NTERHEMISPHERIC COHERENCE OF THE SLEEPLECTROENCEPHALOGRAM IN MICE WITH CONGENITAL CALLOSAL
YSGENESIS
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. VYAZOVSKIY, P. ACHERMANN, A. A. BORBELYND I. TOBLER*
nstitute of Pharmacology and Toxicology, University of Zurich, Win-erthurerstrasse 190, CH-8057 Zurich, Switzerland
bstract—Regional differences in the effect of sleep depriva-ion on the sleep electroencephalogram (EEG) may be relatedo interhemispheric synchronization. To investigate the rolef the corpus callosum in interhemispheric EEG synchroni-ation, coherence spectra were computed in mice with con-enital callosal dysgenesis (B1) under baseline conditionsnd after 6-h sleep deprivation, and compared with the spec-ra of a control strain (C57BL/6).
In B1 mice coherence was lower than in controls in alligilance states. The level of coherence in each of the threeotally acallosal mice was lower than in the mice with onlyartial callosal dysgenesis. The difference between B1 andontrol mice was present over the entire 0.5–25 Hz frequencyange in non-rapid eye movement sleep (NREM sleep), and inll frequencies except for the high � and low � band (3–7 Hz)
n rapid eye movement (REM) sleep and waking. In controlice, sleep deprivation induced a rise of coherence in the �and of NREM sleep in the first 2 h of recovery. This effectas absent in B1 mice with total callosal dysgenesis andttenuated in mice with partial callosal dysgenesis. In bothtrains the effect of sleep deprivation dissipated within 4 h.
ey words: sleep regulation, interhemispheric EEGynchronisation, corpus callosum, local sleep, sleep depri-ation.
he dynamics of low frequency power of the sleep elec-roencephalogram (EEG) may be an indicator of regulatoryrocesses occurring during sleep (Borbely, 1982). In-reased sleep pressure causes not only an increase oflow-wave activity (SWA) in non-rapid eye movementleep (NREM) sleep (SWA, EEG power between 0.75 and.0 Hz), but induces also an interhemispheric shift in EEGower (humans: Achermann et al., 2001; rats: Vyazovskiy
Corresponding author. Tel: �41-1-635-5957; fax: �41-1-635-5707.-mail address: [email protected] (I. Tobler).bbreviations: ANOVA, analysis of variance; EEG,lectroencephalogram; EMG, electromyogram; GABA, �-aminobutyriccid; NREM sleep, non-rapid eye movement sleep; REM sleep, rapid
bye movement sleep; SD, sleep deprivation; SWA, slow-wave activity.
t al., 2002). This shift seems to reflect differences of sleepintensity” between the hemispheres, which may arise as aonsequence of the asymmetric activation of the cortexuring waking (humans: Kattler et al., 1994; rat: Vya-ovskiy et al., 2000). The higher EEG � power may be aign of increased synchronization between cortical neu-ons. It is well known that the synchronization of thalami-ally generated activity in �- and spindle-frequencies mayrise from an intracortical neuronal network generatingynchronous slow (�1 Hz) oscillations (Steriade et al.,991; Timofeev and Steriade, 1996). Such low frequencyscillations are a typical feature of normal physiologicalleep in the cat (Steriade et al., 2001; Destexhe et al.,999) and in humans (Achermann and Borbely, 1997;teriade and Amzica, 1998).
In the anesthetized cat it has been shown that activityf cortical cells is influenced by both ipsilateral thalamicrojections and input from the contralateral hemisphereSteriade et al., 1993; Cisse et al., 2003). Such interhemi-pheric connections may have functional significance,ince synchronization of neuronal responses between leftnd right visual cortices elicited by visual stimulation inats was abolished after callosotomy (Engel et al., 1991).imilarly, after callosotomy the increase of interhemi-pheric EEG coherence induced by visual stimuli wasbolished in ferrets (Kiper et al., 1999). These data indi-ate that corpus callosum may play an important functionalole for interhemispheric coordination. A large degree ofemispheric independence during unihemispheric sleep inolphins (Oleksenko et al., 1992) may be related to thetrong reduction of the corpus callosum in Cetaceans (Tar-ley and Ridgway, 1994).
