Craniofacial Muscles

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3 Extraocular Muscle Structure and Function43contain SERCA1. Overall, calcium handling is also signi fi cantly different in EOMthan in limb and body skeletal muscles. The EOM are more resistant to necrosisinduced by elevated cytosolic calcium levels (Khurana et al. 1995 ; Zeiger et al.2010 ) . This increased calcium buffering capacity in EOM is due to a combinationof factors: abundant sarcoplasmic reticulum (which increases SERCA content),high concentrations of parvalbumin, a small cytosolic Ca 2+ -binding protein, andmitochondria serving as fast Ca 2+ sinks (Andrade et al. 2005 ; Celio and Heizmann1982 ) . This enhanced ability to regulate cytosolic Ca 2+ concentration plays a role incontrolling contractile amplitude in the EOM.The EOM are constantly active, have some of the fastest contractile properties(Close and Luff 1974 ) , are very fatigue-resistant (Fuchs and Binder 1983 ) , andwhile they normally need to produce only enough force to move the eye, they arenot intrinsically weaker than limb skeletal muscles (Frueh et al. 2001 ) . The basesfor these properties as well as the maintenance of these properties during eye movementsare an area of continued investigation. It has long been known that the EOMhave an extremely high density of mitochondria compared to non-cranial skeletalmuscles (Mayr 1971 ; Davidowitz et al. 1980 ) . In addition, the EOM mitochondriahave a different mitochondrial biogenesis program than the one used by limb skeletalmuscle (Andrade et al. 2005 ) . Despite their large mitochondrial volume density,paradoxically the EOM mitochondria have lower respiratory capacity (Patel et al.2009 ) . In addition, key enzymes controlling glycogen synthesis and breakdown arerepressed in the EOM, and glycogen content is correspondingly reduced (Porteret al. 2001 ; Fischer et al. 2002 ) , suggesting that the EOM are probably less dependenton glycogen as a metabolic fuel than other skeletal muscles. It is also possiblethat the EOM rely on constant transport of blood-borne glucose and fatty acidsthrough their extensive microvascular network (Kjellgren et al. 2004 ). Overall, thepattern is consistent with the EOM relying to a large extent on mitochondria as themain source of energy under all conditions. One example is the use of lactate as asubstrate for its aerobic metabolism (Andrade and McMullen 2006 ) . In limb skeletalmuscles lactate is usually the end product of glycolysis and is associated withmuscle fatigue. In the EOM, the presence of lactate dehydrogenase B allows theoxidation of lactate back to pyruvate for entry to the Krebs cycle; therefore, lactatecan sustain EOM activity and slow the progression of fatigue (Fig. 3.10 ).The EOM contain high levels of both oxidative and glycolytic enzymes. An analysisof serially sectioned and histochemically stained EOM myo fi bers demonstratedthat, except for the myo fi bers expressing MyHC-slow tonic, all fi bers express bothsuccinic dehydrogenase and a -glycerophosphate dehydrogenase (Asmussen et al.2008 ) . This demonstrates that single EOM myo fi bers combine high levels of bothoxidative and glycolytic pathways, in stark contrast to limb skeletal muscle. Wheneach enzyme was plotted against myo fi ber area or whether the fi ber was fast orslow, a continuum of fi bers emerged, with only the slow tonic-positive myo fi bers ina group by themselves. Again it appears that the fi ber type system used in limb andbody skeletal muscles does not fi t the picture in EOM.
