Modulation of acetylcholine release in human cortical slices: Possible implications for Alzheimer's disease

Feuerstein, Thomas J.; Seeger, W.

doi:10.1016/s0163-7258(97)00006-5

Cited by 25 publications

(11 citation statements)

References 59 publications

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“…1). In analogy to these results, it is probable that the same type of presynaptic 5-HT heteroreceptor on cholinergic nerves is also involved in the inhibition of electrically evoked [ 3 H]ACh release in slices of the rat hippocampus (Maura et al, 1989;Vizi and Kiss, 1998), guinea pig caudate nucleus (Bianchi et al, 1989), and human neocortex (Feuerstein and Seeger, 1997) as well as K ϩ -induced [ 3 H]ACh release in rat striatal slices (Gillet et al, 1985;Jackson et al, 1988). A decrease in electrically evoked [ 3 H]ACh release by the 5-HT receptor agonist CP-93129 (in the absence of TTX) was also observed (5-9 months after grafting) in hippocampal slices from rats that had undergone electrolytic or aspirative (Suhr et al, 1999) fimbria-fornix lesions and 2 weeks later had received intrahippocampal suspension grafts of fetal septal tissue.…”

Section: A General Aspectsmentioning

confidence: 68%

“…The cerebral cholinergic system plays a major role for memory and cognition, and an increase in ACh concentration in the synaptic cleft represents a therapeutic option in dementia associated with Alzheimer's disease. The role of cholinergic-serotoninergic interactions in cognition has been extensively reviewed Steckler and Sahgal, 1995;Buhot, 1997;Feuerstein and Seeger, 1997;Ruotsalainen et al, 1998;Buhot et al, 2000). The interneuronal, somadendritic, and/or presynaptic location of any 5-HT receptor type mediating an increase in ACh release (and, hence, representing a putative target for pharmacotherapy of Alzheimer's dementia) will be discussed with particular care.…”

Section: A General Aspectsmentioning

confidence: 99%

“…Using neocortical synaptosomes one group has classified the inhibitory presynaptic 5-HT receptor on the cholinergic nerve terminals in the human brain as 5-HT 3 (Maura et al, 1992) (section III.C. ), whereas others studying hippocampal slices claimed that it belongs to the 5-HT 1F subclass (Feuerstein and Seeger, 1997). In the latter study an involvement of 5-HT 1B/1D receptors was excluded by the low potency of 5-CT, which fits better to the pharmacological profile of, e.g., 5-HT 1F receptors.…”

Section: Classification and Development Ofmentioning

confidence: 99%

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5-HT Receptor Regulation of Neurotransmitter Release

Fink¹,

Göthert²

2007

Pharmacol Rev

323

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Section: A General Aspectsmentioning

confidence: 68%

Section: A General Aspectsmentioning

confidence: 99%

Section: Classification and Development Ofmentioning

confidence: 99%

See 1 more Smart Citation

5-HT Receptor Regulation of Neurotransmitter Release

Fink¹,

Göthert²

2007

Pharmacol Rev

323

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“…These methods typically include radio-labeled (usually tritium) precursor loading and electrical or neurochemical depolarization and the subsequent measurement of tritium overflow. For example, electrically-evoked ACh release from human neocortical slices was demonstrated to decrease with age (Feuerstein and Seeger, 1997). Although the nature of the stimuli used in these studies potentially allow the dissociation of effects of different modes of neuronal activity, the available evidence indicates that overflow data obtained from brain tissues from patients, animals modeling disorders and/or treated with drugs, typically have been interpreted as indicating aberrant tonic levels of neurotransmission (eg, Engler et al, 2006;Roberts et al, 2005).…”

Section: Traditional Measures Of Neurotransmitter Release/levels Favomentioning

confidence: 99%

Abnormal Neurotransmitter Release Underlying Behavioral and Cognitive Disorders: Toward Concepts of Dynamic and Function-Specific Dysregulation

Sarter

Bruno

Parikh

2006

Neuropsychopharmacol

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Abnormalities in the regulation of neurotransmitter release and/or abnormal levels of extracellular neurotransmitter concentrations have remained core components of hypotheses on the neuronal foundations of behavioral and cognitive disorders and the symptoms of neuropsychiatric and neurodegenerative disorders. Furthermore, therapeutic drugs for the treatment of these disorders have been developed and categorized largely on the basis of their effects on neurotransmitter release and resulting receptor stimulation. This perspective stresses the theoretical and practical implications of hypotheses that address the dynamic nature of neurotransmitter dysregulation, including the multiple feedback mechanisms regulating synaptic processes, phasic and tonic components of neurotransmission, compartmentalized release, differentiation between dysregulation of basal vs activated release, and abnormal release from neuronal systems recruited by behavioral and cognitive activity. Several examples illustrate that the nature of the neurotransmitter dysregulation in animal models, including the direction of drug effects on neurotransmitter release, depends fundamentally on the state of activity of the neurotransmitter system of interest and on the behavioral and cognitive functions recruiting these systems. Evidence from evolving techniques for the measurement of neurotransmitter release at high spatial and temporal resolution is likely to advance hypotheses describing the pivotal role of neurotransmitter dysfunction in the development of essential symptoms of major neuropsychiatric disorders, and also to refine neuropharmacological mechanisms to serve as targets for new treatment approaches. The significance and usefulness of hypotheses concerning the abnormal regulation of the release of extracellular concentrations of primary messengers depend on the effective integration of emerging concepts describing the dynamic, compartmentalized, and activitydependent characteristics of dysregulated neurotransmitter systems.

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“…Examples are colocalizations with serotonin in the nuclei raphes, with dopamine in the midbrain and striatum, with Á-aminobutyric acid and acetylcholine in the cortex and with corticotropin-releasing hormone in the hypothalamus [1,4]. Examples for direct neuromodulatory effects of SP are the regulation of acetylcholine release in the human cortex [5] and the modulation of noradrenergic neurotransmission in the locus ceruleus [6].…”

mentioning

confidence: 99%

Substance P and Affective Disorders: New Treatment Opportunities by Neurokinin 1 Receptor Antagonists?

et al. 2002

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Substance P (SP) is a neuropeptide which is abundant in the periphery and the central nervous system, where it is colocalized with other neurotransmitters such as serotonin or dopamine. SP has been proposed to play a role in the regulation of pain including migraine and fibromyalgia, asthma, inflammatory bowel disease, emesis, psoriasis as well as in central nervous system disorders. This review summarizes our current knowledge of the role of SP in the pathogenesis of neuropsychiatric disorders with special emphasis on affective disorders including bipolar disorders. It also reviews current treatment approaches with neurokinin 1 receptor antagonists which appear to be promising drugs for the future treatment of affective disorders.

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Modulation of acetylcholine release in human cortical slices: Possible implications for Alzheimer's disease

Cited by 25 publications

References 59 publications

5-HT Receptor Regulation of Neurotransmitter Release

5-HT Receptor Regulation of Neurotransmitter Release

Abnormal Neurotransmitter Release Underlying Behavioral and Cognitive Disorders: Toward Concepts of Dynamic and Function-Specific Dysregulation

Substance P and Affective Disorders: New Treatment Opportunities by Neurokinin 1 Receptor Antagonists?

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