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Selective impairment of learning and blockade of long-term potentiation by an N-methyl-D-aspartate receptor antagonist, AP5
TLDR
It is reported that chronic intraventricular infusion of D, L-AP5 causes a selective impairment of place learning, which is highly sensitive to hippocampal damage7, without affecting visual discrimination learning,which is not8 and suggest that NMDA receptors are involved in spatial learning, and add support to the hypothesis that LTP is involved in some, but not all, forms of learning. Expand
Intracellular injections of EGTA block induction of hippocampal long-term potentiation
TLDR
It is reported that intracellular injections of the calcium chelator EGTA block the development of LTP and this results strongly suggest that LTP is caused by a modification of the postsynaptic neurone and that its induction depends on the level of free calcium. Expand
Patterned stimulation at the theta frequency is optimal for the induction of hippocampal long-term potentiation
TLDR
The results indicate that patterns of stimulation resembling spike discharge patterns of hippocampal neurons in animals in exploratory situations are effective in inducing LTP and suggest temporal constraints on the mechanisms involved in triggering synaptic plasticity. Expand
The neurobiology of learning and memory
TLDR
Current progress and emerging concepts derived from the simple system approach using animal models are discussed. Expand
Heterosynaptic depression: a postsynaptic correlate of long-term potentiation
TLDR
It was found that potentiation of one afferent tended to depress the target cell's responses to a second test input, and theories of long-term potentiation which have evolved from work on invertebrate and neuromusclar preparations may not be appropriate to explain synaptic plasticity in hippocampus. Expand
Hippocampal Dysfunction and Cognitive Impairments Provoked by Chronic Early-Life Stress Involve Excessive Activation of CRH Receptors
TLDR
It is found that CRH expression is augmented in hippocampus of middle-aged CES rats, and whether the morphological defects and poor memory performance in these animals involve excessive activation of CRF1 receptors is tested, suggesting that persistently elevated hippocampal CRH–CRF1 interaction contributes importantly to the structural and cognitive impairments associated with early-life stress. Expand
Mechanisms of Late-Onset Cognitive Decline after Early-Life Stress
TLDR
It is demonstrated that a period of early-life “psychological” stress causes late-onset, selective deterioration of both complex behavior and synaptic plasticity in middle-aged, but not young adult, rats exposed to fragmented maternal care during the early postnatal period. Expand
Brain-Derived Neurotrophic Factor Rescues Synaptic Plasticity in a Mouse Model of Fragile X Syndrome
TLDR
The results indicate that the fragile X mutation produces a highly selective impairment to LTP, possibly at a step downstream of actin filament assembly, and suggest a means for overcoming this deficit. Expand
Changes in Synaptic Morphology Accompany Actin Signaling during LTP
TLDR
It is proposed that theta stimulation markedly increases the probability that a spine will enter a state characterized by a large, ovoid synapse and that this morphology is important for expression and later stabilization of LTP. Expand
Cytoskeletal Changes Underlie Estrogen's Acute Effects on Synaptic Transmission and Plasticity
TLDR
It is reported here that acute actions of estrogen are due to selective activation of an actin-signaling cascade normally used in the production of long-term potentiation (LTP), and that the deficits in plasticity arise from acute, as well as genomic, consequences of hormone loss. Expand
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