Requirement for α-CaMKII in experience-dependent plasticity of the barrel cortex

Science

Volumn 272, Issue 5260, 1996, Pages 421-423

  Glazewski, Stanislaw ^b   Chen, Chuan Min ^b   Silva, Alcino ^b   Fox, Kevin ^b  

^a CARDIFF UNIVERSITY   (United Kingdom)

^b NONE

Author keywords

[No Author keywords available]

Indexed keywords

PROTEIN KINASE (CALCIUM,CALMODULIN) II;

ANIMAL EXPERIMENT; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; LONG TERM POTENTIATION; MOUSE; MOUSE MUTANT; NEOCORTEX; NERVE CELL PLASTICITY; NONHUMAN; PRIORITY JOURNAL; SENSORY CORTEX; TACTILE STIMULATION;

EID: 0029871928     PISSN: 00368075     EISSN: None     Source Type: Journal    
DOI: 10.1126/science.272.5260.421     Document Type: Article

References (35)

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21. All but the D1 vibrissa were removed for a period of 18 days without follicle damage [X. Li et al., J. Comp Neurol. 357, 465 (1995)]. Vibnssae were allowed to regrow 8 to 11 days before recording (by 10 to 15 mm). Adults were 6 to 18 months old; adolescents, 1 to 2 months. Age distributions for wild-type, heterozygote, and homozygote mice were indistinguishable (Tukey-Kramer HSD, α = 0 1) because subjects were siblings.
22. Animals were anesthetized with urethane intrapentoneally (1.5 mg per gram of body weight). Fifty vibrissa deflections of 1° at 1 Hz evoked spikes from isolated units (counted in the 5- to 50-ms poststimulus time histogram interval minus spontaneous activity) [see M. Armstrong-James and K. Fox, J. Comp. Neurol. 263, 265 (1987)]. Data were recorded for 842 layer II and III cells in barrel columns surrounding D1.
23. Recording locations within the cytochrome oxidase-stained barrel field [M. M T. Wong-Riley, Brain Res. 171, 11 (1979)] were identified from focal lesions made at the end of each penetration (1 μA, 10 s, dc tip negative). Layers II and III were 30 to 270 μm, the border of layers III and IV from 270 to 300 μm, and layer IV from 300 to 420 μm For each cell, vibrissa dominance (F) = d1/(d1 + p), where d1 is the average D1 vibrissa response and p is the average principal vibrissa response (3). In Fig. 1, the VDH shows the frequency distribution of F. For each animal, WVDI = (0T0 + 1F1 + 2F2 + 3F3 + 4F4 + 5F5 + 6F6 + 7F7 + 8F8 + 9F9)/9N, where F0 is the number of cells for which 0 ≤ F < 0 1, F1 is the number for which 0.1 ≤ F < 0.2, and N is the number of cells in the sample [see (3)]. For each animal, the average D1 (D1) and principal vibrissa responses (P) were calculated [see (5)]. We found that D1, P, and WVDI were normally distributed (Shapiro-Wilk test, W > 0.92. P > 0.1), and these quantities were averaged across each deprivation-genotype-age group for statistical analysis [analysis of variance (ANOVA) and Tukey-Kramer HSD]. The surround receptive field (SRF) vibrissa was taken as a deprived vibrissa that was neither the principal vibrissa nor D1 (for example, D3 for a cell in the D2 barrel).
24. Principal vibrissa responses for undeprived homozygotes and heterozygotes were indistinguishable (principal mean = 1.80 ± 0.50 spikes per stimulus for heterozygotes and 1.65 ± 0.52 for homozygotes) [ANOVA, F(1,8) = 0.14, P = 0.72], as were surround responses (SRF mean = 0.62 ± 0.25 for heterozygotes and 0.41 ± 0.25 for homozygotes) [F(1,8) = 1.11, P = 0.33] and were combined in a single "undeprived mutant" group.
25. Transcription of α-CaMKII is barely detectable at 4 days in rat neocortex [K. E Burgin et al , J. Neurosci. 10, 1788 (1990)], whereas structural plasticity of the barrel map peaks on postnatal day 0 (P0) and is absent by P4 in mice [T. A. Woolsey and J. R. Wann, J. Comp Neurol. 170, 53 (1976)] and rats [B. L. Schlaggar, K. Fox, D. M. M. O'Leary, Nature 364, 623 (1993)]
26. Transcription of α-CaMKII is barely detectable at 4 days in rat neocortex [K. E Burgin et al , J. Neurosci. 10, 1788 (1990)], whereas structural plasticity of the barrel map peaks on postnatal day 0 (P0) and is absent by P4 in mice [T. A. Woolsey and J. R. Wann, J. Comp Neurol. 170, 53 (1976)] and rats [B. L. Schlaggar, K. Fox, D. M. M. O'Leary, Nature 364, 623 (1993)]
27. Transcription of α-CaMKII is barely detectable at 4 days in rat neocortex [K. E Burgin et al , J. Neurosci. 10, 1788 (1990)], whereas structural plasticity of the barrel map peaks on postnatal day 0 (P0) and is absent by P4 in mice [T. A. Woolsey and J. R. Wann, J. Comp Neurol. 170, 53 (1976)] and rats [B. L. Schlaggar, K. Fox, D. M. M. O'Leary, Nature 364, 623 (1993)]
28. Average receptive field sizes and principal vibrissa response latencies were similar for undeprived wild types, heterozygotes, and homozygotes, respectively, in layers II and III (1.63 ± 0.87 vibrissae, n = 62 cells, 1.56 ± 0 63, n = 76; 1.59 ± 0.87, n = 62) and IV (1 38 ± 0 63, n = 26, 1.37 ± 0.49, n = 27; 1.14 ± 0.35, n = 21). Average latencies were also similar in layers II and III (mean ± SD = 14.8 ± 5 5; 16 1 ± 8.2; and 14.5 ± 6.4 ms) and IV (11.7 ± 5.0; 15.3 ± 8, and 11 ± 5.0 ms). Median response latencies were also similar in layers II and III [median, interquartile range = 14,7; 16,10; and 14,7.5) and IV (10,9; 14,2, and 10,8] (P > 0 347, Welch ANOVA and P > 0 178, Mann-Whitney U test) Vibrissae evoking a response ≥0 5 spike per stimulus were analyzed.
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34. A. Kirkwood, A. Silva, M. F. Bear, ibid , p. 1471 (abstract).
35. All procedures were approved by the animal care committees of the University of Minnesota and Gold Spring Harbor Laboratories We thank X. Li for technical help and P. Chapman and H. Cline for reading the manuscript Supported by NIH grant 27759 to K.F. and grants from the Beckman, Whitehall, and Klingenstein foundations to A.S.