Involvement of excitatory amino acid receptors in long-term potentiation in the Schaffer collateral–commissural pathway of rat hippocampal slices

1991 ◽  
Vol 69 (7) ◽  
pp. 1084-1090 ◽  
Author(s):  
G. L. Collingridge ◽  
J. F. Blake ◽  
M. W. Brown ◽  
Z. I. Bashir ◽  
E. Ryan
Keyword(s):  
Amino Acid ◽  
Synaptic Transmission ◽  
Excitatory Amino Acid ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Excitatory Amino Acid Receptors ◽  
Amino Acid Receptors ◽  
Term Potentiation ◽  
Commissural Pathway

The present article reviews studies from our laboratory, which have shown that excitatory amino acid receptors of the N-methyl-D-aspartate type are involved in the induction of long-term potentiation in the Schaffer collateral–commissural pathway of rat hippocampal slices. The nature of the excitatory amino acid receptors that mediate the response that is modified by the induction of long-term potentiation is also considered. The mechanism of induction of long-term potentiation is discussed, as are some possible stages that are required for the maintenance of this process. Some new data are presented concerning the ability of N-methyl-D-aspartate to potentiate synaptic transmission and to depress the amplitude of the presynaptic fibre volley. Concerning the potentiation, it is shown that brief (1–2 min) perfusion of slices with N-methyl-D-aspartate is sufficient to potentiate synaptic transmission for at least 3 h. The N-methyl-D-aspartate induced depression of the presynaptic fibre volley is shown to be transient and independent of synaptic transmission.Key words: long-term potentiation, N-methyl-D-aspartate, a-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid, synaptic plasticity, hippocampus.

scholarly journals Early low-level developmental arsenic exposure impacts mouse hippocampal synaptic function

2021 ◽  
Author(s):  
Karl F Foley ◽  
Daniel Barnett ◽  
Deborah A Cory-Slechta ◽  
Houhui Xia
Keyword(s):  
Synaptic Transmission ◽  
Hippocampal Slices ◽  
Arsenic Exposure ◽  
Long Term Potentiation ◽  
Epidemiological Studies ◽  
Synaptic Function ◽  
Learning Deficits ◽  
Term Potentiation ◽  
The Impact

Background: Arsenic is a well-established carcinogen known to increase all-cause mortality, but its effects on the central nervous system are less well understood. Recent epidemiological studies suggest that early life exposure to arsenic is associated with learning deficits and behavioral changes, and increased arsenic exposure continues to affect an estimated 200 million individuals worldwide. Previous studies on arsenic exposure and synaptic function have demonstrated a decrease in synaptic transmission and long-term potentiation in adult rodents, but have relied on in vitro or extended exposure in adulthood. Therefore, little is known about the effect of arsenic exposure in development. Objective: Here, we studied the effects of gestational and early developmental arsenic exposure in juvenile mice. Specifically, our objective was to investigate the impact of arsenic exposure on synaptic transmission and plasticity in the hippocampus. Methods: C57BL/6 females were exposed to arsenic (0, 50ppb, 36ppm) in their drinking water two weeks prior to mating and continued to be exposed to arsenic throughout gestation and after parturition. We then performed field recordings in acute hippocampal slices from the juvenile offspring prior to weaning (P17-P23). In this paradigm, the juvenile mice are only exposed to arsenic in utero and via the mothers milk. Results: High (36ppm) and relatively low (50ppb) arsenic exposure both lead to decreased basal synaptic transmission in the hippocampus of juvenile mice. There was a mild decrease in paired-pulse facilitation in juvenile mice exposed to high, but not low, arsenic, suggesting the alterations in synaptic transmission are primarily post-synaptic. Finally, high developmental arsenic exposure led to a significant increase in long-term potentiation. Discussion: These results suggest that indirect, ecologically-relevant arsenic exposure in early development impacts hippocampal synaptic transmission and plasticity that could underlie learning deficits reported in epidemiological studies.

scholarly journals Neuronal NT-3 Is not Required For Synaptic Transmission or Long-Term Potentiation in Area CA1 of the Adult Rat Hippocampus

1999 ◽  
Vol 6 (3) ◽  
pp. 267-275 ◽  
Author(s):  
Long Ma ◽  
Gerald Reis ◽  
Luis F. Parada ◽  
Erin M. Schuman
Keyword(s):  
Synaptic Transmission ◽  
Hippocampal Slices ◽  
Field Potential ◽  
Early Death ◽  
Long Term Potentiation ◽  
Wild Type ◽  
Adult Rat ◽  
Term Potentiation ◽  
Knockout Animals

Neurotrophic factors, including BDNF and NT-3, have been implicated in the regulation of synaptic transmission and plasticity. Previous attempts to analyze synaptic transmission and plasticity in mice lacking the NT-3 gene have been hampered by the early death of the NT-3 homozygous knockout animals. We have bypassed this problem by examining synaptic transmission in mice in which the NT-3 gene is deleted in neurons later in development, by crossing animals expressing the CRE recombinase driven by the synapsin I promoter to animals in which the NT-3 gene is floxed. We conducted blind field potential recordings at the Schaffer collateral–CA1 synapse in hippocampal slices from homozygous knockout and wild-type mice. We examined the following indices of synaptic transmission: (1) input-output relationship; (2) paired-pulse facilitation; (3) post-tetanic potentiation; and (4) long-term potentiation: induced by two different protocols: (a) two trains of 100-Hz stimulation and (b) theta burst stimulation. We found no difference between the knockout and wild-type mice in any of the above measurements. These results suggest that neuronal NT-3 does not play an essential role in normal synaptic transmission and some forms of plasticity in the mouse hippocampus.

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