Curare is a plant alkaloid originally used as a poison on darts and arrows used in hunting. It is a competitive antagonist for the nicotinic acetylcholine receptor, which is found in the neuromuscular junction and autonomic ganglia. We know a lot about this receptor and it's blockade by curare, so most good basic pharmacology textbooks devote a fair amount of space to it and you'll find mention in many physiology and neuroscience textbooks. I'd refer you to Goodman and Gilman Chapter 11 for a general reference.
The basics are as follows:
Curare is a quaternary amine. This means it has a charge on it and cannot cross the blood brain barrier. This was confirmed in 1947 by Scott Smith (pubmed link), an anesthesiologist, who administered very high doses of d-tubocurarine to himself (while under mechanical ventilation), resulting in complete paralysis but no central CNS effects. It's an interesting read if you get the chance, and records very carefully details of the minute by minute response for 4 hours of a series of administrations and reversals (with an acetylcholinesterase inhibitor).
What you get, as reported by Smith and confirmed by others, is blockade of motor outflow with skeletal muscle paralysis (including respiratory muscles) and also probably some ganglionic blockade (this is supported with further research since 1947). There are no changes in sensory inflow or any central effects. The blockade of the nicotinic acetylcholine receptors is reversed with an acetylcholinesterase inhibitor by increasing the amount of acetylcholine in the cleft to the point where it overcomes the competitive inhibition by curare.