PFC regions selectively recruited during working memory (WM) and increases activity in visual processing areas, suggesting that augmenting cholinergic function reduces task effort by improving the visual representation of WM stimuli. Here, we investigated how cholinergic enhancement influenced PFC and visual cortical activity in young and older subjects as WM difficulty was altered. Regional cerebral blood flow (rCBF) was measured using H(2)(15)O-PET in 10 young and 10 older volunteers during a parametrically varied face WM task, following an i.v. infusion of saline and physostigmine. Reaction time decreased during physostigmine relative to placebo in both groups. Prefrontal brain regions selectively recruited in each age group that responded differentially to task demands during placebo, had no significant activity during physostigmine. Medial visual processing areas showed task-selective increases in activity during drug in both groups, while lateral regions showed decreased activity in young and increased activity in older participants at longer task delays. These results are consistent with our previous findings, showing that the modulatory role of the cholinergic system persists during aging, and that the effects of cholinergic enhancement are functionally specific rather than anatomically specific. Moreover, the use of the parametric design allowed us to uncover group specific effects in lateral visual processing areas where increasing cholinergic function produced opposite effects on neural activity in the two age groups.
    Brain research bulletin 07/2009; 79(5):322-32. DOI:10.1016/j.brainresbull.2009.01.013 · 2.72 Impact Factor
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