Also in humans the corpus callosum is involved innterhemispheric EEG synchronization. Thus, interhemi-pheric EEG coherence was decreased in congenitallycallosal infants, children and adults (Kuks et al., 1987;ielsen et al., 1993; Koeda et al., 1995) and after calloso-
omy in adults (Montplaisir et al., 1990). It is possible thathe corpus callosum contributes to the higher interhemi-pheric coherence or interhemispheric correlation in the �nd spindle frequencies that has been found in sleepompared with waking (Corsi-Cabrera et al., 1996; Acher-ann and Borbely, 1998a).
There is a large variation in the size of the corpusallosum in different strains of laboratory mice (reviewed inahlsten, 1989; Lipp and Wahlsten, 1992). Partial or com-
lete callosal agenesis was frequent in strains derivedrom 129 or BALB/c mice (Livy and Wahlsten, 1991). Mice
elonging to 129Sv, 129Ola and BALB/c are widely used in
V. Vyazovskiy et al. / Neuroscience 124 (2004) 481–488482
leep studies (e.g. Tobler et al., 1996; Franken et al., 2001;uber et al., 2000; Meerlo et al., 2001), and stem cells forene targeting are usually derived from the 129Sv and29Ola strain (Simpson et al., 1997). Therefore, mice withongenital callosal deficiencies are interesting models tonvestigate the function of the corpus callosum in EEGynchronization during sleep.
Our aim was to compare interhemispheric EEG coher-nce in a mouse with a high incidence of callosal dysgen-sis (B1, I/LnJ�C57BL/6, Magara et al., 1998; Magara,999) with a control strain (C57BL/6J) that is known toave a normally developed corpus callosum (Wahlsten,982). The mice were investigated also after 6-h sleepeprivation (SD) to test whether the increased sleep pres-ure influences interhemispheric EEG synchronization.
EXPERIMENTAL PROCEDURES
nimals
dult male mice with high incidence of callosal agenesis (B1,�9) and C57BL/6J (control, n�7) mice were used. The B1 miceere obtained by a cross of I/LnJ males with C57BL/6 females,nd subsequent back cross of second and third generation fe-ales with I/LnJ males, followed by subsequent random mating of
heir offspring (Magara, 1999). Histological verification of the de-ree of callosal dysgenesis in B1 mice was based on Nissl-stainedoronal sections (20 �m thick) throughout the extent of the corpusallosum (C57BL/6 mice: approximately between 1 mm anterior toregma to 2.5 mm posterior to bregma). Nissl staining is appro-riate for visualization of the corpus callosum because this struc-ure is largely devoid of cell bodies that are stained with Cresyliolet. The corpus callosum was totally absent in three individuals
total dysgenesis) while in n�6 the corpus callosum was absent inhe frontal region, and preserved at the level of the hippocampusapproximately from 1.5–2.5 mm posterior to bregma).
The C57 and B1 mice were 17.5�0.1 S.E.M. and 19.9�0.2eeks old respectively. The mice were kept individually in Mac-
olon cages (36�20�35 cm) with food and water available adibitum, and maintained in a 12-h light/dark cycle (light from8:00–20:00 h; 7 W OSRAM Dulux EL energy saving lamp (Mu-ich, Germany), approximately 30 lux). Mean ambient tempera-
ure was 22.9�0.1 °C.
