Synaptic enhancement in fascia dentata: Cooperativity among coactive afferents

McNaughton, B. L.; Douglas, R. M.; Goddard, Graham V.

doi:10.1016/0006-8993(78)90030-6

Cited by 621 publications

(252 citation statements)

References 52 publications

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“…1C, F) vs. the previous HFS in which LTP was saturated (E, 24.6 Ϯ 5.8% vs. Ϫ0.3 Ϯ 2.2% [mean Ϯ SEM], n ϭ 8, P ϭ 0.0027, t test). These results are surprising considering that this paradigm biases against additional LTP: decreasing the pEPSP size used for the last HFS decreases cooperativity and thereby should decrease the LTP elicited (29). These results are similar, however, to the finding that LTP could not be elicited when p was large, but could be elicited after it was decreased (30).…”

Section: Resultsmentioning

confidence: 75%

Long-term potentiation involves increases in the probability of neurotransmitter release

Schulz

1997

Proc. Natl. Acad. Sci. U.S.A.

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Biochemistry. In the article ''Identification by mass spectrometry of the phosphorylated residue responsible for activation of the catalytic domain of myosin I heavy chain kinase, a member of the PAK͞STE20 family'' by Joanna Szczepanowska, Xiaolong Zhang, Christopher J. Herring, Jun Qin, Edward D. Korn, and Hanna Brzeska, which appeared in number 16, August 5, 1997, of Proc. Natl. Acad. Sci. USA (94,(8503)(8504)(8505)(8506)(8507)(8508), the authors wish to note that in Fig. 3, the ions of m͞z 1345.3 and 1247.1 were incorrectly identified as b 13 and b 13 ⌬ , respectively, produced by cleavage of the peptide AS(Pi)VVGTTYW-MAPEVVK between E and V (Fig. 3 Inset). In fact, these ions are b 12 and b 12 ⌬ , produced by cleavage of the peptide between P and E. This correction has no effect on the conclusion that the phosphorylated residue is serine. Also, in Table 2, reference numbers 22-24 should be 21-23 (the reference in the legend is cited correctly) and the MIHCK sequence is from residue 624 to residue 638.Cell Biology. In the article ''Subtraction hybridization identifies a transformation progression-associated gene PEG-3 with sequence homology to a growth arrest and DNA damageinducible gene'' by Zao

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Section: Resultsmentioning

confidence: 75%

Long-term potentiation involves increases in the probability of neurotransmitter release

Schulz

1997

Proc. Natl. Acad. Sci. U.S.A.

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“…I also will not discuss at any length the phenomenon of long-term potenriation, or enhancement (L@mo, 1966;Bliss and L@mo, 1973;McNaughton et al, 1978; and many hundreds of others in the years since), the best current example of a neurophysiologically plausible candidate for memory that has proven to be most easily elicited in the hippocampal formation. I consider the existence of LTPiE to be a relatively strong indicator that the hippocampus is involved in memory, but, alone, it is not sufficient to prove the case.…”

Section: The Hippocampus As a Spatial Memory Systemmentioning

confidence: 99%

The hippocampus and space revisited

1991

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The hippocampal formation has long been the focus of intense interest among neuroscientists. The discovery by Scoville and Milner (1957) that the mesial temporal lobe, including the hippocampal formation, played a central role in memory function in humans can be said to have started the modern era of research on this brain system. There followed two decades of animal research aimed at creating experimental models of the memory defects observed in humans, including my dissertation research, which met with scant success (Nadel, 1968). Indeed, when John O'Keefe and I started considering the hippocampus and its possible role in spatial mapping several years later, one of our greatest challenges was to analyze the extant lesion literature in terms of this theory with the minimum amount of special pleading. There were already several hundred such studies, varying extensively in terms of exact size and regional location of the lesion, the means by which the lesion had been created, the kind of animal used, the nature of the task, the kind of motivation employed, and so on. Yet, it was our feeling in 1976, when we terminated the review of the lesion literature, which was ultimately published in The Hippocumpiis CIS a Cognitive Map (O'Keefe and Nadel, 1978), that the spatial hypothesis successfully handled the vast preponderance of these lesion studies as well as what was then known about the physiology of the hippocampal formation.In the years following publication of the book, most published lesion studies were concerned in some way with the spatial map hypothesis; most often, comparisons with rival hypotheses were involved. This was a frustrating period because, although many thought they were testing our ideas, too frequently the major themes we hoped to stress were misconstrued. In this article I dig back into the book we published in 1978 and reiterate some of the themes that were important to us then, and remain so now. By so doing, 1 hope to bring out some of the reasons why we thought, and continue to think, that space is so special as to warrant a structure as compelling as the hippocampal formation.I will concentrate on three major issues. First, I will discuss at some length the fact that our theory was about a ~p a t i a l memory system, not simply a "spatial" system. Second, Iwill discuss our assumption that the spatial memory system we allocated to the hippocampus was but one of many spatial systems, and that the role of these various systems can best be understood if one takes into consideration an animal's behavior in its natural habitat. Third, I will briefly discuss our view that in the human hippocampus, at least in the left hemisphere, the mapping system represents something more abstract than physical space.Before turning to these substantive points, however, a brief digression into methods and first principles is in order. Some years before the book was published, O'Keefe and I published a paper (Nadel and O'Keefe, 1974) in which we presented some of the reasons for hypothesizing that the hippocamp...

