θ-activity-dependent and -independent muscarinic facilitation of long-term potentiation in guinea pig hippocampal slices.

Natsume, Kiyohisa; Kometani, Kaoru

doi:10.1016/s0168-0102(97)01167-x

Cited by 32 publications

(20 citation statements)

References 21 publications

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“…Studies have also established that cholinergic input from the basal forebrain enhances hippocampal plasticity in the form of LTP [1]. Since ERK plays such an important role in other molecular processes, such as LTP, the NGF activation of ERK (especially the rapid effects described in the present study) may not only have trophic effects on cholinergic neurons, but may also play a physiological role in cholinergic neurotransmission in the hippocampus and cerebral cortex, perhaps via the cholinergic role in theta rhythm and thus induction of LTP [21,23,35]. Since hippocampal LTP is diminished in the aged rat [26,30], and cholinergic function plays a role in hippocampal LTP, it is thus feasible that altered NGF signaling, and hence the altered ERK activation, may play a role in age-related memory loss.…”

Section: Mapk Signaling In the Cnsmentioning

confidence: 78%

Age-dependent loss of NGF signaling in the rat basal forebrain is due to disrupted MAPK activation

Williams

Granholm

Sambamurti

2007

Neuroscience Letters

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The loss of Nerve Growth Factor (NGF) and its high affinity receptor TrkA has been implicated in the loss of cholinergic tone and function in Alzheimer's disease (AD) and normal aging. We employed an animal model of aging, the aged rat, which also exhibits memory loss and NGF alterations. Basal forebrain TrkA levels increased after injection of NGF in the hippocampus within one-hour in young rats, but this response was diminished in aged animals as determined by Western blot analysis. Further, NGF activated MAPK pathways without changing total ERK levels and the activation of these pathways was also diminished in aged animals. The exogenous NGF injection did not appear to activate the PI-3K pathway or alter total levels of Akt significantly. These data shed light on mechanisms of NGF signaling in the CNS, and alterations in this signaling cascade associated with age and memory loss. These findings might lead to development of novel treatment therapies for the memory loss associated with AD and other age-associated neurodegenerative diseases.

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Section: Mapk Signaling In the Cnsmentioning

confidence: 78%

Age-dependent loss of NGF signaling in the rat basal forebrain is due to disrupted MAPK activation

Williams

Granholm

Sambamurti

2007

Neuroscience Letters

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“…In addition, ACh has also been shown to suppress glutamatergic transmission (Hounsgaard, 1978b;Hounsgaard, 1978a;Valentino and Dingledine, 1981;Hasselmo and Bower, 1992;Hasselmo and Schnell, 1994;Hasselmo et al, 1995;Levey, 1996;Bouron and Reuter, 1997;Kimura and Baughman, 1997;Patil and Hasselmo, 1999). Paradoxically, it has been shown that when cholinergic suppression of the Schaffer collaterals is strongest is also when induction of LTP in pyramidal dendrites is easiest (Natsume and Kometani, 1997). Therefore, at the point when LTP is most easily induced in pyramidals, ACh also provides presynaptic suppression of recurrent collaterals fibers further biasing the synaptic transmission levels toward allowing greater perforant path synaptic efficacy, and therefore much higher probability of perforant path synaptic activity dominating the induced activity in CA1 pyramidals.…”

Section: Relationship To Other Effects Of Acetylcholinementioning

confidence: 99%

Cholinergic suppression of glutamatergic synaptic transmission in hippocampal region CA3 exhibits laminar selectivity: Implication for hippocampal network dynamics

