Properties of rat medial septal neurones recorded in vitro.
Activity of neurones of the rat medial septal nucleus (m.s.) was recorded in in vitro slice preparations. The recorded population could be divided into low (less than 30 M omega)- and high-input-resistance (greater than 30 M omega) neurones. The high-resistance neurones tended to fire spontaneous action potentials and post-synaptic potentials. Some of the spontaneously active cells fired rhythmically at rates of 2-10 Hz. The rhythmicity disappeared following hyperpolarization of the recorded cell. The cells could fire repetitive Ca2+ spikes in the presence of tetrodotoxin (TTX) and intracellular Cs+. Cd2+ blocked this rhythmicity. Most of the m.s. cells had a non-linear voltage-current relation in both the hyperpolarizing and depolarizing directions. Hyperpolarizing rectification was selectively blocked by extracellular Cs+ whereas depolarizing rectification could be blocked by TTX. A recovery from hyperpolarization was associated in many cells with a transient depolarization (anodal break (a.b.) potential). A 20 ms 15 mV hyperpolarization could trigger an a.b. potential. The a.b. potential was reduced by TTX and Cs+ but not by Cd2+ or Mn2+. Depolarization of quiescent neurones triggered action potential discharges. A common pattern of discharge was a burst of two spikes which kept a fairly constant interspike interval. The second spike in a doublet could not follow a rate of 10 Hz depolarizing current pulses. It was also sensitive to topical application of Cd2+. It is therefore suggested that Ca2+ might be involved in the generation of the doublet. Long depolarizing current pulses produced trains of action potentials, showing little accommodation and little after-hyperpolarization, indicating that these cells possess little Ca2+-dependent K+ current. Many cells emitted spontaneous post-synaptic potentials at high rates. These could be blocked by picrotoxin. Stimulation of the lateral septal (l.s.) nucleus produced a Cl-dependent i.p.s.p. The i.p.s.p. was blocked by picrotoxin. Topical application of gamma-aminobutyric acid (GABA) produced a marked Cl(-)-dependent increase in conductance. It is suggested that l.s. projects a GABA-mediated inhibitory connexion to the m.s. Acetylcholine (ACh) depolarized m.s. neurones and caused an increase in input resistance. The response was present in TTX or Cd2+-containing medium. Atropine blocked responses to ACh. 5-Hydroxytryptamine (5-HT) hyperpolarized m.s. neurones in a manner consistent with an increase in K+ conductance. The effects of 5-HT were seen in TTX- and Cd2+-treated m.s. slices.(ABSTRACT TRUNCATED AT 400 WORDS)
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001464:Barium / Q000494:pharmacology; D001921:Brain / Q000502:physiology*; D002104:Cadmium / Q000494:pharmacology; D002586:Cesium / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D009474:Neurons / Q000502:physiology*; D018377:Neurotransmitter Agents / Q000494:pharmacology; D010852:Picrotoxin / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013569:Synapses / Q000502:physiology; D013779:Tetrodotoxin / Q000494:pharmacology
D001464:Barium; D002104:Cadmium; D002586:Cesium; D018377:Neurotransmitter Agents; D010852:Picrotoxin; D013779:Tetrodotoxin