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“…Cooperativity between afferents in producing LLP has previously been demonstrated in various regions of the hippocampus (Lee, 1983;Levy and Steward, 1979;McNaughton et al, 1978). Such effects have been observed also in the presence of GABA antagonists, suggesting that they can be unrelated to changes in inhibitory pathways (Barrionuevo and Brown, 1983;Wigstrijm and Gustafsson, 1983~).…”

Section: Discussionmentioning

confidence: 89%

Hippocampal long-lasting potentiation produced by pairing single volleys and brief conditioning tetani evoked in separate afferents

Gustafsson¹,

Wigström²

1986

J. Neurosci.

156

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Cooperative effects between afferents on the induction of longlasting potentiation (LLP) of synaptic transmission were examined in the CA1 region of the hippocampal slice preparation. Synaptic activity was recorded extracellularly in the dendritic layer (stratum radiatum) as a field EPSP, and the amount of LLP produced was measured from the change in slope of the rising phase of this potential. Experiments were performed with the GABA antagonist picrotoxin in the bath solution in order to facilitate the induction of LLP. It is shown that under these conditions a test input evoked by single volleys (at 0.2 Hz) is potentiated when paired with brief tetani (2-15 impulses at 50 Hz) to a separate population of fibers in the stratum radiatum. For this potentiation to appear, the test input had to occur during the train or precede it by less than 40 msec. Maximal effects were observed with the test volley positioned in the early part of the tetanus, and were largely independent of train duration. The potentiation obtained in this manner reached a peak level after some 20 conjunction events, and its magnitude measured 10 min after conjunction was about half that which could be induced by homosynaptic tetanization. Prior homosynaptic potentiation occluded the potentiation induced by conjunction, suggesting an identity of their underlying mechanisms. A test input to the apical dendritic layer was potentiated also by inputs to the basal dendritic layer, although greater effects were observed with both inputs in the same dendritic layer. It is suggested that the conditioning effect is related to the postsynaptic depolarization created by the tetanus. The results support the recent proposal that LLP is induced by ionic flux through voltage-dependent synaptic channels.In the hippocampus, tetanic activation of afferents leads to a very prolonged increase in synaptic efficacy, known as longlasting potentiation (LLP) (Bliss and Gardner-Medwin, 1973;Bliss and Lomo, 1973;Douglas and Goddard, 1975;Lomo, 1966). Even though considerable work has been devoted to finding the mechanism(s) underlying LLP, this question is still unsettled, and there is even controversy whether the actual modification takes place on the pre-or postsynaptic side (e.g., see Dolphin et al., 1982;Douglas et al., 1982;Lynch et al., 1983; Skrede and Malthe-Sorenssen, 198 1; see also Bliss and Dolphin, 1982).Under normal conditions, LLP is induced by long stimulus trains giving rise to considerable activity in both presynaptic terminals and postsynaptic cells. It has recently been shown, however, that the induction of LLP is greatly facilitated when

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Synaptic enhancement in fascia dentata: Cooperativity among coactive afferents

Cited by 621 publications

References 52 publications

Long-term potentiation involves increases in the probability of neurotransmitter release

Long-term potentiation involves increases in the probability of neurotransmitter release

The hippocampus and space revisited

Hippocampal long-lasting potentiation produced by pairing single volleys and brief conditioning tetani evoked in separate afferents

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