Neuropathic pain can involve exaggerated pain responses often accompanied by sensory deficits with some patients responding poorly to traditional analgesics. Dysfunctional mechanisms, and thus potential drug targets, are conceivably located on peripheral nerves and central neurones. Of interest here are alterations in spinal neuronal excitability contributing to the plasticity of transmission and modulating systems, manifest as altered nociception. Counterparts of clinical symptoms can be studied in animal models. Spinal nerve ligation, employed here, involves unilateral tight ligation of L5/6 spinal nerves of the sciatic nerve and reproducibly induces mechanical and cold allodynia. In vivo electrophysiology was subsequently used to record evoked dorsal horn neuronal responses to electrical and natural stimuli. Activation of voltage-dependent calcium channels (VDCCs) is critical for neurotransmitter release and neuronal excitability, and blockers are antinociceptive in behavioural and clinical studies. Here, effects of N-, P/Q-, T- and L-type VDCC blockers (ω-conotoxin GVIA, ω-agatoxin IVA, ethosuximide and nifedipine, respectively) on evoked neuronal responses were investigated in an attempt to unravel their physiological and pathophysiological roles in sensory transmission. Spinal ω-conotoxin GVIA produced prolonged inhibitions of the evoked neuronal responses in neuropathic and control rats, in a manner increased after neuropathy. Spinal ω-agatoxin IVA exerted inhibitory actions but to a lesser extent. Minimal inhibitions were achieved with spinal ethosuximide and nifedipine. Mechanisms of neuropathic pain are diverse; indicating that combination therapy could be beneficial. The anticonvulsant gabapentin, effective in the clinical treatment of neuropathic pain, has been demonstrated to bind the VDCC α2δ subunit. Here, gabapentin inhibited neuronal responses in neuropathic, but not normal, rats, in line with neuropathy-induced VDCC plasticity. In the presence of gabapentin, morphine exhibited greater inhibitions, again more pronounced after neuropathy. These studies indicate a prominent role for N-type VDCCs in sensory transmission, which is increased after neuropathy, suggestive of a key role in the increased central excitability.