The role of intrinsic and agonist-activated conductances in determining the firing patterns of preoptic area neurons in the guinea pig.
Whole-cell and intracellular recordings were made in coronal hypothalamic slices prepared from ovariectomized female guinea pigs. 62% of preoptic area (POA) neurons fired action potentials in a bursting manner, and exhibited a significantly greater afterhyperpolarization (AHP) than did non-bursting POA neurons. The majority (70%) of POA neurons (n=76) displayed a time-dependent inward rectification (I(h)) that was blocked by CsCl (3 mM) or by ZD 7288 (30 microM). In addition, 51% of the cells expressed a low-threshold spike (LTS) associated with a transient inward current (I(T)) that was blocked by NiCl(2) (200 microM). A smaller percentage of POA neurons (29%) expressed a transient outward, A-type K(+) current that was antagonized by a high concentration of 4-aminopyridine (3 mM). Moreover, POA neurons responded to bath application of the mu-opioid receptor agonist DAMGO (93%) or the GABA(B) receptor agonist baclofen (83%) with a membrane hyperpolarization or an outward current. These responses were accompanied by a decrease in input resistance or an increase in conductance, respectively, and were attenuated by BaCl(2) (100 microM). In addition, the reversal potential for these responses closely approximated the Nernst equilibrium potential for K(+). These results suggest that POA neurons endogenously express to varying degrees an AHP, an I(h), an I(T) and an A-type K(+) current. The vast majority of these neurons also are inhibited upon mu-opioid or GABA(B) receptor stimulation via the activation of an inwardly-rectifying K(+) conductance. Such intrinsic and transmitter-activated conductances likely serve as important determinants of the firing patterns of POA neurons.
Wagner
E J
EJ
Department of Physiology and Pharmacology, L334, Oregon Health Sciences University, 3181 S.W. Sam Jackson Park Road, Portland, OR 97201, USA. wagnere@ohsu.edu
Reyes-Vazquez
C
C
Ronnekleiv
O K
OK
Kelly
M J
MJ
D015761:4-Aminopyridine / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects* / Q000502:physiology; D000818:Animals; D001418:Baclofen / Q000494:pharmacology; D017609:Barium Compounds / Q000494:pharmacology; D002586:Cesium / Q000494:pharmacology; D002712:Chlorides / Q000494:pharmacology; D020875:Enkephalin, Ala(2)-MePhe(4)-Gly(5)- / Q000494:pharmacology; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D005260:Female; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008564:Membrane Potentials; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D009532:Nickel / Q000494:pharmacology; D010052:Ovariectomy; D018408:Patch-Clamp Techniques; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology; D011301:Preoptic Area / Q000187:drug effects / Q000502:physiology*; D011743:Pyrimidines / Q000494:pharmacology; D011930:Reaction Time; D013779:Tetrodotoxin / Q000494:pharmacology
D017609:Barium Compounds; D002712:Chlorides; D018690:Excitatory Amino Acid Agonists; D015221:Potassium Channels; D011743:Pyrimidines; C024986:barium chloride; D020875:Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; C082246:ICI D2788; D002586:Cesium; D013779:Tetrodotoxin; C022838:nickel chloride; D009532:Nickel; D015761:4-Aminopyridine; C028019:cesium chloride; D001418:Baclofen