urgery
he local governmental commission for animal research approvedhe experiments, that were conducted according to the local andnternational guidelines on the ethical use of animals. All effortsere made to minimize suffering of the animals and the amount ofnimals used was minimal to allow statistical group comparison.t surgery the mice weighed 27.2 g�1.1 and 29.2 g�1.0 (C57 and1, respectively). Under deep equithesin (pentobarbital/chloralydrate) anesthesia (dose 0.4 ml/100 g, i.p.) the mice were im-lanted with gold-plated, round-tipped miniature screws (0.9 mmiameter) that served as EEG electrodes. The epidural electrodesere placed bilaterally over the parietal cortex (3 mm lateral toidline, 2 mm posterior to bregma) and frontal cortex (1.5 mm
ateral to midline and 1.5 mm anterior to bregma). The commoneference electrode was placed above the cerebellum (2 mmosterior to lambda, on midline). Two gold wires (diameter.2 mm) inserted into the neck muscles served to record thelectromyogram (EMG). The electrodes were connected to stain-
ess steel wires that were fixed to the skull with dental cement. Ateast 3 weeks were allowed for recovery after surgery and adap-
ation to the recording conditions. c
xperimental protocol and data acquisition
he EEG and EMG were recorded continuously for 48 h. A 24-haseline day was followed by 6-h SD starting at light onset and8-h recovery. SD was performed by introducing objects (e.g.esting material) into the cage, and later by tapping on the cagehenever the animal appeared drowsy and/or the EEG exhibitedlow waves. Halfway through the SD the mice were transferred toew cages to provide additional stimulation. To minimize stress,ome sawdust and nesting material from the old cage was trans-erred to the new one. The mice were never disturbed duringeeding and drinking.
The EEG and EMG signals were amplified (amplification fac-or approx. 2000), conditioned by analog filters (high-pass filter:3 dB at 0.016 Hz; low-pass filter: 3 dB at 40 Hz, less than 35B at 128 Hz) sampled with 512 Hz, digitally filtered (EEG: low-ass FIR filter 25 Hz; EMG: band-pass FIR filter 20–50 Hz) andtored with a resolution of 128 Hz. Ambient temperature inside theage was sampled at 4-s intervals.
igilance states
he three vigilance states NREM sleep, REM sleep and wakingere scored for 4-s epochs. Vigilance states were determinedff-line by visual inspection of the left parietal EEG and EMGecords and the values of EEG power in the slow-wave range0.75–4.0 Hz; see Tobler et al., 1997).
EG coherence and EEG correlation analysis
or coherence and correlation analyses bipolar fronto-parietalerivations in the left and right hemisphere were used. To excludehe influence of the common cerebellar referential electrode thatould artificially enhance coherence, the parieto-cerebellar signalf each side was subtracted from the fronto-cerebellar signal.nterhemispheric coherence spectra were computed using
elch’s averaged periodogram method (Welch, 1967) for artifactree 12-s epochs of a specific state (six 2-s epochs correspondingo three consecutive 4-s epochs scored as NREM sleep, REMleep or waking). For methodological details see Achermann andorbely (1998a). The frequency resolution was 0.5 Hz and anal-sis was performed between 0.5 and 25 Hz. Power spectra for theeft and right derivations were computed for 12-s epochs (fastourier transform routine, Hanning window, averages of six 2-spochs).
The number of 12-s epochs that was used for the computationf the coherence and power spectra and correlation analysis forhe 12-h baseline light period (total: 3600 12-s epochs) was for57 mice: NREM sleep, 1852.6�36.9 (interindividual range756–2005); REM sleep, 300.0�13.8 (242–351); waking,64.3�117.8 (223–1046); for B1 mice: NREM sleep,840.4�27.1 (1755–2007); REM sleep, 351.1�16.4 (279–428);aking, 314.6�68.5 (72–659).
To assess whether total callosal agenesis would abolish in-erhemispheric EEG synchronization, random coherence wasomputed for each 12-s epoch between the left and the time-eversed right EEG in the mice with total callosal dysgenesisn�3).
