Cholinergic innervation in adult rat cerebral cortex: A quantitative immunocytochemical description

Mechawar, Naguib; Cozzari, Costantino; Descarries, Laurent

doi:10.1002/1096-9861(20001211)428:2<305::aid-cne9>3.0.co;2-y

Cited by 135 publications

(116 citation statements)

References 113 publications

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“…Dopamine projections into V1, however, are relatively sparse (46). Another possibility is that cholinergic nuclei, which are known to be involved in the satiation of thirst (47,48) and which project into V1 (49,50) could signal reward to the visual cortex. Effects similar to the reported voltage sensitivity of G protein coupled ACh receptors (51) could provide a biochemical mechanism of reward inhibition.…”

Section: Discussionmentioning

confidence: 99%

Learning reward timing in cortex through reward dependent expression of synaptic plasticity

Gavornik

Shuler

Loewenstein

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

124

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The ability to represent time is an essential component of cognition but its neural basis is unknown. Although extensively studied both behaviorally and electrophysiologically, a general theoretical framework describing the elementary neural mechanisms used by the brain to learn temporal representations is lacking. It is commonly believed that the underlying cellular mechanisms reside in high order cortical regions but recent studies show sustained neural activity in primary sensory cortices that can represent the timing of expected reward. Here, we show that local cortical networks can learn temporal representations through a simple framework predicated on reward dependent expression of synaptic plasticity. We assert that temporal representations are stored in the lateral synaptic connections between neurons and demonstrate that reward-modulated plasticity is sufficient to learn these representations. We implement our model numerically to explain reward-time learning in the primary visual cortex (V1), demonstrate experimental support, and suggest additional experimentally verifiable predictions. reinforcment learning ͉ visual cortex O ur brains process time with such instinctual ease that the difficulty of defining what time is, in a neural sense, seems paradoxical. There is a rich literature in experimental neuroscience describing the temporal dynamics of both cellular and system-level neuronal processes and many insightful psychophysical studies have revealed perceptual correlates of time. Despite this, and the clear importance of accurate temporal processing at all levels of behavior, we still know little about how time is represented or used by the brain (1). Temporal processing is classically understood as a higher order function, and although there is some disagreement (2, 3), it is often argued that dedicated structures or regions in the brain are responsible for representing time (4). Because different mechanisms are likely responsible for computing timing at different time scales (1,5,6), and because there is evidence for modality specific temporal mechanisms (7), an alternative possibility is that timing processes develop locally within different brain regions.Recent evidence indicates that temporal representations are expressed in primary sensory cortices (8-10) and that rewardbased reinforcement can affect the form of stimulus driven activity in the primary somatosensory cortex (11-13). In particular, Shuler and Bear (9) showed that neurons in rat primary visual cortex can develop persistent activity, evoked by brief visual stimuli, that robustly represents the temporal interval between a visual stimulus and paired reward (Fig. 1). A mechanistic framework capable of describing how a neural substrate can learn the observed temporal representations does not exist.Here, we explain how these temporal signals can be encoded in recurrent excitatory synaptic connections and how a local network can learn specific temporal instantiations through reward modulated plasticity. Although our model is potentially ...

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Section: Discussionmentioning

confidence: 99%

Learning reward timing in cortex through reward dependent expression of synaptic plasticity

Gavornik

Shuler

Loewenstein

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

124

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“…These findings indicate that the slow pathway acts within a neural network to regulate the particular excitability state of a neuron. Such a process is thought to be involved in the release of modulatory transmitters from cortical projections to regulate attention and working memory (Goldman-Rakic, 1999;Mechawar et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

M₁Muscarinic Receptors Inhibit L-type Ca²⁺Current and M-Current by Divergent Signal Transduction Cascades

et al. 2006

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2 )], whereas M-current did not. Western blot and imaging studies confirmed acute activation of cPLA 2 by muscarinic stimulation. Third, in type IIa PLA 2 [secreted (sPLA 2 )] ؊/؊ / cPLA 2 ؊/؊ double-knock-out SCG neurons, muscarinic inhibition of L-current decreased. In contrast, M-current inhibition remained unaffected but recovery was impaired. Our results indicate that L-current is inhibited by a pathway previously shown to control M-current over-recovery after washout of muscarinic agonist. Our findings support a model of M 1 R-meditated channel modulation that broadens rather than restricts the roles of phospholipids and fatty acids in regulating ion channel activity.

