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41 Despite their presence throughout the central nervous system, the impact of axonally 42 expressed gamma-amino-butyric-acid type-A receptors (GABAARs) on neuronal signaling is just 43 beginning to be understood. A recently published article by Jason Pugh and Craig Jahr (2011) 44 tackled this important issue by investigating GABAAR-mediated function in axons of cerebellar 45 granule cells. Their results indicate parallel fiber GABAARs enhance neurotransmitter release 46 probability and boost axonal and somatic excitability. 47 48 Introduction to the work of Jason Pugh and Craig Jahr 49 Bernard Katz once said, “The more one finds out about properties of different synapses, 50 the less grows one’s inclination to make general statements about their mode of action.” This 51 maxim can be extended beyond synaptic transmission to neuronal signaling in general. For 52 example, it is widely appreciated that dendritic integration leads to an all-or-none action 53 potential (AP) initiated near the soma which then propagates to the axon terminal. The terminal 54 bouton is depolarized, leading to Ca influx and subsequent neurotransmitter release. Although 55 this model is highly instructive, research over the past few decades revealed additional 56 computational features of neurons. It is now known APs can travel backwards in an antidromic 57 fashion away from the soma and into dendrites (Stuart et al. 1997). Moreover, mounting 58 evidence indicates APs can also be generated in the axon where they travel antidromically 59 towards the soma (Paradiso and Wu 2009). 60 Action potentials are not alone in their ability to influence neural computation. While sub61 threshold membrane potential fluctuations can lead to the production or negation of APs, they 62 themselves can provide meaningful information to the system (Alle and Geiger 2008). Sub63 threshold events generally originate from ligand-gated ion channels expressed in the plasma 64 membrane. While the role that somato-dendritic ion channels play in supporting graded 65 potentials and AP generation has been relatively well characterized, the contribution of channels 66 expressed in axonal compartments to these signals is less clear. Interestingly, it is now known 67 that GABAARs are expressed in certain axons throughout the brain and spinal cord (Trigo et al. 68 2008). In mature animals, GABAAR activation typically hyperpolarizes the membrane potential 69 due to low intracellular Cl concentrations. However, compared with the soma and dendrites, 70 axonal compartments can maintain more Cl, resulting in a higher Cl reversal potential, and 71 GABAAR activation depolarizes the membrane potential (Price and Trussell 2006). Given the 72 widespread expression of GABAARs in the central nervous system, determining when and 73 where these channels exert their depolarizing action is essential to advancing our knowledge of 74