Cocoa-based products are among the most craved confections worldwide. While recent literature highlighted beneficial effects on human health, potential deleterious effects of cocoa are comparatively under-researched. Cocoa is derived from Theobroma cocoa, botanically related to other plants of the Rubiaceae, Theaceae, and Sterculiaceae families, which are used to produce coffee, tea, and other stimulating herbal-based products that have been linked to icto- and epileptogenesis based on animal studies and clinical data. The extracts from these plants share indeed several bioactive compounds, including polyphenols and methylxanthines. Especially the latter have been associated with an increase in epileptic seizures and with a reduction of anti-seizure drug efficacy, among other effects on neuronal excitability. While there is a host of studies on coffee and caffeine in this regard, comparatively little is however known about cocoa. Thus, given the hitherto absence of suitable animal models, an ex vivo and in vitro approach was chosen here in an effort to contribute elucidating putative effects of cocoa compounds on the neural circuitry and potentially related to icto- and epileptogenesis. Using the mouse as an experimental model organism, the research presented revealed heightened neural excitability, as examined through fEPSP recordings on hippocampal slices, and diminished expression of the GABAA 1 receptor subunit and Synapsin I and II as determined using western blots. Implications of the data regarding the safety profile of cocoa in certain subgroups at risk, specifically pregnant women, neonates, and epilepsy patients, as well as possible mechanisms through which cocoa compounds might influence neural excitability and neurogenesis are discussed.