Blockade of hippocampal long-term potentiation by saccharin

Morishita, Wade; Xie, Zheng; Chirwa, S.S.; May, P. B. Y.; Sastry, B.R.

doi:10.1016/0306-4522(92)90117-k

Cited by 3 publications

(4 citation statements)

References 27 publications

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“…However, both are referred to as "LTP" in the titles or abstracts of the respective articles. There are also reports of enhanced LTP through caloric restriction (Hori et al 1992) and prevention of LTP induction by the sugar substitute saccharin (Morishita et al 1992) as well as by cocaine (Smith et al 1993). Again, the common denominator linking these observations is the term "long-term potentiation" in the title of the reports.…”

Section: Multiple Definitions Of Ltpmentioning

confidence: 99%

“…Among the dozens of compounds shown to retard the induction of LTP in the hippocampus, only a few directly influence learning, and many others have no effect on learning. For example, saccharin is reported to block the induction of LTP in area CA1 of the hippocampus (Morishita et al 1992), but chronic and acute administration induces no obvious memory deficits, and in some cases enhances retention (Stefurak & van der Kooy 1992). Another study suggesting a dissociation between LTP and learning involved the gene deletion technique.…”

Section: Pharmacological and Genetic Manipulations Of Ltpmentioning

confidence: 99%

“…Another example of confusing synapse and system levels of analysis appears when S&M dismiss LTP as a learning mechanism because the effects of saccharin on a hippocampal slice (Morishita et al 1992) differ from the effects of oral ingestion of saccharin by an intact animal on a task that does not require the hippocampus (Stefurak & van der Kooy 1992).…”

Section: Without Ltp the Learning Circuit Is Brokenmentioning

confidence: 99%

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Long-term potentiation: What's learning got to do with it?

1997

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Long-term potentiation (LTP) is operationally defined as a long-lasting increase in synaptic efficacy following high-frequency stimulation of afferent fibers. Since the first full description of the phenomenon in 1973, exploration of the mechanisms underlying LTP induction has been one of the most active areas of research in neuroscience. Of principal interest to those who study LTP, particularly in the mammalian hippocampus, is its presumed role in the establishment of stable memories, a role consistent with “Hebbian” descriptions of memory formation. Other characteristics of LTP, including its rapid induction, persistence, and correlation with natural brain rhythms, provide circumstantial support for this connection to memory storage. Nonetheless, there is little empirical evidence that directly links LTP to the storage of memories. In this target article we review a range of cellular and behavioral characteristics of LTP and evaluate whether they are consistent with the purported role of hippocampal LTP in memory formation. We suggest that much of the present focus on LTP reflects a preconception that LTP is a learning mechanism, although the empirical evidence often suggests that LTP is unsuitable for such a role. As an alternative to serving as a memory storage device, we propose that LTP may serve as a neural equivalent to an arousal or attention device in the brain. Accordingly, LTP may increase in a nonspecific way the effective salience of discrete external stimuli and may thereby facilitate the induction of memories at distant synapses. Other hypotheses regarding the functional utility of this intensely studied mechanism are conceivable; the intent of this target article is not to promote a single hypothesis but rather to stimulate discussion about the neural mechanisms underlying memory storage and to appraise whether LTP can be considered a viable candidate for such a mechanism.

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Section: Multiple Definitions Of Ltpmentioning

confidence: 99%

Section: Pharmacological and Genetic Manipulations Of Ltpmentioning

confidence: 99%

Section: Without Ltp the Learning Circuit Is Brokenmentioning

confidence: 99%

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Long-term potentiation: What's learning got to do with it?

1997

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“…Earlier studies have recorded the relationship between iron and glutamate. It is reported that microinjection of excitatory amino acids inhibitor into the striatum of brain leads to alterations of iron concentrations in the ipsilateral globus pallidus and substantia nigra pars reticulate [14][15][16]. Our previous data also showed that the iron content was increased in the caudate putamen after microinjection of glutamate into substantia nigra [17].…”

Section: Introductionmentioning

confidence: 87%

Effect of Glutamate on Brain Iron Metabolism and the Regulation Mechanism

Zhang¹,

Di²

2015

J Drug Metab Toxicol

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Glutamate is an excitatory transmitter and can induce neurotoxicity, it can also increase the iron concentrations in the brain, but little is known about the detailed molecular regulation mechanism of iron metabolism by Glu. Based on our previous data, iron metabolism related proteins might be associated with the increase of brain iron contents induced by neurotransmitter. To investigate the issues, the iron contents, non-transferrin-bound iron (NTBI) uptake and the expression of iron uptake and iron release proteins were firstly examined in vivo and in vitro with iron histochemistry, inductively coupled plasma mass spectroscopy (ICP-MS), 55 Fe radioactive liquid scintillation counting and western blot methods. Data showed that glutamate induced the increase of total iron contents, storage iron contents and NTBI uptake activity. Moreover, only divalent metal transporter 1, one of iron uptake proteins, was increased in rat brain and PC12 cells treated with glutamate. Further investigations revealed that nuclear factor кB (NF-кB) and protein kinase C (PKC) were involved in the regulation of DMT1 in PC12 cells treated with glutamate. These findings demonstrate that glutamate increases iron contents in the brain through increased NTBI, and that DMT1 is the key molecule underlying regulation of iron metabolism by glutamate, Furthermore, NF-кB and PKC play important roles in the regulatory pathway of DMT1 expression by glutamate. Thus, it implicates that inhibiting the expression of DMT1 and disruption of its regulation pathway might be effective strategies in attenuating glutamate neurotoxicity through decreased iron contents.

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Presynaptic actions of GABA and baclofen in CA1 region of the guinea-pig hippocampusin vitro

Morishita

Sastry

1994

Neuroscience

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Blockade of hippocampal long-term potentiation by saccharin

Cited by 3 publications

References 27 publications

Long-term potentiation: What's learning got to do with it?

Long-term potentiation: What's learning got to do with it?

Effect of Glutamate on Brain Iron Metabolism and the Regulation Mechanism

Presynaptic actions of GABA and baclofen in CA1 region of the guinea-pig hippocampusin vitro

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