Abstract:SUMMARY1. Cat a-motoneurones supplying muscle units of the soleus S type and gastrocnemius S, FR and FF types were injected intracellularly with horseradish peroxidase.2. Ten a-motoneurones of each motor unit type were collected for morphological analysis of the intramedullary parts of their axonal systems including the recurrent axon collaterals.3. The a-motor axon diameters in the spinal cord white matter were significantly smaller for the soleus motor units (mean = 5-2 jtm) than for the gastrocnemius S unit… Show more
“…526)." In particular, Pompeiano and Wand (1976;Wand and Pompeiano, 1979) a size-dependency, and Cullheim and Kellerth (1978) produced convergent anatomical evidence by showing that larger, phasic motoneurons make many more synaptic contacts with Renshaw cells than smaller, tonic motoneurons. The second hypothesis has been well supported since Sherrington's (1906) observations of reciprocal inhibition, but is oddly ignored in many treatments.…”
Section: Evidence For Assumed Distribution Of Renshaw Connectivitymentioning
confidence: 99%
“…Suppose that a co-contractive input, P, to a-MN 1 and a-MN 2 occurs when input A 1 exceeds A 2 and that the activity of a-M N 1 is consequently multiplied by a larger factor than that of a-M Nz due to the size principle (Figure 8). Then R 1 also becomes much more active due to a size-correlated synaptic weighting on a-M N 1 axon collaterals to R 1 ( Cullheim and Kellerth, 1978;Pompeiano, 1984). Because the opposing R 2 has not experienced as large an input increment, R 1 will transiently become more active than R 2 by an amount that scales with the difference between the a-MN output increments due to the change in P. Thus, this system calculates a predicted error due to unequal amplifications of co-contractive inputs.…”
Section: Automatic Compensation By the Renshaw-jain Pathway For Unequmentioning
“…526)." In particular, Pompeiano and Wand (1976;Wand and Pompeiano, 1979) a size-dependency, and Cullheim and Kellerth (1978) produced convergent anatomical evidence by showing that larger, phasic motoneurons make many more synaptic contacts with Renshaw cells than smaller, tonic motoneurons. The second hypothesis has been well supported since Sherrington's (1906) observations of reciprocal inhibition, but is oddly ignored in many treatments.…”
Section: Evidence For Assumed Distribution Of Renshaw Connectivitymentioning
confidence: 99%
“…Suppose that a co-contractive input, P, to a-MN 1 and a-MN 2 occurs when input A 1 exceeds A 2 and that the activity of a-M N 1 is consequently multiplied by a larger factor than that of a-M Nz due to the size principle (Figure 8). Then R 1 also becomes much more active due to a size-correlated synaptic weighting on a-M N 1 axon collaterals to R 1 ( Cullheim and Kellerth, 1978;Pompeiano, 1984). Because the opposing R 2 has not experienced as large an input increment, R 1 will transiently become more active than R 2 by an amount that scales with the difference between the a-MN output increments due to the change in P. Thus, this system calculates a predicted error due to unequal amplifications of co-contractive inputs.…”
Section: Automatic Compensation By the Renshaw-jain Pathway For Unequmentioning
“…The spatial positioning of the neurons in the simulated neuronal columns is specially important because RC synapses on MNs (and vice-versa) occur among synergistic nuclei (McCurdy and Hamm 1994a, b), with synaptic strength depending on the distance between the cells (Cullheim and Kellerth 1978;Windhorst 1996;Burke 2004).…”
Section: Methodsmentioning
confidence: 99%
“…On the other hand, one MN reaches a smaller number of RCs (Cullheim and Kellerth 1978;Burke 2004). The influences of a RC over the MN pool and the influence of a MN over the RC pool diminish with distance, modeled according to Eq.…”
Section: Recurrent Inhibition Synapsesmentioning
confidence: 99%
“…For the synapses from MNs to RCs, the factor a was set at 0.01, because the maximum spread of the MN collaterals reaches 1 mm (Cullheim and Kellerth 1978;Burke 2004). …”
With the advent of new tools and techniques including the retrograde approach, success rates for recanalization of chronic total occlusion (CTO) have improved. Numerous cardiac and extracardiac complications during retrograde CTO recanalization have been described. To date the development of ST-segment elevation myocardial infarction (STEMI) with retrograde recanalization as a result of atheroembolization has not been reported. We report such a case following retrograde recanalization of a totally occluded right coronary artery.
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