Alger B E, Pitler T A, Williamson A
Department of Physiology, University of Maryland School of Medicine, Baltimore 21201.
Brain Res. 1990 Jun 25;521(1-2):118-24. doi: 10.1016/0006-8993(90)91531-k.
The post-tetanic sequelae of trains of synaptic stimuli (50 pulses at 5 or 10 Hz) were studied with intracellular recordings from rat hippocampal neurons in vitro. In a large proportion of CA1 neurons, stimulation of afferent fibers was followed by a prolonged membrane hyperpolarization (peak amplitude approximately 6 mV) that was associated with a decrease in neuronal input resistance (approximately 33%) that lasted from tens of seconds to over 1 min. Antidromic stimulation or activation of cells with intracellular current injection did not elicit this post-tetanic hyperpolarization (PTH). The PTH could be elicited in chloride (Cl-)-loaded cells, its null potential shifted in response to changes in extracellular potassium ([K+]o), and it was significantly reduced by 5-10 mM extracellular cesium (Cs+). The K(+)-dependent PTH may also be calcium (Ca2+) dependent as its amplitude and associated conductance increase were sensitive to changes in [Ca2+]o. The PTH was enhanced by treatments that increase Ca2+ entry into cells including perfusion with elevated [Ca2+]o, with picrotoxin or with tetraethylammonium ion (TEA). The K+ conductance blocker 4-AP had no consistent effect on the PTH. The PTH was potently blocked by the membrane-permeant forms of cAMP, dibutyryl- and 8-bromo-cAMP. However, phorbol esters that activate protein kinase C and carbachol, which usually block the same potential that is blocked by cAMP, did not depress the PTH. The cardiac glycosides dihydro-ouabain and strophanthidin had only small and variable effects on the PTH.(ABSTRACT TRUNCATED AT 250 WORDS)