The effect of SD on interhemispheric coherence in NREMleep was assessed for the first 6 h of recovery. To minimizendividual and inter-interval variability in the amount of data con-ributing to the analysis, coherence spectra were computed for theinimal common amount of artifact-free 12-s epochs in NREM
leep per 2-h interval (�212 epochs, i.e. 42.4 min).Interhemispheric correlation between EEG amplitude (�V) of
he left and right derivation (Pearson correlation coefficients) wasomputed for the same number of 12-s epochs that entered the
V. Vyazovskiy et al. / Neuroscience 124 (2004) 481–488 483
Before computing averages, Fisher’s z-transformation waspplied to coherence and correlation values.
For signal analysis the software package MATLAB (The Mathorks, Inc., Natick, MA, USA) was used and for statistical anal-
sis SAS (SAS Institute, Inc., Cary, NC, USA).
RESULTS
EG coherence and EEG correlation during baseline
nterhemispheric EEG coherence was lower in B1 mice thann controls (individual examples in NREM sleep and REMleep: Figs. 1 and 2; mean coherence spectra: Fig. 4). InREM sleep coherence was reduced over the entire fre-uency range, whereas in REM sleep and waking the valuesid not differ in the high �/low range (REM sleep: 4.0–.5 Hz and 6.0–6.5 Hz; waking: 3–7 Hz). The decrease ofoherence in B1 mice depended on the degree of callosalysgenesis (Fig. 4). In all three mice with total callosal dys-enesis interhemispheric coherence in NREM sleep was
-2000
200
C57BL/6J mouse (control)
B1 mouse (total callosal dysgenesis)
-2000
200
µVRIGHT
LEFT
NR
-2000
200
Seconds
0 3 6 9
-2000
200
ig. 1. Left panels: Two examples of raw 12-s EEG records of NREM snd a B1 mouse with total callosal dysgenesis. Middle panels: The volt
or corresponding consecutive sampling intervals (1/128 s) for the 12-sanels: Interhemispheric coherence spectra (left-right) for frequencies
ower than in any of the mice with partial dysgenesis. In L
ddition, in each mouse with total callosal dysgenesis (n�3)oherence in each vigilance state was above the correspond-
ng random level of coherence (mean curves: Fig. 4).The coherence spectra in REM sleep and waking were
haracterized by the prominent peak within the frequencyand in both B1 and control mice. The peak occurred inignificantly higher frequencies in C57 mice than in B1ice in both REM sleep (C57, 7.4�0.1 Hz; B1,.6�0.1 Hz, unpaired t-test, P�0.0001) and in wakingC57, 7.3�0.3 Hz; B1, 6.1�0.1 Hz, unpaired t-test,�0.001), and differed between REM sleep and waking in1 mice only (paired t-test, P�0.01).
The computation of coherence for the three vigilancetates in control mice revealed vigilance state specificatterns of interhemispheric coherence (Fig. 3, left panel).oherence was higher in NREM sleep than in REM sleepnd waking in the low � band. In the band coherence inEM sleep and waking exceeded the NREM sleep level.
0.0
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1.0
interhemispheric coherence
0.0
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12
Frequency (Hz)
0 5 10 15 20 250.0
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1.0
r2=0.43
µV
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r2=0.36
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r2=0.02
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interhemisphericcorrelation
µV
EMS) from the right and left derivations for a control C57BL/6J mouses of the left derivation were plotted as a function of the right derivationdepicted in the left panels. The lines depict a linear regression. Right0.5 and 25 Hz of the corresponding 12-s EEG record.
EMS
leep (NRage value
epochsbetween
ittle or no difference between vigilance states was found
aptf
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V. Vyazovskiy et al. / Neuroscience 124 (2004) 481–488484
t frequencies above 10 Hz. This is in contrast to EEGower spectra (Fig. 3, right panel) where differences be-ween vigilance states were present also within the higherrequency range (Fig. 3).
