Calcium spikes and calcium currents in neurons from the medial preoptic nucleus of rat.
Ca2+ spikes, their contribution to firing patterns, and the underlying Ca2+ currents in neurons of the medial preoptic nucleus of rat were investigated by tight-seal whole-cell recordings in a slice preparation. Two different types of spikes were recorded: Low-threshold spikes were generated from membrane potentials <-75 mV. High-threshold spikes were recorded when K+ currents were reduced, and were readily evoked from membrane potentials near -40 mV. Both types of spikes were blocked by substitution of Co2+ for Ca2+ in the external medium, but were insensitive to 2.0 microM TTX. Under voltage-clamp conditions, two main types of Ca2+ currents were characterized: low-threshold currents that activated at membrane potentials >-60 mV, and high-threshold currents that activated at potentials >-30 mV. The low-threshold current and the low-threshold spike were more sensitive to block by external Ni2+ than to block by Cd2+, whereas the high-threshold current and the high-threshold spike were more sensitive to block by external Cd2+ than to block by Ni2+. Significant fractions of the high-threshold currents were blocked by 10 microM nifedipine, 1.0 microM omega-conotoxin GVIA, 50 nM omega-agatoxin IVA and 1.0 microM omega-conotoxin MVIIC, suggesting the presence of L-, N-, P- and Q-type Ca2+ channels. There were also a high-threshold current component insensitive to the above mentioned toxins. It is proposed that the low-threshold current serves as a trigger for short bursts of fast spikes from hyperpolarized levels, whereas the high-threshold current is involved in the Cd2+-sensitive burst firing seen in relatively depolarized neurons.
Sundgren-Andersson
A K
AK
Department of Neurochemistry and Neurotoxicology, Stockholm University, S-106 91 Stockholm, Sweden.
Johansson
S
S
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D002104:Cadmium / Q000493:pharmacokinetics; D002118:Calcium / Q000493:pharmacokinetics*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000378:metabolism; D003035:Cobalt / Q000493:pharmacokinetics; D004558:Electric Stimulation; D007700:Kinetics; D008297:Male; D009474:Neurons / Q000737:chemistry* / Q000378:metabolism*; D009532:Nickel / Q000493:pharmacokinetics; D009543:Nifedipine / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D010455:Peptides / Q000494:pharmacology; D010507:Periodicity; D011188:Potassium / Q000493:pharmacokinetics; D015221:Potassium Channels / Q000502:physiology; D011301:Preoptic Area / Q000166:cytology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000493:pharmacokinetics; D015222:Sodium Channels / Q000502:physiology; D013111:Spider Venoms / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology; D020867:omega-Agatoxin IVA; D020866:omega-Conotoxin GVIA
D002121:Calcium Channel Blockers; D015220:Calcium Channels; D010455:Peptides; D015221:Potassium Channels; D015222:Sodium Channels; D013111:Spider Venoms; D020867:omega-Agatoxin IVA; D002104:Cadmium; D003035:Cobalt; D013779:Tetrodotoxin; D009532:Nickel; D020866:omega-Conotoxin GVIA; D012964:Sodium; D009543:Nifedipine; D011188:Potassium; D002118:Calcium