Here is also a quite good, brief summary that backs up what Andy is saying - http://www.ncbi.nlm.nih.gov/books/NBK11117/
Note that this talks about postsynaptic effects. GABA is the major inhibitory major neurotransmitter in the brain, which it can do by activating GABAA channels (composed of a variety of subunits) on, I think, mostly post-synaptic membranes, but also at pre-synaptic and ‘extra-synaptic’ sites. There is another type of GABA receptor, the ‘metabotropic’ G protein coupled GABAB, which can also mediate pre- and post-synaptic inhibition.
Excitatory and inhibitory neurons can synapse on the same neuron - this is not uncommon. And there is a lot of input, e.g., from neuropeptides and other substances like a major inhibitory transmitter such as endocannabinoids (e.g., activating the cannabinoid CB1 receptor in the brain, one of the most abundant central G protein-coupled receptors), that modulate either excitatory or inhibitory synapses.
Quite often you have to look at synapses in the brain as part of a network, e.g., inhibitory input onto an excitatory neurone (e.g., GABA onto a glutamate neurone), excitatory input onto an inhibitory neurone, inhibitory input onto an inhibitory neurone, etc.