Synaptic plasticity in the hippocampus during afferent activation reproducing the pattern of the theta rhythm (theta plasticity)

Am, Kleshchevnikov

doi:10.1007/bf02465325

Cited by 11 publications

(5 citation statements)

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“…Input frequencies in hippocampal networks are determined in large part by population oscillatory events. Theta (4–12 Hz) oscillations are present in local field potential recordings collected from the hippocampus of adult animals while they explore and solve mazes and have been shown to have a role in synaptic plasticity ( Kleshchevnikov, 1999 ) and learning and memory ( Buzsáki, 2005 , Hasselmo and Stern, 2014 ). Stimulation patterns set to mimic APs riding on an endogenous theta wave, i.e.…”

Section: Late Postnatal Changes In Network Oscillations and Excitabilmentioning

confidence: 99%

“…Theta power is reduced relative to more mature animals and CA1 pyramidal neurons do not burst. The result is an increased proclivity to induce LTD during bouts of theta ( Kleshchevnikov, 1999 ). (C) An illustration of a filtered EEG trace recorded in area CA1 of the hippocampus at 30 days of age.…”

Section: Developmental Changes In Metaplasticity Align With Hippocampmentioning

confidence: 99%

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Multiple forms of metaplasticity at a single hippocampal synapse during late postnatal development

McHail

Dumas

2015

Developmental Cognitive Neuroscience

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Metaplasticity refers to adjustment in the requirements for induction of synaptic plasticity based on the prior history of activity. Numerous forms of developmental metaplasticity are observed at Schaffer collateral synapses in the rat hippocampus at the end of the third postnatal week. Emergence of spatial learning and memory at this developmental stage suggests possible involvement of metaplasticity in the final maturation of the hippocampus. Three distinct metaplastic phenomena are apparent. (1) As transmitter release probability increases with increasing age, presynaptic potentiation is reduced. (2) Alterations in the composition and channel conductance properties of AMPARs facilitate the induction of postsynaptic potentiation with increasing age. (3) Low frequency stimulation inhibits subsequent induction of potentiation in animals older but not younger than 3 weeks of age. Thus, many forms of plasticity expressed at SC-CA1 synapses are different in rats younger and older than 3 weeks of age, illustrating the complex orchestration of physiological modifications that underlie the maturation of hippocampal excitatory synaptic transmission. This review paper describes three late postnatal modifications to synaptic plasticity induction in the hippocampus and attempts to relate these metaplastic changes to developmental alterations in hippocampal network activity and the maturation of contextual learning.

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Section: Late Postnatal Changes In Network Oscillations and Excitabilmentioning

confidence: 99%

Section: Developmental Changes In Metaplasticity Align With Hippocampmentioning

confidence: 99%

Multiple forms of metaplasticity at a single hippocampal synapse during late postnatal development

McHail

Dumas

2015

Developmental Cognitive Neuroscience

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“…In the present study we found a decrease in mechanical threshold and increase in number of action potentials produced by threshold and suprathreshold stimulation in rats consuming alcohol, but not in ddC-treated rats. The increase in number of short ISIs, in response to both threshold and suprathreshold mechanical stimulation, in alcohol fed rats, will increase temporal summation in postsynaptic spinal dorsal horn neurons; increasing the range of ISIs, near 100 ms, as observed in rats consuming alcohol, causes greater temporal summation of C-fiber-evoked excitatory postsynaptic currents in dorsal horn neurons [35], and in the same range of ISIs, temporal summation of afferent activity appears to be an important factor in human pain perception [36–41].…”

Section: Discussionmentioning

confidence: 99%

Mechanically-Evoked C-Fiber Activity in Painful Alcohol and AIDS Therapy Neuropathy in the Rat