Kremin¹,

Hasselmo²

2007

Neuroscience

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ACh may help set the dynamics within neural systems to facilitate the learning of new information. Neural models have shown that if new information is encoded at the same time as retrieval of existing information already stored, the memories will interfere with each other. Structures such as the hippocampus have a distinct laminar organization of inputs that allows this hypothesis to be tested. In region CA1 of the rat hippocampus, the cholinergic agonist carbachol (CCh) suppresses transmission in stratum radiatum (SR), at synapses of the Schaffer collateral projection from CA3, while having lesser effects in stratum lacunosum-moleculare (SLM), the perforant path projection from entorhinal cortex (Hasselmo and Schnell, 1994). The current research extends support of this selectivity by demonstrating laminar effects in region CA3. CCh caused significantly greater suppression in SR than in SLM at low concentrations, while the difference in suppression was not significant at higher concentrations. Differences in paired-pulse facilitation suggest pre-synaptic inhibition substantially contributes to the suppression and is highly concentration and stratum dependent. This selective suppression of the recurrent excitation would be appropriate to set CA3 dynamics to prevent runaway modification of the synapses of excitatory recurrent collaterals by reducing the influence of previously stored associations and allowing incoming information from the perforant path to have a predominant influence on neural activity. Keywords perforant path; recurrent collaterals; presynaptic; muscarinic; acetylcholine Acetylcholine (ACh) has been shown to play a vital role in learning and memory ((for a review see Hagan and Morris, 1988;Rasmusson, 2000)). An extensive range of experiments using ACh agonists and antagonists (Davis et al., 1971;Ghoneim and Mewaldt, 1977;Kopelman, 1986;Hagan and Morris, 1988;Whishaw, 1989;Fibiger, 1991) indicate a vital role for ACh in the encoding of new memories. Selective lesions of the primary cholinergic input to the hippocampus using IgG-192 saporin have been shown to influence attention and various aspects of cognitive behavior (Baxter et al., 1997;Janisiewicz et al., 2004), including causing transient impairments of spatial memory function (Vuckovich et al., 2004), but they may not Corresponding Author: 5858 Horton Street, Suite 200, Emeryville, CA 94608, Email: tkremin@gallo.UCSF.edu, . Section Editor: Dr. Geoffrey Schoenbaum Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. always have strong mnemonic effects as some levels of hippocampal ACh may remain (C...

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“…These behavioral eVects could be due to the eVects of acetylcholine (ACh) on a number of cellular neurophysiological properties. For example, activation of muscarinic receptors has been shown to enhance LTP in the CA1 region of the hippocampus (Auerbach & Segal, 1994;Blitzer, Gil, & Landau, 1990) in dentate gyrus (Natsume & Kometani, 1997), and in piriform cortex (Patil, Linster, Lubenov, & Hasselmo, 1998). In addition to this enhancement of LTP, other eVects may also contribute to setting dynamics in the hippocampus appropriate for encoding information (Hasselmo & Schnell, 1994).…”

Section: Introductionmentioning

confidence: 99%

Muscarinic suppression in stratum radiatum of CA1 shows dependence on presynaptic M1 receptors and is not dependent on effects at GABAB receptors

Kremin

Gerber

Giocomo

et al. 2006

Neurobiology of Learning and Memory

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Cholinergic modulation of synaptic transmission is vital to memory processes and may be responsible for setting network dynamics in the hippocampus appropriate for encoding of information. Sheridan and Sutor (1990) found evidence suggesting M1 receptors cause presynaptic inhibition of glutamatergic transmission, while Dutar and Nicoll (1988a) research supports a role of the M2 receptor. We examined muscarinic inhibition of fEPSPs in stratum radiatum of mice lacking m1 subtype receptors (KO) compared to wild type (WT) controls. WT mice exhibit greater suppression of transmission by muscarine as compared to KO in a dose dependent fashion. Oxotremorine shows no signiWcant diVerence in suppression between WT and KO, while MCN-A-343, an M1 agonist, exhibits a signiWcant diVerence between KO and WT, with KO showing no suppression. One hundred micromolar SGS-742, a selective GABA B antagonist, fails to aVect either normal transmission or muscarinic suppression in either WT or KO suggesting that diVerences in suppression between the groups is not attributable to diVerences in GABA B receptor activation due to muscarinic activation of GABAergic interneurons. These Wndings support a role for presynaptic m1 mAChRs in modulation of synaptic transmission in CA1, but indicate that other muscarinic receptor subtypes, such as M2, are also involved in suppression of synaptic potentials. 

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θ-activity-dependent and -independent muscarinic facilitation of long-term potentiation in guinea pig hippocampal slices.

Cited by 32 publications

References 21 publications

Age-dependent loss of NGF signaling in the rat basal forebrain is due to disrupted MAPK activation

Age-dependent loss of NGF signaling in the rat basal forebrain is due to disrupted MAPK activation

Cholinergic suppression of glutamatergic synaptic transmission in hippocampal region CA3 exhibits laminar selectivity: Implication for hippocampal network dynamics

Muscarinic suppression in stratum radiatum of CA1 shows dependence on presynaptic M1 receptors and is not dependent on effects at GABAB receptors

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