scholarly journals Morphine and opioid peptides reduce inhibitory synaptic potentials in hippocampal pyramidal cells in vitro without alteration of membrane potential.

1981 ◽  
Vol 78 (8) ◽  
pp. 5235-5239 ◽  
Author(s):  
G. R. Siggins ◽  
W. Zieglgansberger
1997 ◽  
Vol 78 (3) ◽  
pp. 1735-1739 ◽  
Author(s):  
Denis Paré ◽  
Elen Lebel ◽  
Eric J. Lang

Paré, Denis, Elen LeBel, and Eric J. Lang. Differential impact of miniature synaptic potentials on the somata and dendrites of pyramidal neurons in vivo. J. Neurophysiol. 78: 1735–1739, 1997. We studied the impact of transmitter release resistant to tetrodotoxin (TTX) in morphologically identified neocortical pyramidal neurons recorded intracellularly in barbiturate-anesthetized cats. It was observed that TTX-resistant release occurs in pyramidal neurons in vivo and at much higher frequencies than was previously reported in vitro. Further, in agreement with previous findings indicating that GABAergic and glutamatergic synapses are differentially distributed in the somata and dendrites of pyramidal cells, we found that most miniature synaptic potentials were sensitive to γ-aminobutyric acid-A (GABAA) or α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) antagonists in presumed somatic and dendritic impalements, respectively. Pharmacological blockage of spontaneous synaptic events produced large increases in input resistance that were more important in dendritic (≈50%) than somatic (≈10%) impalements. These findings imply that in the intact brain, pyramidal neurons are submitted to an intense spike-independent synaptic bombardment that decreases the space constant of the cells. These results should be taken into account when extrapolating in vitro findings to intact brains.


Cephalalgia ◽  
2000 ◽  
Vol 20 (6) ◽  
pp. 533-537 ◽  
Author(s):  
T Leniger ◽  
M Wiemann ◽  
D Bingmann ◽  
A Hufnagel ◽  
U Bonnet

Clinical studies indicate anti-migraneous efficacy of the probably GABAergic anti-convulsants valproate and gabapentin. For the GABAergic anticonvulsants vigabatrin and tiagabine, studies about antimigraneous efficacy are missing. The aim of this study was to test the GABAergic potency of these drugs in vitro before further clinical studies. Intracellular recordings were obtained from hippocampal pyramidal cells. Spontaneous GABAergic hyperpolarizations (SGH) elicited by 75 μ m 4-aminopyridine were used to test the effect of these drugs on GABA-dependent potentials. Tiagabine (0.1 m m) prolonged the duration of SGH. Furthermore, monophasic SGH turned over into triphasic typical GABAergic membrane potential fluctuations within 20 min. In contrast, valproate, gabapentin, and vigabatrin failed to affect SGH up to 60 min of application. The reason for the fast action of tiagabine on SGH may be caused by a faster increase of synaptic GABA levels compared with other drugs. As migraine therapy benefits from an augmentation of GABA activity, we recommend clinical studies of tiagabine as a fast-acting agent in migraine attacks.


2001 ◽  
Vol 85 (6) ◽  
pp. 2381-2387
Author(s):  
Valeri Lopantsev ◽  
Philip A. Schwartzkroin

Changes in intracellular chloride concentration, mediated by chloride influx through GABAA receptor–gated channels, may modulate GABAB receptor–mediated inhibitory postsynaptic potentials (GABAB IPSPs) via unknown mechanisms. Recording from CA3 pyramidal cells in hippocampal slices, we investigated the impact of chloride influx during GABAA receptor–mediated IPSPs (GABAA IPSPs) on the properties of GABAB IPSPs. At relatively positive membrane potentials (near −55 mV), mossy fiber–evoked GABAB IPSPs were reduced (compared with their magnitude at −60 mV) when preceded by GABAAreceptor–mediated chloride influx. This effect was not associated with a correlated reduction in membrane permeability during the GABAB IPSP. The mossy fiber–evoked GABAB IPSP showed a positive shift in reversal potential (from −99 to −93 mV) when it was preceded by a GABAA IPSP evoked at cell membrane potential of −55 mV as compared with −60 mV. Similarly, when intracellular chloride concentration was raised via chloride diffusion from an intracellular microelectrode, there was a reduction of the pharmacologically isolated monosynaptic GABABIPSP and a concurrent shift of GABAB IPSP reversal potential from −98 to −90 mV. We conclude that in hippocampal pyramidal cells, in which “resting” membrane potential is near action potential threshold, chloride influx via GABAA IPSPs shifts the reversal potential of subsequent GABAB receptor–mediated postsynaptic responses in a positive direction and reduces their magnitude.


1981 ◽  
Vol 221 (2) ◽  
pp. 402-408 ◽  
Author(s):  
Q.J. Pittman ◽  
G.R. Siggins

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