Ultrastructural localization of cholinergic muscarinic receptors in rat brain cortical capillaries

Luiten, P.G.M.; Jong, G.I. de; Zee, Eddy A. van der; Dijken, Henk van

doi:10.1016/0006-8993(96)00195-3

Cited by 25 publications

(14 citation statements)

References 31 publications

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“…It can be argued that the cholinergic effects shown in this study reflect more general changes in blood flow and/or volume associated with the cerebral microvasculature rather than more specific changes in deoxyhemoglobin concentration that colocalize with changing neuronal activity Peterson et al, 1998;Polley et al, 1999a). Indeed, basal forebrain stimulation has been shown to increase cerebral blood flow (for review, see Dauphin and MacKenzie, 1995), and both muscarinic (Luiten et al, 1996;Elhusseiny et al, 1999) and nicotinic (Kalaria et al, 1994) receptors are found on cerebral blood vessels. It may be that the small arterioles and capillaries located in deeper cortical layers express cholinergic receptors and play a larger role in cholinergic-mediated cerebral blood flow, a possibility that would require some time for a cholinergic agent to penetrate the cortex before exerting its effect on the deeper vessels and, therefore, would be consistent with our time course results.…”

Section: Source Of the Imaged Intrinsic Signalsmentioning

confidence: 99%

In vivo modulation of a cortical functional sensory representation shortly after topical cholinergic agent application

Penschuck

Chen-Bee

Prakash

et al. 2002

J of Comparative Neurology

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The aim of the present study was to determine whether cholinergic increase in the size of a functional representation (collective evoked response from a large population of neurons) can be observed shortly (within an hour) after treatment onset and whether nicotinic receptors can participate in this type of modulation. Cholinergic agonist application has been found previously to increase the response of a single cortical neuron to a stimulus. Also, pairing cholinergic basal forebrain stimulation with delivery of a tone has been reported to increase the size of that tone's functional representation. Whereas the increase in a single cortical neuron response can occur within seconds after cholinergic agonist application, to date the increase in the size of a functional representation has only been investigated within one to several weeks after the onset of pairing basal forebrain stimulation with tone delivery. Furthermore, primarily muscarinic receptors have been implicated in these types of changes in cortical activity. By using optical imaging of intrinsic signals in vivo, we found that the size of a whisker's functional representation in the primary somatosensory cortex of the rat increases substantially within 69 or 46 minutes after topical application of either a muscarinic or nicotinic agonist to the exposed cortex, respectively, and decreases within 23 minutes after topical application of a muscarinic antagonist. For each cholinergic agent, we verified that delivery of a cholinergic agent by means of topical application can lead to the agent's successful penetration through the cortical layers in the time allotted to complete an imaging experiment. Furthermore, the time course of penetration for each agent was characterized. Based on the combined imaging/penetration results, we speculate on potential sites of cholinergic action in the cortex. Irrespective of the exact mechanism of action, we demonstrate here that an increase in the size of a functional sensory representation can occur shortly by means of activation of either nicotinic or muscarinic receptors.

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Section: Source Of the Imaged Intrinsic Signalsmentioning

confidence: 99%

In vivo modulation of a cortical functional sensory representation shortly after topical cholinergic agent application

Penschuck

Chen-Bee

Prakash

et al. 2002

J of Comparative Neurology

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“…An impaired microvascular system may represent a major variable contributing to the vulnerability of these neurons. Basal forebrain cholinergic projections innervate and dilate cortical microvessels directly, as well as indirectly via a local cortical nitric oxide relay (Raszkiewicz et al ., 1992; Vaucher & Hamel, 1995; Luiten et al ., 1996; Vaucher et al ., 1997a; Barbelivien et al ., 1999). Ischemic events and microvascular disorder have been suggested to reduce cortical cholinergic activity and cholinergic innervation (Kalaria, 2002).…”

Section: Introductionmentioning

confidence: 99%

Microsphere embolism‐induced cortical cholinergic deafferentation and impairments in attentional performance

Craft

Mahoney²,

DeVries

et al. 2005

Eur J of Neuroscience

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Ischemic events have been hypothesized to play a critical role on the pathogenesis of dementia and the acceleration of cognitive impairments. This experiment was designed to determine the consequences of microvascular ischemia on the cortical cholinergic input system and associated attention capacities. Injections of microspheres ( approximately 50 microm diameter; approximately 5000 microspheres/100 microL) into the right common carotid artery of rats served as a model of microvascular ischemia and resulted in decreases in the density of cholinergic fibers in the ipsilateral medial prefrontal cortex and frontoparietal areas. Furthermore, dense astrogliosis, indicated by glial fibrillary acidic protein (GFAP) immunohistochemistry, was observed in the globus pallidus, including the areas of origin of cholinergic projections to the cortex. Fluoro-Jade B staining indicated that loss of neurons in the cortex was restricted to areas of microsphere-induced infarcts. Attentional performance was assessed using an operant sustained attention task; performance in this task was previously demonstrated to reflect the integrity and activity of the cortical cholinergic input system. Embolized animals' performance was characterized by a decrease in the animals' ability to detect signals. Their performance in non-signal trials remained unaffected. The residual density of cholinergic axons in prefrontal and frontoparietal areas correlated with the animals' performance. The present data support the hypothesis that microvascular ischemia results in loss of cortical cholinergic inputs and impairs associated attentional performance. Microsphere embolism represents a useful animal model for studying the role of interactions between microvascular disorder and impaired forebrain cholinergic neurotransmission in the manifestation of cognitive impairments.

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“…In the rat, focal stimulation of these neurons increases ipsilateral cortical blood flow [247][248][249] . Both cholinergic and serotonergic receptors have been identified on the perivascular endfeet of astrocytes [250][251][252] . It appears that the cortical vasodilation is mediated by both muscarinic and nicotinic cholinergic receptors.…”

Section: Neural Controlmentioning

confidence: 99%

The Cerebral Microcirculation

Tuma

2008

Microcirculation

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Ultrastructural localization of cholinergic muscarinic receptors in rat brain cortical capillaries

Cited by 25 publications

References 31 publications

In vivo modulation of a cortical functional sensory representation shortly after topical cholinergic agent application

In vivo modulation of a cortical functional sensory representation shortly after topical cholinergic agent application

Microsphere embolism‐induced cortical cholinergic deafferentation and impairments in attentional performance

The Cerebral Microcirculation

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