44 L.K. McLoon et al.Fig. 3.10 Use of lactate inEOM. ( a ) Proposed fl ow ofsubstrates in an EOM fi ber.Blood glucose entersglycolysis as glucose-6-phosphate (glucose-6-P).Glycogen content is low andglycogenolysis is greatlydown-regulated. The lactatedehydrogenase (LDH)reaction fl ows in the directionof lactate oxidation topyruvate, which enters themitochondrial Krebs cycle.( b ) Electron micrographillustrating the highmitochondrial content of anEOM fi berAGlucoseLactateExtraocular muscle fiberGlycogenGlucose-6-PGlycolysisLDHPyruvateKrebs cycleOxPhosMitochondriaB3.8 Myonuclear Turnover and RegenerationAnother unusual property of adult EOM is its ability to remodel portions of itsmyo fi bers throughout life. Using bromodeoxyuridine labeling and immunohistochemicaltechniques, it was shown that the EOM retain a population of activatedsatellite cells (McLoon and Wirtschafter 2003 ) , and these cells replicate and appear
Page 2: Craniofacial Muscles
Page 5 and 6: EditorsLinda K. McLoonDepartment of
Page 7 and 8: viContents8 Masticatory Muscle Resp
Page 9 and 10: viiiContributorsMark Lewis School o
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Page 13 and 14: 1 The Craniofacial Muscles: Argumen
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Page 17 and 18: Chapter 2Head Muscle DevelopmentIta
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Page 35 and 36: Part IIIExtraocular Muscles
Page 37 and 38: 32 L.K. McLoon et al.Fig. 3.1 Diagr
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Page 53 and 54: 48 L.K. McLoon et al.Fuchs AF, Bind
Page 55 and 56: 50 L.K. McLoon et al.Tajbakhsh S, R
Page 57 and 58: 52 V.E. DasFig. 4.1 Initial studies
Page 59 and 60: 54 V.E. DasFig. 4.2 Schematic view
Page 61 and 62: 56 V.E. DasFig. 4.3 Top panel —co
Page 63 and 64: 58 V.E. Das4.3 Motor Control of Con
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Page 75 and 76: 70 V.E. Das4.6 SummaryThe oculomoto
Page 77 and 78: 72 V.E. DasHoerantner R, Kaltofen T
Page 79 and 80: 74 V.E. DasTweed DB, Haslwanter TP,
Page 81 and 82: 76 F. Pedrosa Domellöfcompletely d
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Page 91 and 92: 86 F. Pedrosa DomellöfReferencesAg
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112 B.J. Sessle et al.zygomaticus m
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114 B.J. Sessle et al.Fig. 7.1 ( a
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116 B.J. Sessle et al.Most of the m
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118 B.J. Sessle et al.lie immediate
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120 B.J. Sessle et al.(Dubner et al
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122 B.J. Sessle et al.Fig. 7.3 An e
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124 B.J. Sessle et al.that each out
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126 B.J. Sessle et al.2010 ; Plowma
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128 B.J. Sessle et al.activities. S
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130 B.J. Sessle et al.Moayedi M, We
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132 S.L. Hebert et al.type 3 and cr
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134 S.L. Hebert et al.This early de
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136 S.L. Hebert et al.that EMG valu
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138 S.L. Hebert et al.Newton JP, Ab
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Chapter 9Structure and Function of
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9 Structure and Function of the Lar
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Chapter 10Motor Control and Biomech
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10 Motor Control and Biomechanics o
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186 J.C. Stemple et al.established
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188 J.C. Stemple et al.of protein d
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190 J.C. Stemple et al.the depictio
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192 J.C. Stemple et al.Fig. 11.2 Ul
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194 J.C. Stemple et al.11.6 Larynge
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196 J.C. Stemple et al.Neurapraxia,
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198 J.C. Stemple et al.of the preci
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200 J.C. Stemple et al.Gardner GM,
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202 J.C. Stemple et al.Rhee HS, Luc
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Part VITongue Musculature
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208 A. Sokoloff and T. BurkholderTh
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Chapter 13Tongue Biomechanics and M
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Fig. 13.1 Retrogradely labeled enti
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13 Tongue Biomechanics and Motor Co
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Chapter 14Tongue Muscle Responseto
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14 Tongue Muscle Response to Neurom
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Part VIIFacial Muscles
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266 A.O. Grobbelaar and A.C.S. Wool
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288 J. Park et al.Table 16.1 Disord
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290 J. Park et al.Table 16.2 Jankov
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292 J. Park et al.16.2.3 Pathophysi
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294 J. Park et al.evident eyelid sq
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296 J. Park et al.Focal motor seizu
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298 J. Park et al.Fig. 16.1 Content
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300 J. Park et al.Botox ® in human
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302 J. Park et al.Long-term effect
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304 J. Park et al.is as high as 50%
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306 J. Park et al.Table 16.4 Drugs
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308 J. Park et al.septum should be
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310 J. Park et al.16.9 Hemifacial S
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312 J. Park et al.16.9.5 TreatmentB
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314 J. Park et al.regeneration beca
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316 J. Park et al.Alderson K, Holds
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318 J. Park et al.Grandas F, Elston
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320 J. Park et al.McCord CD Jr (198
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Part VIIISummary and Conclusions
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326 L.K. McLoon and F.H. Andrade17.
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332 L.K. McLoon and F.H. AndradeDie
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334 L.K. McLoon and F.H. AndradeSam
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IndexAAbducens nucleusvs. lateral r
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Index339Embryonic myosin heavy chai
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IndexLLagophthalmos , 304, 308Lamin
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Indexmuscular dystrophy , 187-190my
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Index345hydrostat mass reduction ,
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