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<DIV><FONT face=Arial size=2>Dear colleagues,</FONT></DIV>
<DIV><FONT face=Arial size=2></FONT> </DIV>
<DIV><FONT face=Arial size=2>The following article is now available
at: <BR></FONT><FONT face=Arial size=2><A
href="http://www.cs.stir.ac.uk/~vcu/papers/IJNS2007.pdf">http://www.cs.stir.ac.uk/~vcu/papers/IJNS2007.pdf</A></FONT></DIV><FONT
face=Arial size=2>
<DIV><BR>Cutsuridis, V. (2007)<BR>Does Abnormal Spinal Reciprocal Inhibition
Lead to Co-contraction</DIV>
<DIV>of Antagonist Motor Units? A Modeling Study</FONT></DIV>
<DIV><FONT face=Arial size=2>International Journal of Neural
Systems, 17(4): 319-327<BR> <BR>ABSTRACT<BR></FONT><FONT
face=Arial size=2><FONT face=CMR9 size=1><FONT size=2>It is suggested that
co-contraction of antagonist motor units <BR>perhaps due to abnormal disynaptic
I</FONT></FONT><I><FONT face=CMMI7>a </I></FONT><FONT face=CMR9>reciprocal
inhibition is <BR>responsible for Parkinsonian rigidity. A neural model of
Parkinson’s <BR>disease bradykinesia is extended to incorporate the effects of
spindle <BR>feedback on key cortical cells and examine the effects of dopamine
depletion <BR>on spinal activities. Simulation results show that although
reciprocal inhibition is<BR>reduced in DA depleted case, it doesn’t lead to
co-contraction of antagonist <BR>motor neurons. Implications to Parkinsonian
rigidity are discussed.</FONT></FONT><FONT face=Arial><FONT size=2>
<BR></FONT></FONT></DIV>
<DIV><FONT face=Arial size=2></FONT> </DIV>
<DIV><FONT face=Arial size=2></FONT> </DIV>
<DIV><FONT face=Arial size=2>KEYWORDS: </FONT><FONT face=Arial size=2><FONT
size=2>Parkinson's disease, dopamine, reciprocal inhibition, spinal cord,
<BR>rigidity, neural model</DIV></FONT></FONT>
<DIV><FONT face=Arial size=2></FONT> </DIV></BODY><p>-- </p>
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