Acetylcholine and Prostigmine Electrophoresis at Visual Cortex Neurons

Spehlmann, Rainer

doi:10.1152/jn.1963.26.1.127

Cited by 82 publications

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“…The fact that acetylcholine (ACh) applied directly by microiontophor-esis can excite certain cortical neurones has been known for a number of years (Krnjevic & Phillis, 1963a, b;Spehlmann, 1963). The characteristic slow time course of this action sharply distinguishes it from the quick excitation produced by glutamate, or indeed from the rapid excitatory action of ACh on Renshaw cells.…”

Section: Introductionmentioning

confidence: 99%

The mechanism of excitation by acetylcholine in the cerebral cortex

Krnjević¹,

Pumain²,

Renaud³

1971

The Journal of Physiology

659

131

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SUMMARY1. The muscarinic depolarizing action of ACh on cortical neurones is associated with an increase in membrane resistance (mean / V/.iR = 3-16 mV/Mu).2. ACh also promotes repetitive firing by slowing repolarization after spikes.3. The depolarizing effect has a mean reversal level 6f -86 7 mV (with mean resting potential -56 mV).4. It is concluded that as a muscarinic excitatory agent, ACh probably acts by reducing the resting K+ conductance of cortical neurones, and also the delayed K+ current of the action potential.5. These results are discussed in relation to the possible role of ACh in cortical function.

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Section: Introductionmentioning

confidence: 99%

The mechanism of excitation by acetylcholine in the cerebral cortex

Krnjević¹,

Pumain²,

Renaud³

1971

The Journal of Physiology

659

131

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“…It is particularly relevant that Spehlmann (1963) has shown that the unit (Marrazzi, 1953) and the evoked ACh release from at least the contralateral visual cortex might have been the result of activating this component. This possibility was eliminated in experiments in which the transcallosal fibres were cut without abolishing the contralateral evoked release, thus indicating that a deeper pathway must be involved.…”

mentioning

confidence: 99%

The central release of acetylcholine during stimulation of the visual pathway

Collier¹,

Mitchell²

1966

The Journal of Physiology

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SUMMARY1. -In rabbits anaesthetized with Dial ACh has been collected from the surface of the cerebral cortex during stimulation of the visual pathways.2. The spontaneous release of ACh from the visual and non-visual areas of the cortex was found to be similar.3. Stimulation of the retinae by diffuse light produced a large increase in ACh release from the primary visual receiving areas (4.3 times the spontaneous release) and a smaller increase (1.9 times the spontaneous release) from other parts of the cortex.4. Direct unilateral electrical stimulation of the lateral geniculate body evoked a large increase in ACh release (3.4 times the spontaneous release) from the ipsilateral visual cortex and a smaller increase (1.7 times the spontaneous release) from the contralateral visual area and other regions of the cerebral cortex. The evoked increase from the contralateral cortex was not mediated by transcallosal pathways.5. The increase in ACh release evoked from the visual cortex by stimulation of the ipsilateral lateral geniculate body was dependent on the frequency of stimulation. The evoked release was smallest at low stimulus frequencies and increased to a maximum at 20 stimuli/sec.The evoked ACh release from other areas of the cortex was independent of the frequency at which the lateral geniculate body was stimulated.6. The possible central nervous pathways associated with the spontaneous release of ACh and the release evoked by stimulation of the eyes by light and by direct stimulation of the lateral geniculate body are discussed.7. It is concluded that two ascending cholinergic systems may be involved; the non-specific reticulo-cortical pathways responsible for the e.e.g arousal response, and the more specific thalamo-cortical pathways associated with augmenting and repetitive after-discharge responses. The first system is thought to be concerned with the small but widespread

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“…As shown in Fig. 1, ACh acts post-synaptically on muscarinic receptors in the cortex to produce a slow and prolonged excitation (Krnjević 1963;McCormick and Prince 1986;McCormick 1992;Spehlmann 1963). Presynaptically, evidence suggests that ACh acts differently on intracortical and thalamocortical afferents (Clarke 2004;Gil et al 1997;Kimura 2000;Metherate 2004).…”

Section: Introductionmentioning

confidence: 91%

Mean field model of acetylcholine mediated dynamics in the cerebral cortex

2007

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A recent continuum model of the large scale electrical activity of the cerebral cortex is generalized to include cholinergic modulation. In this model, dynamic modulation of synaptic strength acts over the time scales of nicotinic and muscarinic receptor action. The cortical model is analyzed to determine the effect of acetylcholine (ACh) on its steady states, linear stability, spectrum, and temporal responses to changes in subcortical input. ACh increases the firing rate in steady states of the system. Changing ACh concentration does not introduce oscillatory behavior into the system, but increases the overall spectral power. Model responses to pulses in subcortical input are affected by the tonic level of ACh concentration, with higher levels of ACh increasing the magnitude firing rate response of excitatory cortical neurons to pulses of subcortical input. Numerical simulations are used to explore the temporal dynamics of the model in response to changes in ACh concentration. Evidence is seen of a transition from a state in which intracortical inputs are emphasized to a state where thalamic afferents have enhanced influence. Perturbations in ACh concentration cause changes in the firing rate of cortical neurons, with rapid responses due to fast acting facilitatory effects of nicotinic receptors on subcortical afferents, and slower responses due to muscarinic suppression of intracortical connections. Together, these numerical simulations demonstrate that the actions of ACh could be a significant factor modulating early components of evoked response potentials.

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Acetylcholine and Prostigmine Electrophoresis at Visual Cortex Neurons

Cited by 82 publications

References 0 publications

The mechanism of excitation by acetylcholine in the cerebral cortex

The mechanism of excitation by acetylcholine in the cerebral cortex

The central release of acetylcholine during stimulation of the visual pathway

Mean field model of acetylcholine mediated dynamics in the cerebral cortex

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