SUMMARY1. Extracellular recordings have been obtained from 134 units in the paravermal cortex of lobule V in the anterior lobe of the cerebellum in free-to-move cats. Each unit discharged action potentials in a characteristic pattern with no complex spikes. Previous investigators have described such discharges and have assigned them to Golgi cells. We provide further evidence to support this identification.2. In cats which were sitting quietly, each putative Golgi cell discharged tonically at a low rate (overall mean (±S.D.) was 14-5+7-3 spikes/s). Eighty-one of the neurones were also recorded during steady walking on a moving belt and the discharge rate then averaged 17-7 (S.D. + 19-4) spikes/s.3. All eighty-one putative Golgi cells discharged rythmically during locomotion. Many different patterns of discharge were seen but as a population the neurones were most active in early stance and at the onset of the swing phase of the step cycle in the ipsilateral forelimb.4. Over a range of different walking speeds (0 5-09 m/s) and of different uphill inclines (0-25 deg), putative Golgi cells discharged with similar patterns and rates, despite large changes in the vigour of the locomotor movements and in the amplitude of limb muscle electromyograms.

Experimental therapeutics designed to enhance recovery from spinal cord injury (SCI) primarily focus on augmenting the growth of damaged axons by elevating their intrinsic growth potential and/or by nullifying the influence of inhibitory proteins present in the mature CNS. However, these strategies may also influence the wiring of intact pathways. The direct contribution of such effects to functional restoration after injury has been mooted, but as yet not been described. Here, we provide evidence to support the hypothesis that reorganization of intact spinal circuitry enhances function after SCI. Adult rats that underwent unilateral cervical spared-root lesion (rhizotomy of C5, C6, C8, and T1, sparing C7) exhibited profound sensory deficits for 4 weeks after injury. Delivery of a focal intraspinal injection of the chondroitin sulfate proteoglycan-degrading enzyme chondroitinase ABC (ChABC) was sufficient to restore sensory function after lesion. In vivo electrophysiological recordings confirm that behavioral recovery observed in ChABC-treated rats was consequent on reorganization of intact C7 primary afferent terminals and not regeneration of rhizotomized afferents back into the spinal cord within adjacent segments. These data confirm that intact spinal circuits have a profound influence on functional restoration after SCI. Furthermore, comprehensive understanding of these targets may lead to therapeutic interventions that can be spatially tailored to specific circuitry, thereby reducing unwanted maladaptive axon growth of distal pathways.

SUMMARY1. Cutaneous nerve stimulation was used to study the excitability of the spinoolivocerebellar pathways (SOCPs) to the c2 zone of the paravermal cerebellar cortex in the cat. Non-noxious single-shock stimulation of the right and left superficial radial (SR) nerves via implanted cuff electrodes was used to evoke field potentials in the cerebellar cortex via the SOCPs.2. The evoked potentials were recorded extracellularly either in lobule V of the anterior lobe (three cats) or within the paramedian lobule of the posterior lobe (one cat) with glass-coated tungsten microelectrodes. Measurement of the amplitudes of the responses was used to monitor transmission in the SOCPs in cats at rest and during walking.3. A total of eleven c2 recording sites were investigated in detail. At seven of these sites, responses were recorded both during locomotion and at rest. For all seven sites responses during locomotion were smaller, more variable in amplitude and less securely evoked (average reduction 59%). 4. At five out of the eleven recording sites (45 %) the mean amplitude of responses elicited during different tenths of the step cycle fluctuated sufficiently that the largest response was more than twice the smallest. In the majority of these cases (4/5) the responses were largest in either mid-stance or late swing. These fluctuations in response size occurred without parallel fluctuation in the amplitude of the peripheral nerve volley. At the remaining sites fluctuation of the cerebellar field size was less and in some cases practically absent.5. At six recording sites it was possible to record the climbing fibre potentials evoked by stimulation of both the ipsilateral and contralateral superficial radial nerves. In all six cases the fluctuations in size of the response during locomotion occurred in phase, despite the fact that the two limbs move out of phase.6. The probability that an individual stimulus would evoke any cerebellar response also varied between the different tenths of the step cycle and such variations occurred in parallel with the fluctuations in response size. This shows that the SOCP regulatory mechanisms) must, at least in part, operate at a precerebellar level.MS 8015 R. APPS, M. LIDIERTH AND D. M. ARMSTRONG

Inhibitory mechanisms are essential in suppressing the development of allodynia and hyperalgesia in the normal animal and there is evidence that loss of inhibition can lead to the development of neuropathic pain. We used Fos expression to map the distribution of tonically inhibited cells in the healthy rat lumbar spinal cord. In a control group, Fos-like immunoreactive (Fos-LI) cells were rare, averaging 7.5+/-2.2 cells (mean+/-SEM; N=13 sections) per 20 microm thick section of dorsal horn. This rose to 103+/-11 (mean+/-SEM; N=20) in picrotoxin-treated rats and to 88+/-11 (mean+/-SEM; N=18) in strychnine-treated rats. These changes were significant (ANOVA; P<0.001). There were marked regional variations in the distribution of Fos-LI cells between picrotoxin- and strychnine-treated animals. Picrotoxin induced a significant increase in the number of Fos-LI cells throughout the dorsal horn (lamina I-VI) while strychnine significantly elevated Fos-like immunoreactivity only in deep laminae (III-VI). For both picrotoxin and strychnine, the increase in Fos-like immunoreactivity peaked in lamina V (at 3579+/-319 and 3649+/-375% of control, respectively; mean+/-SEM) but for picrotoxin an additional peak was observed in the outer part of lamina II (1959+/-196%). Intrathecal administration of both GABAA and glycine receptor antagonists has been shown elsewhere to induce tactile allodynia. The present data suggest that this allodynia could arise due to blockade of tonic GABAA and glycine-receptor mediated inhibition in the deep dorsal horn. GABAA antagonists also induce hypersensitivity to noxious inputs. The blockade of tonic inhibition in the superficial dorsal horn shown here may underlie this hyperalgesia.

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