Evidence for synaptic potentiation in a cortical network during learning

Roman, François S.; Stäubli, Ursula; Lynch, Gary

doi:10.1016/0006-8993(87)90089-8

Cited by 170 publications

(105 citation statements)

References 19 publications

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“…Specifically, LTP was evaluated because this form of synaptic plasticity has been implicated in memory formation [116,22,96,132]. Indeed, LTP was impaired in both CA3 and CA1 hippocampal areas of 12-month old rats stressed early in life [31].…”

Section: Disruption Of Ltp Induction Accompanies the Profound Memory mentioning

confidence: 99%

Hippocampal neuroplasticity induced by early-life stress: Functional and molecular aspects

Fenoglio¹,

Brunson²,

Baram³

2006

Frontiers in Neuroendocrinology

192

138

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Whereas genetic factors contribute crucially to brain function, early-life events, including stress, exert long-lasting influence on neuronal function. Here, we focus on the hippocampus as the target of these early-life events because of its crucial role in learning and memory. Using a novel immaturerodent model, we describe the deleterious consequences of chronic early-life 'psychological' stress on hippocampus-dependent cognitive tasks. We review the cellular mechanisms involved and discuss the roles of stress-mediating molecules, including corticotropin releasing hormone, in the process by which stress impacts the structure and function of hippocampal neurons. KeywordsNeonatal; Rat; Human; Stress; Memory; Hippocampus; Corticotropin releasing hormone; CRF; Hypothalamic pituitary adrenal axis; Neuroplasticity Early-life events interact with genetic factors to influence hippocampal function long-termBrain function and dysfunction throughout life are determined by the interaction of genetic factors with 'acquired' environmental events, signals and stimuli [100]. Events that occur early in life are capable of exerting effects that persist throughout adulthood. Here, we focus on the hippocampus as the target of these early-life events because of its crucial role in learning, memory storage and retrieval, and general cognitive function [105,41,65]. Indeed, early-life events, via complex interactions with genetic factors [106,120], have been suspected to be a major determinant of smaller hippocampal volume and long-term cognitive dysfunction in preterm infants [111,17] and may play a role in certain affective and dementing disorders in the adult and aging human [100,26,120]. This review focuses on the mechanisms by which certain early-life events influence populations of hippocampal neurons acutely, and impact the function and integrity of the hippocampus long-term. Studying early-life stress may be used to probe the molecular mechanisms involved in experience-evoked hippocampal neuroplasticityStress may provide a salient example of early-life experience that might exert long-lasting influence on the brain, because (1) over 50% of the world's children are exposed to stress [139] and (2) evidence from both human and animal studies suggests that early-life stress has profound effects on cognitive function and emotional health.Stress has been shown to influence the hippocampus in a number of important ways. Whereas acute mild stress rapidly enhances synaptic efficacy and learning and memory processes [131,45,91,123], chronic or severe activation of the stress response early in life has been shown to be potentially injurious in both humans [6,120,147] and experimental animals [120,31]. For example, severe childhood psychological stress (neglect and abuse) correlates with a higher incidence of learning disabilities later in life, including those learning and memory functions requiring an intact hippocampus [121,50]. Further, MRI studies have suggested that adults subjected to abuse (a measure of chronic stress) ...

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Section: Disruption Of Ltp Induction Accompanies the Profound Memory mentioning

confidence: 99%

Hippocampal neuroplasticity induced by early-life stress: Functional and molecular aspects

Fenoglio¹,

Brunson²,

Baram³

2006

Frontiers in Neuroendocrinology

192

138

View full text Add to dashboard Cite

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“…No neurobiological candidate other than LTP satisfies these requirements for an encoding mechanism. Beyond this, the potentiation effect has a deep relationship with rhythmic patterns of brain activity associated with learning and has been shown to accompany the formation of specific memories (Roman et al, 1987). And, while the issue remains controversial, there is a large literature showing that manipulations that disrupt LTP also interfere with learning (Bliss et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Synaptic plasticity in early aging

Lynch

Rex

Gall

2006

Ageing Research Reviews

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Studies of how aging affects brain plasticity have largely focused on old animals. However, deterioration of memory begins well in advance of old age in animals, including humans; the present review is concerned with the possibility that changes in synaptic plasticity, as found in the long-term potentiation (LTP) effect, are responsible for this. Recent results indicate that impairments to LTP are in fact present by early middle age in rats but only in certain dendritic domains. The search for the origins of these early aging effects necessarily involves ongoing analyses of how LTP is induced, expressed, and stabilized. Such work points to the conclusion that cellular mechanisms responsible for LTP are redundant and modulated both positively and negatively by factors released during induction of potentiation. Tests for causes of the localized failure of LTP during early aging suggest that the problem lies in excessive activity of a negative modulator. The view of LTP as having redundant and modulated substrates also suggests a number of approaches for reversing age-related losses. Particular attention will be given to the idea that induction of brain-derived neurotrophic factor, an extremely potent positive modulator, can be used to provide long periods of normal plasticity with very brief pharmacological interventions. The review concludes with a consideration of how the selective, regional deficits in LTP found in early middle age might be related to the global phenomenon of brain aging. #

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“…LTP is elicited in the piriform cortex only when patterned electrical stimulation, applied to the lateral olfactory tract (LOT), and reward were associated in a learning context. 35 In previous studies, Roman et al 36 showed that LTP in the piriform cortex was gradual and appeared only when there was significant discrimination between the two cues (in this case, patterned stimulation versus natural odor). The authors found a positive correlation between the improvement in behavioral performance and the increase in the slope of the monosynaptic responses recorded in the olfactory cortex.…”

mentioning

confidence: 98%

“…Although most of the LTP research focuses on the hippocampus, the phenomenon is not specific to this structure. Many studies have reported expression of LTP in different parts of the mammalian brain, including the prefrontal cortex, 24 visual cortex, 1 piriform (olfactory) cortex, 35,36,40 superior colliculus 32 and olfactory bulb. 12 In vivo and in vitro studies have shown that patterned electrical stimulations alone are able to elicit LTP in the hippocampus and in many other brain areas.…”

mentioning

confidence: 99%