The interhemispheric EEG correlation was higher bothn NREM sleep and REM sleep in control mice than in B1
nterhemispheric EEG coherence in NREM sleepfter SD
n the first 2-h interval after SD interhemispheric lowrequency coherence in NREM sleep was higher than in
1
10
0.0
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0.4
0.6
0.8
1.0EEG coherence
0 5 10 15 20 25
10100F-value
Freque
ig. 3. Interhemispheric coherence spectra (left) and EEG power spec57BL/6J mice (n�7). Vertical bars in the lower panels represent sigetween the vigilance states (one-way ANOVA, coherence: after Fi
-2000
200
C57BL/6J mouse (control)µVRIGHT
LEFT
RE
Seconds0 3 6 9
-2000
200B1 mouse (total callosal dysgenesis)
Fig. 2. Examples of REM sleep (R
vigilance state’; P�0.01).
he corresponding baseline interval (Fig. 5). This in-rease encompassed a larger frequency range (0.5–.5 Hz) in control mice than in B1 mice (0.5–2 Hz).ithin B1 mice, the coherence increase after SD in the
ow frequency range was smaller in totally acallosalndividuals (Fig. 5). The differences in the low frequencyange between baseline and recovery dissipated withinh (two-way ANOVA for repeated measures, interactionf factors ‘day’ (baseline, recovery)�‘2-h interval’ (1–3)as P�0.05 between 0.5–3.5 and 4.5– 6.5 Hz in controlice and between 0.5–1 and 1.5–2 Hz in B1 mice). The1 and control mice differed in the magnitude of theffect of SD on coherence during the first 2 h of recovery
NREMS-REMSNREMS-WAKINGWAKING-REMS
NREMSREMSWAKING
wer density (µV2/0.5 Hz)
10 15 20 25)
in NREM sleep (NREMS), REM sleep (REMS) and waking for control-values plotted on a log scale for those frequency bins that differed
transformation; EEG power density: after log transformation, factor
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1.0
12Frequency (Hz)
0 5 10 15 20 250.0
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1.0
r2=0.67
µV
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r2=0.47
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µV
interhemispheric coherence
interhemisphericcorrelation
G records. See Fig. 1 for details.
0
0
EEG po
0 5
10100
ncy (Hz
tra (right)nificant Fsher’s z-
MS
EMS) EE
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V. Vyazovskiy et al. / Neuroscience 124 (2004) 481–488 485
Fig. 5). The difference between baseline and recoveryas significantly larger in control mice than in B1 mice
0.5– 6.0 Hz; P�0.05). It should be also noted that in B1ice coherence in frequencies between 4 and 7.5 Hzas actually reduced below baseline. Coherence inigher frequencies above 10 Hz during the first 2-h
nterval after SD was reduced below baseline in mostins in both B1 and control mice (not shown). SD en-anced power in the low frequency range in both strainsdata not shown). The increase in the 1.5–5.5 Hz rangeas 24.6% larger in controls than in B1 mice (P�0.05).
igilance states
inor differences were observed in the 24-h values ofigilance states between the two strains during baseline.1 slept more than control mice (NREM sleep: 11.0�0.2s 9.8�0.3 h; REM sleep: 1.8�0.04 vs 1.4�0.08 h;aired t-test, P�0.01), and were less awake (11.2�0.2s 12.7�0.3 h; P�0.01). Only a negligible amount ofREM sleep occurred during the 6-h SD (C57: 3.11�1.2
Coh
eren
ce
0.0
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0.4
0.6
0.8
1.0NREMS
F-value
partial dysgenesisnormal callosum
total dysgenesis
F
0 5 10 15 20 25
10
100
0 5
REM
random level
ig. 4. Interhemispheric coherence spectra in NREM sleep (NREMSC57BL/6J; n�7) and B1 mice subdivided into mice with partial callosaistology. Random level of coherence is shown for the mice with tot-values plotted on a log scale for those frequency bins that differed ben Fisher’s z-transformed coherence values, factor ‘strain’; P�0.05).
able 1. Effects of corpus callosum deficiency on interhemisphericEG correlationa
Pearson product-moment correlation coefficients between voltagealues of EEG from left and right derivations for control mice (C57BL/J; n�7) and B1 mice (n�9). Mean correlation coefficients (S.E.M. inarentheses) between all artifact-free 12-s epochs of 12-h baseline
ight period in NREM sleep, REM sleep and waking. Letters indicateignificant differences between controls and B1 mice (b P�0.0006;P�0.04; unpaired t-test on Fisher z-transformed correlation val-
ses).
in; B1: 5.7�1.2 min). A long-lasting increase of NREMleep and REM sleep followed SD, while the amount ofaking was below baseline in both strains (not shown).
