TY - JOUR
T1 - The role of intrinsic and agonist-activated conductances in determining the firing patterns of preoptic area neurons in the guinea pig
AU - Wagner, Edward J.
AU - Reyes-Vazquez, Cruz
AU - Rønnekleiv, Oline K.
AU - Kelly, Martin J.
N1 - Funding Information:
The authors thank Jason T. Deignan, Martha A. Bosch and Barry Naylor for outstanding technical assistance. The experiments described in this study were supported by PHS Grants NS35944 and DA00192 (RSDA to Martin J. Kelly).
PY - 2000/10/6
Y1 - 2000/10/6
N2 - 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 (Ih) that was blocked by CsCl (3 mM) or by ZD 7288 (30 μM). In addition, 51% of the cells expressed a low-threshold spike (LTS) associated with a transient inward current (IT) that was blocked by NiCl2 (200 μM). 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 μ-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 BaCl2 (100 μM). 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 Ih, an IT and an A-type K+ current. The vast majority of these neurons also are inhibited upon μ-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.
AB - 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 (Ih) that was blocked by CsCl (3 mM) or by ZD 7288 (30 μM). In addition, 51% of the cells expressed a low-threshold spike (LTS) associated with a transient inward current (IT) that was blocked by NiCl2 (200 μM). 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 μ-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 BaCl2 (100 μM). 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 Ih, an IT and an A-type K+ current. The vast majority of these neurons also are inhibited upon μ-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.
KW - Afterhyperpolarization
KW - Calcium current
KW - Firing
KW - Inward rectification
KW - Preoptic area
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U2 - 10.1016/S0006-8993(00)02698-6
DO - 10.1016/S0006-8993(00)02698-6
M3 - Article
C2 - 11011003
AN - SCOPUS:0034613223
SN - 0006-8993
VL - 879
SP - 29
EP - 41
JO - Brain Research
JF - Brain Research
IS - 1-2
ER -