Acetylcholinesterase induces long-term potentiation in CA1 pyramidal cells by a mechanism dependent on metabotropic glutamate receptors

Appleyard, Margaret E.

doi:10.1016/0304-3940(95)11491-e

Cited by 30 publications

(11 citation statements)

References 24 publications

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“…This action has been shown to be independent of its esterase activity but dependent on direct action of AChE on metabotropic glutamate receptors. Comparable activity of BuChE was not observed (Appleyard, 1995). The distribution of BuChE in the central nervous system varies from species to species.…”

Section: Cholinergic Neurotransmissionmentioning

confidence: 92%

“…For example, infusion of AChE into guinea pig hippocampal slices induces long-term potentiation in the neurons (Appleyard, 1995). This action has been shown to be independent of its esterase activity but dependent on direct action of AChE on metabotropic glutamate receptors.…”

Section: Cholinergic Neurotransmissionmentioning

confidence: 99%

“…It has been suggested that AChE may have functions independent of its enzymatic activity (Greenfield, 1991;Appleyard, 1992Appleyard, , 1995. For example, infusion of AChE into guinea pig hippocampal slices induces long-term potentiation in the neurons (Appleyard, 1995).…”

Section: Cholinergic Neurotransmissionmentioning

confidence: 99%

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Distribution of butyrylcholinesterase in the human amygdala and hippocampal formation

1998

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The distribution of the major cholinergic regulatory enzyme acetylcholinesterase (AChE, EC 3.1.1.7) has been extensively studied in the human brain, but the distribution of the closely related enzyme butyrylcholinesterase (BuChE, EC 3.1.1.8) is largely unknown. Because of the importance of BuChE and AChE in Alzheimer's disease, we have studied the distribution of BuChE in the normal human amygdala and hippocampal formation and compared it with that of AChE by using histochemical techniques. In the amygdala, the distribution of BuChE differed significantly from that of AChE in that BuChE was found primarily in neurons and their dendritic processes, whereas AChE was found predominantly in the neuropil. BuChE-positive neurons were present in up to 10% of the neuronal profiles in lateral, basolateral (basal), basomedial (accessory basal), central, cortical, and medial amygdaloid nuclei. AChE was found primarily in the neuropil in these nuclei with only a few AChE-positive neurons. In the hippocampal formation, BuChE was also found in neurons and not in the neuropil, whereas AChE was found in both neurons and in the neuropil. BuChE and AChE neurons were present in the polymorphic layer of the dentate gyrus, as well as the stratum oriens and stratum pyramidale of the hippocampus proper. There was considerable overlap in shapes, sizes, and numbers of BuChE- and AChE-positive neurons, suggesting that the enzymes were colocalized in neurons of the hippocampal formation. The distinct distribution of BuChE suggests that it may have specific functions including coregulation of cholinergic and noncholinergic neurotransmission in human amygdala and hippocampal formation.

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Section: Cholinergic Neurotransmissionmentioning

confidence: 92%

Section: Cholinergic Neurotransmissionmentioning

confidence: 99%

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Distribution of butyrylcholinesterase in the human amygdala and hippocampal formation

1998

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“…Moreover, the dopamine neurons from substantia nigra pars compacta when stimulated are known to release AChE in a neurotransmitter-like fashion along with dopamine [56]. AChE is also known to induce long-term potentiation (LTP) in pyramidal cells of the hippocampus, by a mechanism dependent on metabotropic glutamate receptors [55,57].…”

Section: Restoration Of Stress-induced Decrease In the Levels Of Neurmentioning

confidence: 99%

Self-Stimulation Rewarding Experience Restores Stress-Induced CA3 Dendritic Atrophy, Spatial Memory Deficits and Alterations in the Levels of Neurotransmitters in the Hippocampus

et al. 2007

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Chronic restraint stress causes spatial learning and memory deficits, dendritic atrophy of the hippocampal pyramidal neurons and alterations in the levels of neurotransmitters in the hippocampus. In contrast, intracranial self-stimulation (ICSS) rewarding behavioral experience is known to increase dendritic arborization, spine and synaptic density, and increase neurotransmitter levels in the hippocampus. In addition, ICSS facilitates operant and spatial learning, and ameliorates fornix-lesion induced behavioral deficits. Although the effects of stress and ICSS are documented, it is not known whether ICSS following stress would ameliorate the stress-induced deficits. Accordingly, the present study was aimed to evaluate the role of ICSS on stress-induced changes in hippocampal morphology, neurochemistry, and behavioral performance in the T-maze. Experiments were conducted on adult male Wistar rats, which were randomly divided into four groups; normal control, stress (ST), self-stimulation (SS), and stress + self-stimulation (ST + SS). Stress group of rats were subjected to restraint stress for 6 h daily over 21 days, SS group animals were subjected to SS from ventral tegmental area for 10 days and ST + SS rats were subjected to restraint stress for 21 days followed by 10 days of SS. Interestingly, our results show that stress-induced behavioral deficits, dendritic atrophy, and decreased levels of neurotransmitters were completely reversed following 10 days of SS experience. We propose that SS rewarding behavioral experience ameliorates the stress-induced cognitive deficits by inducing structural and biochemical changes in the hippocampus.

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“…38 It has also been reported that secreted AChEs potentiate synaptic responses evoked in guinea pig hippocampus. 3 The aim of this present study was to investigate the diverse effect of carbamate ChEIs on carbacholstimulated muscular nAChR functions on TE671 cell line. The human rhabdomyosarcoma-derived cell line, TE671, is rich in fetal type muscular nAChRs, 24 and convenient to handle.…”

mentioning

confidence: 99%

Anticholinesterase induces nicotinic receptor modulation

Sung¹,

Kim²,

Lee

et al. 1998

Muscle Nerve

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Acetylcholinesterase induces long-term potentiation in CA1 pyramidal cells by a mechanism dependent on metabotropic glutamate receptors

Cited by 30 publications

References 24 publications

Distribution of butyrylcholinesterase in the human amygdala and hippocampal formation

Distribution of butyrylcholinesterase in the human amygdala and hippocampal formation

Self-Stimulation Rewarding Experience Restores Stress-Induced CA3 Dendritic Atrophy, Spatial Memory Deficits and Alterations in the Levels of Neurotransmitters in the Hippocampus

Anticholinesterase induces nicotinic receptor modulation

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