The role of glutamate and GABA co-release in developing and adult brain is still not well understood. In our previous work we documented the co-existence of glutamate (VGLUT) and GABA (VGAT) transporters at synaptic and vesicular level. By immunoisolation VGLUT2 as well as VGLUT3 are found on VGAT vesicles. The presence of VGLUT on GABAergic vesicles enhances vesicular uptake of GABA. Post-embedding immuno-electron microscopy reveals the presence of VGLUT2 in GABAergic cerebellar basket cell terminals as well as the presence of VGAT in subsets of glutamatergic i.e., hippocampal and cerebellar mossy fiber terminals while it is absent in others i.e. cerebellar parallel and climbing fiber terminals. The co-existence of GABA in these terminals may provide the mossy fibers with a putative mechanism to autoregulate synaptic release via activation of presynaptic GABAA and/or GABAB receptors. In our present study we provide morphological evidence for a modulation of GABAergic properties during progression of kindling induced epilepsy. Quantitative postembedding immunogold labelling reveals changes in the amounts of synaptophysin, VGLUT, the glutamate decarboxylase GAD and VGAT depending on the kindling progression. Taken together, the GABAergic properties in some glutamatergic terminals may regulate synaptic plasticity in the normal adult CNS and changes under pathological conditions as a compensatory mechanism to protect against pathological glutamatergic overexcitation.