The lamprey is a lower vertebrate model system for studying locomotor network function. Neural networks in the spinal cord, which generate basic locomotor outputs, are activated and modulated by descending inputs from the brain. The lamprey recovers locomotor function after being paralysed by complete spinal lesions that remove these descending inputs, and thus prevent the activation of locomotor networks (Cohen et al. 1988). As in mammalian systems, the analysis of functional recovery in the lamprey has focused on regrowth of ascending and descending axons across lesion sites. However, there is evidence that regrowth alone cannot account for the recovery (Mackler & Selzer, 1985; McClellan, 1994). A complementary approach is to investigate how plasticity may alter network properties in locomotor networks to optimise function below lesion sites after injury. This plasticity could be evoked as a result of neuromodulator or activity-dependent effects on network cellular or synaptic properties, or through intrinsic changes in cellular or synaptic properties i.e. homeostatic or adaptive plasticity (Turrigiano, 1999). A potential role for adaptive plasticity has initially been examined by pharmacologically disrupting network function. Larval animals were anaesthetised by immersion in Tricaine methane-sulphonate (100-200mg/l) and the trunk region of the spinal cord was isolated. Spinal cords were then incubated in tetrodoxin (TTX, 1.5μM), 6-cyano-7-nitroquinoxaline-2,3-dione plus DL-2-amino-5-phosphonopentanoic acid (CNQX, 10μM; AP5, 50μM respectively), or CNQX (10μM) for 24 hours. TTX abolishes all action potential-evoked synaptic transmission in the network by blocking presynaptic Na⁺ channels, while CNQX and AP5 block postsynaptic AMPA and NMDA receptors, respectively. Intracellular recording was used to investigate several electrophysiological parameters to identify potential changes in presynaptic and postsynaptic properties, including the resting membrane potential, input resistance and the amplitude and frequency of spontaneous miniature EPSPs and IPSPs. The resting membrane potential of cells in TTX (-61.50±2.28mV, n=10) and CNQX/AP5-treated cords (-56.17±3.45mV, n=6) was significantly depolarised relative to control (-72.71±2.29mV, n=7; p<0.05, ANOVA with post-hoc Fishers pairwise comparison). There was also an increase in the frequency of spontaneous miniature EPSPs in TTX (3.23±0.29Hz, n=12) and CNQX/AP5 (3.01±0.41Hz, n=7) when compared with control (1.66±0.32Hz, n=10; p<0.05, ANOVA with post-hoc Fishers pairwise comparison). These changes were not seen when only postsynaptic AMPA receptors were blocked. Together, these effects suggest changes in presynaptic and postsynaptic properties. Disrupting network activity can thus evoke adaptive plasticity. This now provides a basis for examining the role of adaptive changes in locomotor networks below lesion sites in the recovery of locomotor function after complete spinal lesions.