DISCUSSION
he corpus callosum is involved in interhemisphericEG synchronisation
ice with a dysgenesis of the corpus callosum showed aeduced interhemispheric coherence of the EEG comparedith the control strain. Although the small sample size pre-luded a statistical analysis, the magnitude of the effecteemed to be related to the degree of acallosality. In totallycallosal mice coherence was lower than in mice with partialallosal dysgenesis. This indicates that cortico–cortical cal-
osal connections play an important role in synchronising theEG between the two hemispheres. However, since in miceith callosal dysgenesis the random coherence level waslearly exceeded, other commissural connections or re-outed callosal fibers must be also involved. It is known thatallosal fibers may cross the midline via the ventral hip-ocampal commissure in ddN mice (Ozaki et al., 1987) or
hrough the anterior commissure in hybrids of 129J and BAL-cWah1, totally lacking corpus callosum (Livy et al., 1997).lose phase relationships of neuronal firing between con-
ralateral reticular nuclei in anesthetized cats provided elec-rophysiological evidence for direct thalamic connectionsTimofeev and Steriade, 1996).
Similar to coherence, EEG correlation in NREM sleepnd REM sleep was lower in the B1 mice than in controls.lso in the ddN strain interhemispheric correlation coeffi-ients obtained for 2 min of waking EEG per mouse were
ower in acallosal mice than in mice with a preserved callo-
REMS
WAKING
y (Hz)
15 20 25 0 5 10 15 20 25
sleep (REMS) and waking for control mice with a normal callosumesis (n�6) and total callosal dysgenesis (n�3) according to post hocl dysgenesis. Vertical bars in the lower panels represent significante two strains (the B1 mice were pooled for statistics; one-way ANOVA
V. Vyazovskiy et al. / Neuroscience 124 (2004) 481–488486
igilance-state specific EEG coherence
nother major result was a pronounced vigilance state-pecific pattern of interhemispheric EEG coherence.hus there was a higher coherence within the � band inREM sleep compared with both REM sleep and wak-
ng. This result is consistent with the sleep state-specificoherence found in humans (Achermann and Borbely,998a). The decline of coherence with increasing fre-uency that was observed also in humans (Achermannnd Borbely, 1998a) may indicate that interhemisphericynchronisation mediated by the corpus callosum isore efficient for lower frequency EEG activity. In con-
rast, higher frequency activity is synchronized only overmall cortical territories (Destexhe et al., 1999).
A distinct peak of coherence within the band wasresent in both C57 and B1 mice in REM sleep and inaking. Coherent -activity between the left and rightippocampus was observed in progeny of hybrids of57BL/6J and 129S6/SvEvTac mouse strains (Buzsakit al., 2003). The frequency where the coherence peakccurred was lower in B1 mice than in C57 in both REMleep and waking. Strain differences in oscillationsuggested a gene with a major effect (Franken et al.,998). -Activity was markedly slower in mice deficientor Acad, an enzyme involved in fatty acid �-oxidationTafti et al., 2003). Interhemispheric coherence in B1ice did not differ from the control strain in 4.0 – 6.5 Hz
n REM sleep and in 3–7 Hz during waking. Theserequencies correspond to the oscillatory activity re-orded from individual hippocampal cells that lies be-ween 3 and 6 Hz (Klausberger et al., 2003). The peak in
10100
Coh
eren
ce (
reco
very
- b
asel
ine)
-0.1
0.0
0.1
0.2
10100
F-value
2-h intervals after SD:1 2
partial dysgenesisnormal callosum
total dysgenesis
0 510
100
Frequ
010
ig. 5. Interhemispheric coherence spectra in NREM sleep for the 212SD). Curves depict within each panel the difference between recoveallosum (C57BL/6J; n�7) and B1 mice subdivided into mice with partost hoc histology. Vertical bars in the lower panels represent significignificantly by SD within a strain (open bars, enhanced; black bars, reice. ANOVA as in Fig. 4.
