Involvement of M2 receptor in an enhancement of long-term potentiation by carbachol in Schaffer collateral-CA1 synapses of hippocampal slices

Shimoshige, Yukinori; Maeda, Takehiko; Kaneko, Shuji; Akaike, Akinori; Satoh, Masamichi

doi:10.1016/s0168-0102(96)01147-9

Cited by 39 publications

(22 citation statements)

References 18 publications

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“…Several in vitro studies have demonstrated a cholinergic enhancement of hippocampal LTP using cholinergic agonists or AChE inhibitors [21,23,83]. In anesthetized rats, hippocampal LTP facilitated by tetanic stimulation of the MS was blocked by systemic administration of cholinergic antagonists [24,25] and MS tetanus delivered longer than 5 min before hippocampal LTP induction will not potentiate hippocampal responses [25].…”

Section: Septohippocampal Cholinergic Modulation Of Ltpmentioning

confidence: 99%

“…LTP was first described in the hippocampus of anesthetized and behaving animals [19,20], and there has been much evidence that acetylcholine modulates hippocampal LTP. Application of the cholinergic agonists enhanced hippocampal LTP in vitro [21][22][23]. In anesthetized rats, hippocampal LTP was facilitated by tetanic stimulation of the MS, and this facilitation was blocked by systemic administration of cholinergic antagonists [24,25].…”

Section: Introductionmentioning

confidence: 97%

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Vestibular stimulation enhances hippocampal long-term potentiation via activation of cholinergic septohippocampal cells

Tai

Leung

2012

Behavioural Brain Research

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Section: Septohippocampal Cholinergic Modulation Of Ltpmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

Vestibular stimulation enhances hippocampal long-term potentiation via activation of cholinergic septohippocampal cells

Tai

Leung

2012

Behavioural Brain Research

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“…The hippocampus expresses all five mAChR subtypes (Levey et al, 1995;Fisahn et al, 2002), in which they modulate various ionic channels and regulate excitability of neurons (for review, see Nicoll et al, 1990). Application of mAChR agonists to hippocampal slices produces network oscillations (Huerta and Lisman, 1993;Fisahn et al, 1998Fisahn et al, , 2002, which modulate the induction of hippocampal long-term potentiation (LTP) (Williams and Johnston, 1988;Huerta and Lisman, 1993;Shimoshige et al, 1997), a cellular model for learning and memory in the vertebrate CNS (for review, see Lynch, 2004), and oscillations in the whole animal are considered to reflect learning processes (Winson, 1978). In fact, malfunction of the cholinergic system in some mental disorders causes memory impairment (Blokland, 1996).…”

Section: Introductionmentioning

confidence: 99%

“…Relatively high concentrations of mAChR agonists were used in previous studies (Huerta and Lisman, 1993;Auerbach and Segal, 1996;Shimoshige et al, 1997); however, neural activities in physiological conditions would never raise local ACh concentrations to such a high level in the intact brain, partly because there exist cholinesterase enzymes and ACh is markedly susceptible to hydrolysis by the enzymes. Conversely, most of the cholinergic agonists used in previous studies, such as carbachol [carbamoylcholine (CCh)] or bethanechol (carbamoyl-␤-methylcholine), are completely resistant to hydrolysis by cholinesterase and have far longer duration of actions than ACh.…”

Section: Introductionmentioning

confidence: 99%

Modulation of Synaptic Plasticity by Physiological Activation of M₁Muscarinic Acetylcholine Receptors in the Mouse Hippocampus

Shinoe¹,

Matsui²,

Taketo³

et al. 2005

J. Neurosci.

234

179

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The muscarinic acetylcholine receptor (mAChR) has been considered one of the neurotransmitter receptors regulating hippocampal synaptic plasticity, which likely plays a critical role in learning and memory. In previous studies, however, muscarinic agonists were used at relatively high concentrations, and the subtype selectivity of muscarinic antagonists was not satisfactory. Thus, it remains to be answered whether physiological levels of ACh are involved in the regulation of synaptic plasticity and which mAChR subtypes are responsible for such effects. We found in this study that a low concentration (50 nM) of carbachol enhanced long-term potentiation (LTP) of excitatory synaptic transmission in mouse hippocampal slices. Notably, this enhancing effect was abolished in M 1 mAChR knock-out (KO) but not in M 3 mAChR KO mice, although LTP itself was intact in both mutant mice. Furthermore, we found that repetitive stimulation in the stratum oriens, which presumably triggered the release of endogenous ACh from cholinergic terminals, could enhance LTP in wild-type mice but not in M 1 mAChR KO mice. These results suggest that physiologically released ACh from cholinergic fibers modulates hippocampal synaptic plasticity through the postsynaptic M 1 mAChR activation.

