The overall aim of this work was to establish the role of group I mGluR and KCNQ/M channels in aspects of the neurophysiology of area CA1 of the rat hippocampus. Specifically we studied the role of these putative drug targets in a form of epileptiform activity and in the slow fEPSP recorded using extracellular methods. First, we have described here the extracellular recording of an excitatory slow fEPSP which is predominantly mediated by acetylcholine, as evidenced by the increase in physostigmine and inhibition in the presence of atropine. This type of response is significantly enhanced by two KCNQ/M channels blockers Iinopiridine and XE-991 highlighting an involvement of M currents. Furthermore, this response has a glutamatergic component, as application of a glutamate uptake inhibitor (L-trans-PDC) significantly affected the slow fEPSP. Specifically, the response is 4-CPG sensitive but not MCPG sensitive suggesting an involvement of group I mGluRs in the modulation of this response. Another interesting finding was given by KCNQ/M channels which play a role in the regulation of synchronous population firing activity in the absence of synaptic acivity (low Ca2+ epileptiform activity). More specifically, application of retigabine, a KCNQ/M channel modulator, completely abolished the bursts, in an XE-991-sensitive manner. Furthermore, application of the KCNQ/M channel blockers, linopirdine or XE-991 alone, abolished the gamma frequency, but not the higher-frequency population spike firing observed during low Ca2+/high K+ bursts. Finally, it has been demonstrated that activation of group I mGluRs by application of the potent agonist DHPG causes a dramatic long lasting alteration in the frequency of low Ca2+ epileptiform activity. This long lasting effect on the burst frequency, is MCPG sensitive (group 1/11 mGluRs antagonist), showing a strong modulation by mGluRs in this non-synaptic epileptiform acitvity. Application of two tyrosine phosphatase inhibitors, PAD and SDV blocked the DHPG effect on the bursting frequency, providing that tyrosine phosphorylation is involved in DHPG-induced synaptic plasticity.