, 2007). Compounds acting on nAChRs are being developed for treating neurological diseases and disorders, including STI571 AD (Levin, McClernon, & Rezvani, 2006; Levin & Rezvani, 2002), Parkinson��s disease (Park et al., 2007; Quik, Bordia, et al., 2007; Quik, Cox, et al., 2007; Villafane et al., 2007), attention-deficit hyperactivity disorder (Potter & Newhouse, 2008), schizophrenia (Tizabi, 2007), and epilepsy (Shin et al., 2007). In order to understand how to treat nAChR-related disorders and diseases, it is critical to understand how these receptors participate in normal brain function. This entails not only understanding the biophysical properties of ion channel function and their pattern of expression but also how these receptors are regulating excitability and circuit behavior.

The primary cholinergic input to the hippocampus comes from the medial septum and diagonal band of Broca (MSDB), and the activation of both nAChRs and muscarinic ACh receptors (mAChRs) can initiate and sustain network oscillations important for cognitive function (Cobb & Davies, 2005; Dutar et al., 1995; Frotscher & L��r��nth, 1985; Lawrence, Grinspan, Statland, & McBain, 2006; Lawrence, Statland, Grinspan, & McBain, 2006; L��r��nth & Frotscher, 1987). In addition to the primary cholinergic input from the MSDB, there is also a significant gamma-aminobutyric acid (GABA)-ergic input. Hippocampal GABAergic interneurons, which express both nAChRs and mAChRs, can coordinate the activity of large numbers of principal cells.

The phasic GABAergic input, in concert with the tonic cholinergic excitation of interneurons, is thought to induce rhythmic inhibition of pyramidal cells (Buzsaki, 2002; Freund & Antal, 1988; Griguoli & Cherubini, 2011; Jones et al., 1999; Stewart & Fox, 1990; T��th, Freund, & Miles, 1997). Additionally, inputs to the hippocampus from the entorhinal Batimastat cortex (EC) are thought to regulate hippocampal theta rhythm (Buzsaki, 2002). Nevertheless, it is unclear precisely how both mAChRs and nAChRs, working in concert, can modulate the oscillatory properties of neurons within the hippocampus. Understanding how cholinergic receptor signaling regulates hippocampal network activity is critical since dysregulation of normal oscillations may induce hyperexcitability, leading to both seizures (Bertrand, Weiland, Berkovic, Steinlein, & Bertrand, 1998; Damaj, Glassco, Dukat, & Martin, 1999; Turski, Ikonomidou, Turski, Bortolotto, & Cavalheiro, 1989) and cognitive deficits linked with AD (Fodale, Quattrone, Trecroci, Caminiti, & Santamaria, 2006). The nAChRs (in particular the ��7 subtype) are thought to be participating in various mechanisms of neuroprotection (Dineley, 2007; Parri, Hernandez, & Dineley, 2011; Shen & Yakel, 2009).