Characterization of a slow cholinergic post-synaptic potential recorded in vitro from rat hippocampal pyramidal cells

• Published in: The Journal of physiology Vol. 352; no. 1; pp. 173 - 188
• Main Authors: Cole, A E, Nicoll, R A
• Format: Journal Article
• Language: English
• Published: Oxford The Physiological Society 01-07-1984; Blackwell
• Subjects: Acetylcholine - pharmacology; Action Potentials - drug effects; Animals; Biological and medical sciences; Cadmium - pharmacology; Carbachol - pharmacology; Central nervous system; Central neurotransmission. Neuromudulation. Pathways and receptors; Cholinergic Fibers - physiology; Fundamental and applied biological sciences. Psychology; Hippocampus - cytology; Hippocampus - physiology; In Vitro Techniques; Membrane Potentials - drug effects; Neurons - physiology; Parasympathomimetics - pharmacology; Rats; Synapses - physiology; Tetrodotoxin - pharmacology; Vertebrates: nervous system and sense organs; Vertebrata; Mammalia; Rat; Rodentia; Central nervous system; Neurotransmitter; Brain (Vertebrata); Acetylcholine; Pyramidal neuron; Excitatory postsynaptic potential; Hippocampus; Rhinencephalon
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1113/jphysiol.1984.sp015285

Intracellular recording from CA1 pyramidal cells in the hippocampal slice preparation was used to compare the action of exogenously
applied acetylcholine (ACh) and cholinomimetics to the effect of electrically stimulating sites in the slice known to contain
cholinergic fibres. ACh depolarized pyramidal cells with an associated increase in input resistance, blocked a calcium-activated
potassium conductance (GK(Ca], and blocked accommodation of action potential discharge. All of these actions were blocked
by the muscarinic antagonist, atropine. Repetitive electrical stimulation of stratum (s.) oriens evoked a series of fast excitatory
post-synaptic potentials (e.p.s.p.s) followed by an inhibitory post-synaptic potential. These potentials were followed by
a slow e.p.s.p. that lasted 20-30 s. The slow e.p.s.p. was selectively enhanced by eserine and blocked by atropine. Ionophoretic
application of ACh closely mimicked the time course of the slow e.p.s.p. The slow e.p.s.p. was blocked by tetrodotoxin and
cadmium, indicating that it was dependent on propagated action potentials and on calcium. Considerably higher stimulus strengths
were needed to elicit a slow e.p.s.p. than to elicit the earlier synaptic potentials. The size of the slow e.p.s.p. was markedly
increased by repetitive stimulation. Stimulation of the alveus, s. oriens, s. pyramidale and fimbria all evoked a slow e.p.s.p.,
while stimulation of s. radiatum was relatively ineffective. The input resistance of the cell increased during the slow e.p.s.p.
Hyperpolarizing the cell decreased the size of the slow e.p.s.p. and at membrane potentials of -70 mV or greater, little response
was recorded. Stimulation of s. oriens blocked GK(Ca) and accommodation of action potential discharge. These effects, which
could be seen in the absence of any change in membrane potential, were enhanced by eserine and blocked by atropine. The present
electrophysiological results establish that CA1 pyramidal cells receive a cholinergic input and demonstrate that this input
can dramatically alter the firing properties of these neurones for tens of seconds in the absence of any marked effect on
membrane potential. Such an action contrasts with previously characterized synaptic potentials in this region of the brain.