Chen

Levine

2007

Mol Pain

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While altered activities in sensory neurons were noticed in neuropathic pain, caused by highly diverse insults to the peripheral nervous system, such as diabetes, alcohol ingestion, cancer chemotherapy and drugs used to treat AIDS, other infections and autoimmune diseases, as well as trauma, our understanding of how these various peripheral neuropathies manifest as altered neuronal activity is still rudimentary. The recent development of models of several of those neuropathies has, however, now made it possible to address their impact on primary afferent nociceptor function. We compared changes in mechanically-evoked C-fiber activity, in models of painful peripheral neuropathy induced by drinking ethanol (alcohol) or administering 2',3'-dideoxycytidine (ddC), a nucleoside reverse transcriptase inhibitor for AIDS therapy, two comorbid conditions in which pain is thought to be mediated by different second messenger signaling pathways. In C-fiber afferents, ddC decreased conduction velocity. In contrast, alcohol but not ddC caused enhanced response to mechanical stimulation (i.e., decrease in threshold and increase in response to sustained threshold and supra-threshold stimulation) and changes in pattern of evoked activity (interspike interval and action potential variability analyses). These marked differences in primary afferent nociceptor function, in two different forms of neuropathy that produce mechanical hyperalgesia of similar magnitude, suggest that optimal treatment of neuropathic pain may differ depending on the nature of the causative insult to the peripheral nervous system, and emphasize the value of studying co-morbid conditions that produce painful peripheral neuropathy by different mechanisms.

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“…We would add to this discussion the idea that novelty-or stress-induced depotentiation and LTD reflect active memory reversal processes, which can involve CaMKII, NCAM and cytokine actions (discussed above), as well as activation of b-adrenergic receptors, the amygdala (Katsuki et al, 1997;Nakao et al, 2004), and glutamate (NMDA) receptor activity (Nicoll et al, 1998;Kemp et al, 2000;Mockett et al, 2002;Villarreal et al, 2002;Daoudal and Debanne, 2003;Kosub et al, 2005). The depotentiation process, which can be triggered by exploration-related (theta) activity (Staubli and Lynch, 1990;Larson et al, 1993;Staubli and Chun, 1996;Holscher et al, 1997;Scafidi, 1997, 1999;Kleshchevnikov, 1999;Hyman et al, 2003), would reverse hippocampal plasticity that had been induced by recent learning experiences. This process is adaptive because when previously induced plasticity is ''reset'' to a depotentiated state by exploration, novelty, or a stressful experience, the hippocampus can then generate a representation of the new experience via the induction of endogenous LTP on a ''refreshed'' or ''uncluttered'' baseline state of plasticity.…”

Section: Does Stress Induce An Endogenous Form Of Ltd/depotentiation?mentioning

confidence: 94%

Competitive interactions between endogenous LTD and LTP in the hippocampus underlie the storage of emotional memories and stress-induced amnesia

et al. 2005

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ABSTRACT:This speculative review serves two purposes. First, it as an extension of the ideas we developed in a previous review (Diamond et al., Hippocampus, 2004;14:281-291), and second, it is a rebuttal to Abraham's (Hippocampus, 2004;14:675-676) critique of that review. We had speculated on the functional significance of the finding that post-training LTP induction produces retrograde amnesia. We noted the similarities between the findings that strong tetanizing stimulation can produce LTP and retrograde amnesia, and that a strong emotional experience can produce a long-lasting memory and retrograde amnesia, as well. The commonalities between LTP induction and emotional learning provided the basis of our hypothesis that an emotional experience generates endogenous LTD/depotentiation, which reverses synaptic plasticity formed during previous learning experiences, and endogenous LTP, which underlies the storage of new information. Abraham raised several concerns with our review, including the criticism that our speculation ''falters because there is no evidence that stress causes LTD or depotentiation,'' and that research on stress and hippocampus has ''failed to report any LTP-like changes.'' Abraham's points are well-taken because stress, in isolation, does not appear to generate long-lasting changes in baseline measures of hippocampal excitability. Here, within the context of a reply to Abraham's critique, we have provided a review of the literature on the influence of stress, novelty, fear conditioning, and the retrieval of emotional memories on cognitive and physiological measures of hippocampal functioning. An emphasis of this review is our hypothesis that endogenous forms of depotentiation, LTD and LTP are generated only when arousing experiences occur in conjunction with memory-related activation of the hippocampus and amygdala. We conclude with speculation that interactions among the different forms of endogenous plasticity underlie a form of competition by synapses and memories for access to retrieval resources. V V C 2005 Wiley-Liss, Inc.

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Synaptic plasticity in the hippocampus during afferent activation reproducing the pattern of the theta rhythm (theta plasticity)

Cited by 11 publications

References 70 publications

Multiple forms of metaplasticity at a single hippocampal synapse during late postnatal development

Multiple forms of metaplasticity at a single hippocampal synapse during late postnatal development

Mechanically-Evoked C-Fiber Activity in Painful Alcohol and AIDS Therapy Neuropathy in the Rat

Competitive interactions between endogenous LTD and LTP in the hippocampus underlie the storage of emotional memories and stress-induced amnesia

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