GABA and chloride ionsWatch
The monocarboxylic amino acid neurotransmitters (GABA, taurine and glycine) are largely inhibitory, while the dicarboxylic ones (glutamate and aspartate) are excitatory. The particular GABA receptors that use chloride to produce hyperpolarization are GABA-A (with "A" as subscript - not possible to execute on TSR) and GABA-C. The GABA-A receptor is probably pentameric or tetrameric (has 4 or 5 sub-units (2 alpha, 2 beta and 1 gamma sub-units in the benzodiazepine receptors [benzodiazepines are one group of drugs used to treat anxiety = anxiolytics e.g. lorazepam, chlordiazepoxide] that assemble around a central pore). It is an ionotropic receptor.
In the CNS, GABA receptors are present between e.g. cerebellar Purkinje neurons and their synaptic connections in Deiter's nucleus, between the vestibular nucleus (the nucleus of the vestibulocochlear nerve (8th cranial nerve)) and trochlear neurones.
Chloride ions, being of course -vely charged, when they enter the post-synaptic neurone, cause hyperpolarization by increasing the net -ve charge inside the neuronal cell membrane.
There are 3 main types of chloride channels - the type relevant to GABA are the ligand-gated channels; Because Cl- conc-n is about 100+ mM outside cells and 20 mM inside, the gradient is inward, so opening of chloride channels leads to net negativity moving inwards leading to an IPSP (inhibitory post-synaptic potential = hyperpolarization).
((The GABA-B receptor is a metabotropic receptor i.e. it operates through a G-protein coupled mechanism - GPCR.))
I hope this helps improve your essay slightly!
M (clinical pharmacologist)