he band observed in REM sleep and waking may arise h
rom direct interhippocampal connections, which arereserved in acallosal mice (Magara, 1999).
ncreased sleep pressure enhanced interhemisphericoherence of EEG SWA
o test whether interhemispheric synchronisation of SWAs subject to increased sleep pressure, coherence spectraere analyzed after 6-h SD. An increased coherence wasbserved in low frequencies in NREM sleep in C57 miceompared with baseline, and the increase was larger than
n B1 mice. The negligible change of low frequency coher-nce in the totally acallosal mice indicated that the corpusallosum plays a role in the increased interhemisphericynchronisation after SD. The degree of acallosality did not
nfluence the decrease of coherence in higher frequenciesfter SD, indicating that other pathways are involved. Atronger functional coupling between the hemispheres un-er increased sleep pressure via the corpus callosum maynderlie the increase of coherence in SWA after SD. Inumans, no significant change of interhemispheric EEGoherence in 0.75–1.5 Hz band was found in the course ofbaseline night (Achermann and Borbely, 1998b). How-
ver, sleep pressure differences within a night may not bearge enough to affect coherence.
echanisms underlying the interhemispheric EEGynchronisation
he mechanisms leading to interhemispheric synchroniza-ion and its function during sleep are still unknown. It haseen shown that activity of cortical neurons is driven by a
ocal intracortical network as well as by neurons from
3
control miceB1 micecontrols vs B1
5 10
)
010
effect of SD:
ree 12-s epochs (42.4 min) per 2-h interval after 6-h sleep deprivationls and the corresponding baseline interval. Control mice with normalal dysgenesis (n�6) and total callosal dysgenesis (n�3) according tolues plotted for those frequency bins where coherence was affectedr where the effect of SD differed significantly between control and B1
ency (Hz
5
artifact-fry intervaial callosant F-vaduced) o
omotopic regions of the contralateral hemisphere (Cisse
V. Vyazovskiy et al. / Neuroscience 124 (2004) 481–488 487
t al., 2003). GABAergic mechanisms may be involvedecause stimulation of commissural callosal fibers in brainlices of rats induced GABA-mediated inhibitory post-syn-ptic potentials in the agranular frontal cortex (Kawaguchi,992). The spatial correlation of neuronal activity duringleep may serve to strengthen synaptic connections,hereby enhancing efficacy of functional coupling betweenhe hemispheres. This idea supports the theory of a “syn-ptic,” use-dependent function of sleep (Krueger and Obal,003). Use-dependent lateralised enhancement of EEGower may be related to a local increase of synchronisa-ion between neurons (Vyazovskiy et al., 2000). In con-rast, callosal connections mediate more global synchroni-ation. The observation of the wide-range synchronisationf �-activity, a marker of sleep homeostasis, is consistentith the hypothesis that sleep may serve global synapticownscaling (Tononi and Cirelli, 2003).
In conclusion, the data indicate that the corpus callo-um is involved in EEG synchronization between the hemi-pheres. Enhanced sleep pressure led to an increase inoherence in the range of � frequencies suggesting thatnterhemispheric interactions between homologous corti-al regions during sleep may have a functional Borbe|Aaly982; Tobler et al., 1997 significance.
cknowledgements—The study was supported by the Swiss Na-ional Science Foundation grants 3100-053005.97 and 3100A0-00567 and Human Frontier Science Program RG 0131/2000.
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