Single synaptic terminal attached to freshly isolated superior cervical ganglion (SCG) neurons, or "soma-attached terminal", were identified using hmmuno staining, electron microscopy (EM) and fluorescent FM1-43 imaging. Using electrochemical carbon fiber electrode (CFE) (for secretion), fura-2 (for hntracellular [Ca~+]j) and FM 1-43 (for synapse visualization), we have examined the existence and role of Ca2+ stores in a single terminal. Activation of either IP-3 or ryanodine Ca2+ stores was sufficient to trigger quantal secretion from tbe terminals. ATP is a fast neurotransmitter in both the central and peripheral neuron systems. CFE, patch clamp, and together with fura-2 Ca2+ imaging were employed to investigate the ATP-induced quantal secretion from free pre-synaptic terminals. We concluded that ATP-induced Ca2+ influx through P2X channels located in free pre-synaptic terminals alone was sufficient to trigger secretion, while ATP-induced intracellular Ca2+ release via P2Y/G-protein pathway played an additional modulation role. We investigated the mechanisms of mAChRs inhibition on nAChRs. lmM methacoline (Mch), the agonist of muscarinic receptors, almost completely suppressed lOOuM nicotine-induced current (M-inhibition). The results of temperature experiments supposed that the inhibition of nicotine current mediated by Mch involved pathway linked to G protein. Pertussis toxine (PTX) pretreatment overnight, or whole-cell dialysis with Bapta (20mM) or GDP 3 s attenuated M-inhibition. The agonists or antagonists of PKA and PKC had effects on M-inhibition. We concluded that the inhibition effect of Mch on nicotine current was mediated by intracellular second messages activated by G-proteins. Release of neurotransmitter is dependent on encoding of action potentials (AP) in single cells. Pattern of APs are dependent on ionic channels on plasma membrane, including Ca2+ channels and Ca2+-activated K+ channels. The two types of Ca2+ dependent K+ channels regulate APs pattern differently. The large conductance Ca2+-activated K+ (BKCa) channels are responsible for the repolarization and the fast afterhyperpolarization of AP, can regulate the duration of AP, and change the Ca2+ influx during APs. The small conductance Ca2+-activated K+ (SKCa) channels are responsible for the slow afterhyperpolarization of a train APs, and also can regulate APs pattern. The subsequence of inactivation of BKCa current and enhancement of SKCa current during the higher electrical firing would result in the action potential adaptation to protect cells from the harm of excess high frequency stimulation. KCa channels can regulate neurotransmitters release, so it is important to study the antagonists inhibition of KCa channels. Here we investigated the inhibition of BmPOS and BmTX3 on KCa channels.