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“…and perfused transcardially with 4% paraformaldehyde dissolved in 0.1 M phosphate buffer, pH 7.4. The brains were removed and postfixed in the same solution for 24 h. Blocks of tissue containing the PFC, cholinergic nuclei, or Hipp were sectioned in either the coronal or sagittal plane at 20 or 50 m. Series of two to four consecutive sections were incubated with the mouse monoclonal antibody against purified rat brain choline acetyltransferase (ChAT) (gift from Dr. C. Cozzari, University of Rome, Italy and Dr. B. K. Hartman, University of Minnesota, Minneapolis, MN), guinea pig polyclonal antibody against recombinant GST-tagged vGluT2 (Millipore), guinea pig polyclonal antibody against rat synthetic linear vGluT1 peptide (Millipore), rabbit polyclonal antibody against recombinant mouse calbindin (CB) (Millipore), or rabbit polyclonal antibody against muscle parvalbumin (PV) (Swant) as described previously (Umbriaco et al, 1994;Mechawar et al, 2000;Henny and Jones, 2008). Briefly, at room temperature (RT), free-floating sections were rinsed in PBS (0.1 M, pH 7.4) and preincubated for 2 h in PBS containing 2% normal horse serum (Vector Laboratories), 1% bovine serum albumin (Roth), and 0.2% Triton X-100 (Roth) to block unspecific staining.…”

Section: Methodsmentioning

confidence: 99%

Cholinergic Control in Developing Prefrontal–Hippocampal Networks

Janiesch¹,

Krüger²,

Poschel³

et al. 2011

J. Neurosci.

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The cholinergic drive enhances input processing in attentional and mnemonic context by interacting with the activity of prefrontalhippocampal networks. During development, acetylcholine modulates neuronal proliferation, differentiation, and synaptic plasticity, yet its contribution to the maturation of cognitive processing resulting from early entrainment of neuronal networks in oscillatory rhythms remains widely unknown. Here we show that cholinergic projections growing into the rat prefrontal cortex (PFC) toward the end of the first postnatal week boost the generation of nested gamma oscillations superimposed on discontinuous spindle bursts by acting on functional muscarinic but not nicotinic receptors. Although electrical stimulation of cholinergic nuclei increased the occurrence of nested gamma spindle bursts by 41%, diminishment of the cholinergic input by either blockade of the receptors or chronic immunotoxic lesion had the opposite effect. This activation of locally generated gamma episodes by direct cholinergic projections to the PFC was accompanied by indirect modulation of underlying spindle bursts via cholinergic control of hippocampal theta activity. With ongoing maturation and switch of network activity from discontinuous bursts to continuous theta-gamma rhythms, accumulating cholinergic projections acting on both muscarinic and nicotinic receptors mediated the transition from high-amplitude slow to low-amplitude fast rhythms in the PFC. By exerting multiple actions on the oscillatory entrainment of developing prefrontal-hippocampal networks, the cholinergic input may refine them for later gating processing in executive and mnemonic tasks.

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Cholinergic innervation in adult rat cerebral cortex: A quantitative immunocytochemical description

Cited by 135 publications

References 113 publications

Learning reward timing in cortex through reward dependent expression of synaptic plasticity

Learning reward timing in cortex through reward dependent expression of synaptic plasticity

M₁Muscarinic Receptors Inhibit L-type Ca²⁺Current and M-Current by Divergent Signal Transduction Cascades

Cholinergic Control in Developing Prefrontal–Hippocampal Networks

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Cholinergic innervation in adult rat cerebral cortex: A quantitative immunocytochemical description

Cited by 135 publications

References 113 publications

Learning reward timing in cortex through reward dependent expression of synaptic plasticity

Learning reward timing in cortex through reward dependent expression of synaptic plasticity

M1Muscarinic Receptors Inhibit L-type Ca2+Current and M-Current by Divergent Signal Transduction Cascades

Cholinergic Control in Developing Prefrontal–Hippocampal Networks

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M₁Muscarinic Receptors Inhibit L-type Ca²⁺Current and M-Current by Divergent Signal Transduction Cascades