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While it is well established that the \u03b8 activity depends on cholinergic inputs from the medial septum\/vertical limb of the diagonal band nucleus (MS\/DBv) and \u03b8 discharges of GABAergic interneurons, and can be induced with cholinergic receptor agonists, it is not clear how the increased excitation of pyramidal cells could occur with increased discharges of GABAergic interneurons during \u03b8 waves. Here, we show that the characteristic \u03b8 activity in adult rat hippocampal CA1 pyramidal cells is associated with GABAergic postsynaptic depolarization and a shift of the reversal potential from Cl<jats:sup>\u2212<\/jats:sup>toward HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>(whose ionic gradient is regulated by carbonic anhydrase). The \u03b8 activity was abolished by GABA<jats:sub>A<\/jats:sub>receptor antagonists and carbonic anhydrase inhibitors, but largely unaffected by blocking glutamate receptors. Carbonic anhydrase inhibition also impaired spatial learning in a watermaze without affecting other sensory\/locomotor behaviors. Thus HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>-mediated signaling, as regulated by carbonic anhydrase, through reversed polarity of GABAergic postsynaptic responses is implicated in both \u03b8 and memory consolidation in rat spatial maze learning. We suggest that this mechanism may be important for the phase forward shift of the place cell discharges for each \u03b8 cycle during the animal's traversal of the place field for that cell.<\/jats:p>","DOI":"10.1152\/jn.2001.85.1.269","type":"journal-article","created":{"date-parts":[[2017,12,21]],"date-time":"2017-12-21T10:42:48Z","timestamp":1513852968000},"page":"269-279","source":"Crossref","is-referenced-by-count":49,"title":["Theta Rhythm of Hippocampal CA1 Neuron Activity: Gating by GABAergic Synaptic Depolarization"],"prefix":"10.1152","volume":"85","author":[{"given":"Miao-Kun","family":"Sun","sequence":"first","affiliation":[{"name":"Laboratory of Adaptive Systems, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wei-Qin","family":"Zhao","sequence":"additional","affiliation":[{"name":"Laboratory of Adaptive Systems, National Institute of 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