Micro RNAs (miRs) are short non-coding RNA sequences with a role in regulating gene expression. MiR 134 influences spine density (1) and volume (2) and is upregulated in epilepsy (1). MiR 134 knockdown protects against seizures (1), though the underlying mechanisms are still not clear. We explored the effects of miR 134 on neuronal excitability and ex vivo epileptiform activity using an acute brain slice model of epilepsy. Adult male Sprague Dawley rats (200-300g) were treated with an antagomir to miR 134 or vehicle control, delivered via intracerebroventricular injection, carried out under anaesthesia with inhalational isofluorane (~2.5% in O2). Ex vivo brain slices were prepared 2-4 days later. Epileptiform activity was induced by bath perfusion with 9 mM K+ and recorded with extracellular micropipettes in hippocampal CA1. Intrinsic neuronal properties were probed using patch clamp recordings in baseline K+ conditions. MiR 134 knockdown via antagomir injection delayed the onset of epileptiform in ex vivo slices by 182 s relative to control (n = 9 control slices; 11 treated slices; Mann Whitney U test p = 0.002). MiR 134 knockdown had a tendency to increase action potential (AP) rising slope in single neurons, but this did not survive multiple comparisons (control: 179 ± 82 mV/ms, n = 6 neurons; treated: 251 ± 18 mV/ms, n=7 neurons; independent samples t test p = 0.043, α=0.025). We did not observe any other effects of the antagomir on intrinsic neuronal properties including: input resistance, resting membrane potential, AP amplitude, AP half width, maximum firing rate, miniature EPSC (mEPSC) amplitude, or mEPSC frequency. Thus, although miR 134 is protective against epileptiform activity in ex vivo brain slices, this is not associated with any robust changes to intrinsic excitability in CA1 neurons. In fact, the only change that approaches significance is a counterintuitive increase in action potential rising slope. We hypothesise that the delay to activity onset is associated with a synaptic change, as suggested previously (1), rather than the intrinsic neuronal properties tested thus far in our recordings. Additional work will probe synaptic strength in treated slices to test this. However, our data so far suggest that miR 134 alters seizure thresholds by relatively specific effects on neurons. A better understanding of the impact of miR 134 on neuronal excitability and connectivity will enhance its position as a potential novel therapy in epilepsy.