Reduction in postsynaptic inhibition during maintained electrical stimulation of different nerves in the cat hindlimb

Abstract

1. Steady-state postsynaptic potentials (PSPs) were generated by prolonged (approximately 1 s) high-frequency (100-200 Hz) electrical stimulation of nerves in the cat hindlimb. The characteristics of these steady-state PSPs were compared for two polysynaptic afferent pathways (ipsilateral cutaneous sural vs. contralateral peroneal nerves), two animal preparations (decerebrate vs. chloralose), and two motoneuron pools (medial gastrocnemius vs. lateral gastrocnemius-soleus). 2. PSPs from both nerves usually (36 of 51 cases) contained a mixture of depolarizing and hyperpolarizing components. In all 36 cases where the PSP contained a hyperpolarizing component, a consistent qualitative pattern emerged during prolonged stimulation: the hyperpolarization reached a peak approximately 20 ms after stimulation onset and then decayed with a biphasic time course that consisted of an initial rapid phase (20-40 ms) and a later slower phase (200-400 ms) before the steady-state value was reached. This pattern occurred regardless of the differences in polysynaptic afferent pathways, animal preparations, and motoneuron pools. 3. The consistency of this overall pattern was remarkable, given the existence of several quantitative differences among the PSPs. These differences include the following: hyperpolarizing components were least common in the sural and peroneal PSPs in the decerebrate preparation. And only these sural and peroneal PSPs tended to have prolonged afterpotentials after stimulus cessation. The steady-state sural PSPs in the decerebrate preparation tended to generate the largest PSPs and, moreover, these PSPs did not follow the overall trend of having a statistically significant relation between the amplitude of the initial hyperpolarization and the amount of its decay. Finally, transient sural PSPs in lateral gastrocnemius-soleus motoneurons in the decerebrate preparation tended to have the largest hyperpolarizations. 4. To determine whether the decay of the hyperpolarization and the subsequent dominance of depolarization was due to a decreased inhibition or an increased excitation, injected current pulses were utilized to measure the changes in the cell's input resistance during the course of the synaptic input. A strong decrease in input resistance accompanied the initial period of maximal hyperpolarization (50% with respect to the resting input resistance). Input resistance then returned toward resting values as hyperpolarization faded and depolarization became dominant. However, there remained a persistent decrease in input resistance during the final phase of the PSP that amounted to < 10% of the initial decrease. These findings indicated that much of the reduction in hyperpolarization reflected a progressive decrease in synaptic efficacy for the inhibition.(ABSTRACT TRUNCATED AT 400 WORDS)

Spastic Long-Lasting Reflexes in the Awake Rat After Sacral Spinal Cord Injury

“…6 and 7). Long-duration cutaneous-evoked EPSPs are not seen in intact spinal cords of unanesthetized animals (Crenna et al 1982;Heckman et al 1994), and consistent with this, in normal awake rats, longlasting reflexes cannot be evoked even with a conditioning stimulation that evokes EMG (Fig. 7).…”

“…In normal and acute spinal rats, caudal trunk stimulation does not by itself evoke a longlasting reflex, although in acute spinal rats, a weak tonic contraction can be evoked by strong C-fiber stimulation. Thus the long-lasting reflexes in chronic spinal rats are more excitable and lower threshold, as in other animal models of spasticity (Taylor et al 1999), and similar to the exaggerated flexor withdrawal reflexes seen in spastic humans after chronic spinal cord injury (Hornby et al 2003;Kuhn and Macht 1948;Roby-Brami and Bussel 1987).…”

“…Furthermore, the characteristics of this reflex are consistent with triggered spasms in the tail. That is, the high reflex excitability (from rest), involvement of both low-and high-threshold afferents, and enhancement with repetition are similar to the characteristics of triggered spasms Hornby et al 2003;Kuhn and Macht 1948).…”

“…However, these EPSPs do not initially evoke large spastic reflexes because of the lack of motoneuron excitability (Bennett et al 2001c;Li et al 2004a). For example, in acute spinal rats and cats, there are unusually long polysynaptic EPSPs (ϳ200 -500 ms) in response to a low-threshold cutaneous stimulation pulse (Baker and Chandler 1987;Crenna et al 1982;Li et al 2004a) that are not seen in spinal cord intact preparations (Crenna et al 1982;Heckman et al 1994). However, these EPSPs do not trigger spasms immediately after injury.…”

Adjustable Amplification of Synaptic Input in the Dendrites of Spinal Motoneurons In Vivo

“…All procedures were approved by the animal care committee at Northwestern University. Full details are available in previous publications (Heckman et al, 1994;Lee and Heckman, 1998a). Briefly, all surgical preparations of the spinal cord and hindlimb were done under deep gaseous anesthesia (1.5-3.0% isoflurane in a 3:1 mixture of O 2 and N 2 O).…”