PMID- 1721875
OWN - NLM
STAT- MEDLINE
DCOM- 19920203
LR  - 20190721
IS  - 0014-4819 (Print)
IS  - 0014-4819 (Linking)
VI  - 86
IP  - 2
DP  - 1991
TI  - Components of the dynamic response of mammalian muscle spindles that originate in 
      the sensory terminals.
PG  - 359-66
AB  - One component of the dynamic response of muscle spindles is characterized by a 
      phase lead and frequency dependent sensitivity in response to sinusoidal 
      stretches at frequencies around 1 Hz. Possible mechanisms producing this 
      component, designated the "mid-frequency" dynamics, were investigated by testing 
      the hypotheses that they arise from the mechanical behavior of the intrafusal 
      muscle and alternatively from within the sensory terminals. Destruction of the 
      myofibrillar structure of the intrafusal muscle fibers did not alter the 
      mid-frequency dynamics, indicating that they do not arise from viscoelastic 
      properties of the intrafusal muscle. An Arrhenius plot of the temperature 
      dependence of the mid-frequency dynamics yielded an equivalent activation energy 
      of 6.5 Kcal/M in the temperature range 23-42 degrees C and a 3-fold higher 
      activation energy at lower temperatures. These observations are consistent with a 
      dynamic process associated with a membrane-bound biochemical process. The 
      addition of Ca++ and Ca(++)-activated-K+ (K(Ca] channel blockers (ZnCl2, Apamin 
      and TEA) to the bathing solution altered the response dynamics by reducing the 
      mid-frequency phase lead. The results suggest a negative feedback on the membrane 
      potential generated by K+ efflux following a Ca++ influx that opens K(Ca) 
      channels. A quantitative model fit to the experimental data yields a time 
      constant of about 80 ms representing the limiting process associated with 
      activation of the K(Ca) channels in this system. The results indicate that the 
      mechanism underlying the mid-frequency dynamics includes at least two processes: 
      one, not identified in this study, generates the phase lead and another, 
      involving Ca++ and K(Ca) channels, provides a negative feedback that modifies the 
      phase lead.
FAU - Kruse, M N
AU  - Kruse MN
AD  - Department of Physiology, University of Minnesota, Minneapolis 55455.
FAU - Poppele, R E
AU  - Poppele RE
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - Germany
TA  - Exp Brain Res
JT  - Experimental brain research
JID - 0043312
RN  - 0 (Calcium Channel Blockers)
RN  - 0 (Chlorides)
RN  - 0 (Ion Channels)
RN  - 0 (Potassium Channels)
RN  - 0 (Zinc Compounds)
RN  - 24345-16-2 (Apamin)
RN  - 86Q357L16B (zinc chloride)
RN  - J41CSQ7QDS (Zinc)
SB  - IM
MH  - Animals
MH  - Apamin/pharmacology
MH  - Calcium Channel Blockers/pharmacology
MH  - Cats
MH  - Chlorides/pharmacology
MH  - Elasticity
MH  - Freezing
MH  - In Vitro Techniques
MH  - Ion Channels/drug effects
MH  - Muscles/innervation/*physiology
MH  - Nerve Endings/*physiology
MH  - Neurons, Afferent/*physiology
MH  - Potassium Channels/drug effects
MH  - Temperature
MH  - Viscosity
MH  - Zinc/pharmacology
MH  - *Zinc Compounds
EDAT- 1991/01/01 00:00
MHDA- 1991/01/01 00:01
CRDT- 1991/01/01 00:00
PHST- 1991/01/01 00:00 [pubmed]
PHST- 1991/01/01 00:01 [medline]
PHST- 1991/01/01 00:00 [entrez]
AID - 10.1007/BF00228959 [doi]
PST - ppublish
SO  - Exp Brain Res. 1991;86(2):359-66. doi: 10.1007/BF00228959.