The ionic mechanisms of rhythmic burst firing and single spike, tonic discharge were investigated with extracellular and intracellular recordings of single neurones in the guinea-pig nucleus reticularis thalami (NRT) maintained as a slice in vitro. 2. Activation of cortical/thalamic afferents to NRT neurones resulted in a short latency burst of action potentials which could be followed by a rhythmic sequence of oscillatory burst firing. Intracellularly, this oscillatory activity was associated with an alternating sequence of low threshold Ca2+ spikes separated by after-hyperpolarizing potentials. Intracellular injection of short duration hyperpolarizing current pulses resulted in a similar sequence of oscillatory burst firing, suggesting that this activity is an intrinsic property of NRT cells. The frequency of rhythmic burst firing was highly voltage and temperature dependent and was between 7-12 Hz at -65 to -60 mV at 38 degrees C. In addition, at depolarized membrane potentials, oscillatory burst firing was typically followed by a prolonged tail of single spike activity. 3. Application of the Na+ channel poison tetrodotoxin blocked the generation of fast action potentials, but left intact the rhythmic sequence of low threshold Ca2+ spikes separated by after-hyperpolarizing potentials (AHPs). The reversal potential of the AHPs was -94 mV, suggesting that it was mediated by an increase in K+ conductance. Extracellular application of tetraethylammonium or apamin, or intracellular injection of Cs+ or the Ca2+ chelating agent EGTA, blocked the Ca2+ spike AHP, indicating that it is mediated by a Ca(2+)-activated K+ current. 4. Block of the AHP resulted in the marked enhancement of a slow after-depolarizing potential (ADP). The slow ADP occurred only following the generation of low threshold Ca2+ spikes. Replacement of extracellular Ca2+ with Mg2+ or Sr2+ resulted in an abolition of the slow ADP. In addition, the increase in [Mg2+]o resulted in an abolition of the low threshold Ca2+ spike. In contrast, replacement of extracellular Ca2+ with Ba2+ did not abolish the slow ADP. These results indicate that the ADP can be activated by either Ca2+ or Ba2+, but not by Mg2+ or Sr2+. 5. Replacement of extracellular Na+ with choline+ did not abolish the slow ADP, while replacement with N-methyl-D-glucamine+ did, indicating that the slow ADP can be supported by choline+, but not by N-methyl-D-glucamine+. Neither chemical affected the low threshold Ca2+ spike. These results are consistent with the slow ADP being mediated by a Ca(2+)-activated non-selective cation (CAN) current.(ABSTRACT TRUNCATED AT 400 WORDS)