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“…It has been shown that muscarinic receptor stimulation can induce LTP at the Schaffer collateral-CA1 synapses. This muscarinic-induced LTP (LTPm) resembles LTP produced by tetanic stimulation (Marchi and Raitieri 1989;Blitzer et al 1990;Markram and Segal 1990;Shimoshige et al 1997). With this background, the aim of this study was to investigate the effect of PACAP-38 in the hippocampus, the brain region that has been long known to be essential for learning and memory (Abel and Kandel 1998).…”

mentioning

confidence: 99%

PACAP-38 Enhances Excitatory Synaptic Transmission in the Rat Hippocampal CA1 Region

Roberto¹,

Brunelli²

2000

Learn. Mem.

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Specific receptors for pituitary adenylate cyclase-activating polypeptide (PACAP), a novel peptide with neuroregulatory and neurotrophic functions, have been identified recently in different brain regions, including the hippocampus. In this study, we examined the effects of PACAP-38 on the excitatory postsynaptic field potentials (fEPSPs) evoked at the Schaffer collateral-CA1 synapses. Brief bath application of PACAP-38 (0.05 nM) induced a long-lasting facilitation of the basal transmission. Enhancement of this response was occluded in part by previous high-frequency-induced long-term potentiation (LTP). PACAP-38 did not significantly alter the paired-pulse facilitation (PPF). PACAP-38 has been shown to have a presynaptic effect on the septohippocampal cholinergic terminals, which results in an increase in basal acetylcholine (ACh) release. To assess whether the PACAP-38 enhancement of CA1 synapses was related to the activation of the cholinergic system we examined the effect of this peptide in the presence of atropine, a muscarinic receptor antagonist. The enhancement of the fEPSPs by PACAP-38 was blocked by bath application of atropine. These results show that PACAP-38 induces facilitation of hippocampal synaptic transmission through activation of the cholinergic system via the muscarinic receptors.Pituitary adenylate cyclase-activating polypeptide (PACAP) is a new member of a neuropeptide family that includes vasoactive intestinal peptide (VIP), glucagon, secretin, and growth hormone, and whose members are thought to play an important role in neuronal function (Miyata et al. 1989; Arimura 1998). PACAP has been isolated from the ovine hypothalamus on the basis of its ability to stimulate adenylate cyclase in rat anterior pituitary cells (Miyata et al. 1989) and it is present in the central nervous system (CNS) and in a variety of peripheral tissues (Masuo et al. 1992;Arimura and Shioda 1995;Shioda et al. 1997). Two distinct forms of this neuropeptide, PACAP-38 and PACAP-27, with 38 or 27 amino acids, respectively, have been characterized (Arimura and Shioda 1995). PACAP-38 and PACAP-27 possess similar biological activity (Miyata et al. 1990). PACAP-38 is the prevailing form in mammalian tissues (Arimura 1992). The amino-acid sequence of PACAP-38 is well-preserved in different species and is identical in sheep, rats, and humans (Arimura 1992). Two types of high-affinity PACAP receptors have been identified: The PACAP type-I receptor (PACAPRI), which specifically binds PACAP-38 and PACAP-27 with higher affinity than it binds VIP; and the PACAP type-II receptor (PACAPRII), which has high homology with the VIP receptor and binds PACAP-38, PACAP-27, and VIP with the same high affinity (Arimura 1992;Sokolov and Kleschevnikov 1995). PACAPRI is mainly distributed in the CNS, including the septum, hippocampus, cerebellar cortex, amygdala, nucleus accumbens, hypothalamus, and the entorhinal cortices (Masuo et al. 1992(Masuo et al. ,1993 and it is positively coupled to adenylate cyclase and phospholipase C, whereas PACA...

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Involvement of M2 receptor in an enhancement of long-term potentiation by carbachol in Schaffer collateral-CA1 synapses of hippocampal slices

Cited by 39 publications

References 18 publications

Vestibular stimulation enhances hippocampal long-term potentiation via activation of cholinergic septohippocampal cells

Vestibular stimulation enhances hippocampal long-term potentiation via activation of cholinergic septohippocampal cells

Modulation of Synaptic Plasticity by Physiological Activation of M₁Muscarinic Acetylcholine Receptors in the Mouse Hippocampus

PACAP-38 Enhances Excitatory Synaptic Transmission in the Rat Hippocampal CA1 Region

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Involvement of M2 receptor in an enhancement of long-term potentiation by carbachol in Schaffer collateral-CA1 synapses of hippocampal slices

Cited by 39 publications

References 18 publications

Vestibular stimulation enhances hippocampal long-term potentiation via activation of cholinergic septohippocampal cells

Vestibular stimulation enhances hippocampal long-term potentiation via activation of cholinergic septohippocampal cells

Modulation of Synaptic Plasticity by Physiological Activation of M1Muscarinic Acetylcholine Receptors in the Mouse Hippocampus

PACAP-38 Enhances Excitatory Synaptic Transmission in the Rat Hippocampal CA1 Region

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Modulation of Synaptic Plasticity by Physiological Activation of M₁Muscarinic Acetylcholine Receptors in the Mouse Hippocampus