Bulbospinal inhibition of PAD elicited by stimulation of afferent and motor axons in the isolated frog spinal cord and brainstem

1992 ◽  
Vol 88 (1) ◽  
pp. 106-116 ◽  
Author(s):  
H. González ◽  
I. Jiménez ◽  
P. Rudomin
Keyword(s):  
Spinal Cord ◽  
Motor Axons ◽  
Frog Spinal Cord ◽  
Inhibition Of Pad ◽  
Stimulation Of

Habituation of a monosynaptic response in frog spinal cord: evidence for a presynaptic mechanism

1976 ◽  
Vol 39 (4) ◽  
pp. 661-666 ◽  
Author(s):  
P. B. Farel ◽  
R. F. Thompson
Keyword(s):  
Spinal Cord ◽  
Rana Catesbeiana ◽  
Membrane Conductance ◽  
Resting Membrane Potential ◽  
Extracellular Potassium ◽  
Initial Value ◽  
Lateral Column ◽  
Frog Spinal Cord ◽  
Before And After ◽  
Stimulation Of

1. Using the isolated spinal cord of bullfrogs (Rana catesbeiana), intracellular correlates of habituation-like depression of the monosynaptic response elicited in motoneurons by lateral column (LC) stimulation were investigated. The following properties of the motoneuron were compared before and after response depression produced by stimulation of the LC at 0.5/s: resting membrane potential, membrane conductance, critical firing level, and rheobasic current. No alteration was found in any of these parameters. 2. To determine whether transmitter release mechanisms were changing over trials, the LC was stimulated with pairs of stimuli separated by 6 ms presented at 0.5/s. While the amplitude of the first EPSP declined (74% of initial value), the amplitude of the second EPSP increased (111% of initial value). Facilitation ratios thus increased. 3. The following conclusions can thus be drawn: 1) habituation involves a process intrinsic to the LC-motoneuron synapse; 2) habituation is not totally mediated by receptor desensitization; 3) habituation is not mediated by a mechanism extrinsic to the LC-motoneuron synapse that depolarizes terminal endings, e.g., presynaptic inhibition or accumulation of extracellular potassium; 4) habituation is not produced by transmitter depletion. Any of these possibilities has as a necessary consequence that facilitiation ratios remain unchanged. 4. Possible mechanisms that could mediate habituation are: 1) alterations in mobilization and/or release of transmitter; 2) decreased probability of invasion of terminal branches of the presynaptic fiber by the action potential.

Drastic Decrease in Isoflurane Minimum Alveolar Concentration and Limb Movement Forces after Thoracic Spinal Cooling and Chronic Spinal Transection in Rats

2005 ◽  
Vol 102 (3) ◽  
pp. 624-632 ◽  
Author(s):  
Steven L. Jinks ◽  
Carmen L. Dominguez ◽  
Joseph F. Antognini
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Minimum Alveolar Concentration ◽  
Tail Flick ◽  
Noxious Stimulation ◽  
Partial Recovery ◽  
Spinal Transection ◽  
Thoracic Spinal ◽  
Cord Injury ◽  
Stimulation Of

Background Individuals with spinal cord injury may undergo multiple surgical procedures; however, it is not clear how spinal cord injury affects anesthetic requirements and movement force under anesthesia during both acute and chronic stages of the injury. Methods The authors determined the isoflurane minimum alveolar concentration (MAC) necessary to block movement in response to supramaximal noxious stimulation, as well as tail-flick and hind paw withdrawal latencies, before and up to 28 days after thoracic spinal transection. Tail-flick and hind paw withdrawal latencies were measured in the awake state to test for the presence of spinal shock or hyperreflexia. The authors measured limb forces elicited by noxious mechanical stimulation of a paw or the tail at 28 days after transection. Limb force experiments were also conducted in other animals that received a reversible spinal conduction block by cooling the spinal cord at the level of the eighth thoracic vertebra. Results A large decrease in MAC (to </= 40% of pretransection values) occurred after spinal transection, with partial recovery (to approximately 60% of control) at 14-28 days after transection. Awake tail-flick and hind paw withdrawal latencies were facilitated or unchanged, whereas reflex latencies under isoflurane were depressed or absent. However, at 80-90% of MAC, noxious stimulation of the hind paw elicited ipsilateral limb withdrawals in all animals. Hind limb forces were reduced (by >/= 90%) in both chronic and acute cold-block spinal animals. Conclusions The immobilizing potency of isoflurane increases substantially after spinal transection, despite the absence of a baseline motor depression, or "spinal shock." Therefore, isoflurane MAC is determined by a spinal depressant action, possibly counteracted by a supraspinal facilitatory action. The partial recovery in MAC at later time points suggests that neuronal plasticity after spinal cord injury influences anesthetic requirements.

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