QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

First published online May 26, 2006
Journal of Experimental Biology 209, 2293-2303 (2006)
Published by The Company of Biologists 2006
doi: 10.1242/jeb.01985

This Article Summary Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JEB Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Nguyen, P. V. Search for Related Content PubMed PubMed Citation Articles by Nguyen, P. V.

Comparative plasticity of brain synapses in inbred mouse strains

P. V. Nguyen

Laboratory of Synaptic Plasticity, Department of Physiology and Centre for Neuroscience, University of Alberta School of Medicine, Medical Sciences Building, Edmonton, T6G 2H7, Canada

View larger version (33K): [in a new window]   Fig. 1. Hippocampal slices in an interface chamber. (A) Diagram of a mouse brain showing the positions of the hippocampus and a transverse hippocampal slice. (B) Circuitry and anatomical subregions within a hippocampal slice. (C) Schematic diagram of an interface recording chamber. Hippocampal slices are placed on meshed rings positioned within individual wells. This temperature-regulated chamber allows slices to be perfused with artificial cerebrospinal fluid (ACSF) while exposed to a humidified, oxygenated environment. Adapted from (Young, 2005).

View larger version (28K): [in a new window]   Fig. 2. Different phases of long-term potentiation (LTP). (A) The early phase of LTP (E-LTP; solid circles) is usually induced by one train of high frequency stimulation (HFS; arrowhead) and lasts 1–2 h. A more enduring, late phase of LTP (L-LTP) is induced by three or more trains of HFS (open circles) and is associated with larger amplitudes and steeper initial slopes of fEPSPs for a longer period of time. Note the flat, stable plateau of elevated fEPSP slopes, which is LTP. (B) Different phases of LTP have different mechanisms. E-LTP involves covalent modifications of pre-existing molecules, whereas L-LTP requires transcription and de novo protein synthesis. Adapted from (Woo, 2003).

View larger version (31K): [in a new window]   Fig. 3. Long-term potentiation (LTP) evoked by multiple bursts of stimulation is deficient in some strains of mice. LTP elicited by four 1 s bursts of 100 Hz, interburst interval 20 s, (4x 100 Hz@20s) is reduced in 129/SvEms (A, N=7 mice, 7 slices), DBA (B, N=7 mice, 7 slices) and CBA (C, N=10 mice, 12 slices) as compared to B6 (N=5 mice, 5 slices) hippocampi. Baseline fEPSPs measured during stimulation of a neighbouring pathway that did not experience high-frequency stimulation (no HFS) were unaffected in each strain tested. The B6 curve in A is repeated in B and C for comparison with other strains. Sample sweeps to the right are synaptic responses measured at 90 min post-induction. Taken from (Nguyen et al., 2000b). (Copyright 2000, The American Physiological Society, used with permission.)

View larger version (32K): [in a new window]   Fig. 4. Strain-selective enhancement of long-term potentiation (LTP) by temporally compressed stimulation. (A) There was no significant difference in LTP between B6 (N=7 mice, 7 slices) and 129/SvEms (N=5 mice, 5 slices) hippocampi when the interburst interval was reduced to 3 s. (B,C) LTP in DBA (N=6 mice, 6 slices) and CBA (N=7 mice, 7 slices) strains remained deficient relative to that of the B6 strain. The B6 curve in A is repeated in B and C for comparison with other strains. Sample sweeps were recorded at t=130 min (110 min post-induction). Taken from (Nguyen et al., 2000b). (Copyright 2000, The American Physiological Society, used with permission.)

View larger version (29K): [in a new window]   Fig. 5. Spike discharge properties and glutamatergic receptor currents of CA1 pyramidal neurons are not strain dependent. (A) Membrane excitability: plot of the number of action potentials produced during a 1 s current pulse versus current amplitude in each of the four mouse strains. (B) Spike frequency accommodation: plot of spike number (order in a train) versus delay from onset of current injection. These are averages of fifth-order polynomial curve fits of data obtained from B6 (N=13 cells) 129/SvEms (N=28), DBA (N=14) and CBA (N=21) neurons. (C) Sample traces showing spike frequency accommodation in B6 and 129/SvEms cells. Current injections of 300 pA were used to elicit spiking. (D) Left: ratios of N-methyl-D-aspartate (NMDA) to non-NMDA glutamatergic currents were not significantly different between strains (B6, N=14 cells; 129/SvEms, N=12; DBA, N=5; CBA, N=5). Right: a current–voltage plot comparing the voltage dependence of glutamatergic currents measured in B6 and 129/SvEms neurons. Taken from (Nguyen et al., 2000b). (Copyright 2000, The American Physiological Society, used with permission.)

View larger version (35K): [in a new window]   Fig. 6. Metaplastic inhibition of the late phase of long-term potentiation (L-LTP). (A) Transient depression was observed after 5 Hz low-frequency stimulation for 3 min (LFS) was applied to area CA1 of hippocampal slices from B6 mice. However, fEPSP slopes recovered within 7 min after the end of LFS (open circles). Sample fEPSP traces from one experiment are shown; these were recorded 15 min before (a), during (b), immediately after (c), and 20 min after (d) LFS. (B) Prior LFS at 5 Hz does not affect early LTP induced by a single 100 Hz train. Control slices (open squares) generated LTP that was similar in magnitude and time course to LTP induced in slices that received LFS prior to tetanization (solid circles). Inset: sample fEPSP traces from one experiment, measured 10 min before and 60 min after E-LTP induction. (C) Four successive trains of 100 Hz, spaced 5 min apart, induced robust L-LTP in control slices (open squares) and in slices that received a brief prior episode of LFS (5 Hz, 30 s; solid triangles). No L-LTP was seen in slices that received more prolonged LFS (5 Hz, 3 min; solid circles) prior to HFS. Inset: sample traces from an experiment, measured 10 min before (Control) and 2 h after L-LTP induction. (D) Increasing the time interval between LFS and L-LTP induction abolishes anterograde metaplasticity of L-LTP. Defective L-LTP was observed when LFS was applied 20 min before L-LTP induction (solid circles). By contrast, normal L-LTP was seen when the time interval between LFS and HFS was extended to 40 min (solid triangle). Adapted from (Woo and Nguyen, 2002). (Copyright 2002, Cold Spring Harbor Laboratory Press, used with permission.)