Postsynaptic potentials mediated by GABA and dopamine evoked in stellate glial cells of the pituitary pars intermedia.
Studies have shown that many glial cells in the CNS possess receptors for neurotransmitters and that synapse-like contacts exist between glial cells and axonal terminals. Although synapse-like contacts are present between the glial cells (stellate cells) of the pituitary pars intermedia and the axons from the arcuate nucleus, it is not known whether these cells are under synaptic control. The objective of the present study was to determine whether transmitter-mediated postsynaptic potentials occurred in the stellate cells of the rat pituitary pars intermedia. Whole pituitaries were maintained in vitro, and a stimulating electrode was placed on the stalk to activate afferent fibers. Intracellular recordings were obtained with sharp microelectrodes. Stellate cells showed electrophysiological characteristics of macroglia including a resting potential more negative than -65 mV, low input resistance (< 50 M omega), and no detectable voltage-activated conductances. Single-pulse afferent nerve (stalk) stimulation evoked a [Ca2+]o-dependent postsynaptic response in the stellate cells consisting of a depolarization (< 500 msec) and a long-lasting hyperpolarization (45-75 sec). The depolarization was mimicked by GABA application and blocked by the GABAA antagonist bicuculline (100 microM). Repetitive stimulation of the stalk increased the amplitude and prolonged the GABA-mediated depolarization, during which a decrease in input resistance was observed. The hyperpolarization was mimicked by dopamine and blocked by the D2 antagonists sulpiride (2 microM) and domperidone (10 microM). Nipecotic acid (100 microM; an inhibitor of GABA uptake) or GBR 12909 (15 microM; an inhibitor of dopamine uptake) had minimal effects on the synaptic responses.(ABSTRACT TRUNCATED AT 250 WORDS)
Mudrick-Donnon
L A
LA
Neuroscience Research Group, University of Calgary, Alberta, Canada.
Williams
P J
PJ
Pittman
Q J
QJ
MacVicar
B A
BA
D000818:Animals; D001640:Bicuculline / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D004294:Domperidone / Q000494:pharmacology; D004298:Dopamine / Q000494:pharmacology*; D005071:Evoked Potentials / Q000187:drug effects / Q000502:physiology*; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis; D007150:Immunohistochemistry; D066298:In Vitro Techniques; D008297:Male; D017628:Microglia / Q000187:drug effects / Q000502:physiology*; D009457:Neuroglia / Q000187:drug effects / Q000502:physiology*; D014179:Neurotransmitter Uptake Inhibitors / Q000494:pharmacology; D010879:Piperazines / Q000494:pharmacology; D010902:Pituitary Gland / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013469:Sulpiride / Q000494:pharmacology; D013569:Synapses / Q000187:drug effects / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology*
D005904:Glial Fibrillary Acidic Protein; D014179:Neurotransmitter Uptake Inhibitors; D010879:Piperazines; D004294:Domperidone; D005680:gamma-Aminobutyric Acid; D013469:Sulpiride; C043425:vanoxerine; D002118:Calcium; D004298:Dopamine; D001640:Bicuculline