Characterization of carbachol-induced rhythmic bursting discharges in neurons from guinea pig lateral septum slices.

A brain slice preparation from guinea pigs and intracellular recording techniques were used to examine the effects of carbachol application on the three classes (A, B, and C) of neurons (n = 68, 40 of class A, 12 of class B, 16 of class C) within the mediolateral part of the lateral septum (LSml). Bath application of carbachol elicited a sustained depolarization associated with an increase in membrane input resistance, action-potential firing and triggered rhythmic bursting discharges in 59% of recorded neurons. According to the configuration of these bursts, LSml neurons were classified into type I, II, and III neurons with reference to their response to carbachol. The frequency of spontaneous bursts was increased by depolarization caused by applied DC current in the three types of neurons. Bursts in type II and III neurons were voltage and dose dependent. These dependences were responsible for a continuum of variation in carbachol responses in these two types of neurons. As the neuron depolarized in the presence of carbachol, spontaneous action potentials increased in frequency and slow afterdepolarizing potentials (sADPs) appeared and preceded the occurrence of the first burst. These sADPs from adjacent action potentials appeared to progressively increase to initiate a burst. In the presence of carbachol, sADPs and bursts were also observable after action potentials evoked by depolarizing current pulses at the resting membrane potential (RMP) in LSml neurons. Evoked sADPs and bursts were associated with an apparent increase in input conductance. Application of low Na+ medium blocked both the sADP and bursts. Application of zero Ca2+ medium either 1) blocked completely the generation of sADPs and bursts (n = 16), or 2) did not block bursts (n = 14). Evoked sADPs and bursts were blocked by tetraethylammonium but were resistant to external Cs+. The results indicate that the activation of cholinergic receptors does not differentially affect the three classes of LSml neurons. The responses to carbachol in type II and III neurons form a continuum of variation, whereas these of type I neurons constitute a discrete entity. The selective cholinergic induction of a sADP, and the progressive activation of these sADPs in LSml neurons are thought to be responsible for the onset of the three types of rhythmic bursting discharges. We propose that sADPs and bursts induced by carbachol are generated by a cationic conductance largely permeable to Na+. In a subpopulation of LSml neurons (n = 16), the bursts are dependent on the presence of Ca2+ in the medium.