scholarly journals The time course of minimal excitatory post-synaptic potentials evoked in spinal motoneurones by group la afferent fibres

1971 ◽  
Vol 215 (2) ◽  
pp. 353-380 ◽  
Author(s):  
J. J. B. Jack ◽  
S. Miller ◽  
R. Porter ◽  
S. J. Redman
Keyword(s):  
Time Course ◽  
Synaptic Potentials ◽  
Spinal Motoneurones

Effects of the GABA uptake inhibitor tiagabine on inhibitory synaptic potentials in rat hippocampal slice cultures

1992 ◽  
Vol 67 (6) ◽  
pp. 1698-1701 ◽  
Author(s):  
S. M. Thompson ◽  
B. H. Gahwiler
Keyword(s):  
Time Constant ◽  
Decay Time ◽  
Time Course ◽  
Hippocampal Slice ◽  
Decay Time Constant ◽  
Gabab Receptors ◽  
Gaba Uptake ◽  
Whole Cell ◽  
Synaptic Potentials ◽  
Hippocampal Slice Cultures

1. The effects of the gamma-aminobutyric acid (GABA) uptake blocker tiagabine on inhibitory synaptic potentials (IPSPs) were examined with microelectrode and whole-cell recording from CA3 pyramidal cells in rat hippocampal slice cultures. 2. Tiagabine (10-25 microM) greatly prolonged the duration of monosynaptic IPSPs elicited in the presence of excitatory amino acid antagonists but had no effect on their amplitude. Part of the prolonged time course resulted from a GABAB receptor-mediated component that was not detectable under control conditions. 3. The mean decay time constant of the underlying GABAA receptor-mediated synaptic current was increased from 16 to 250 ms. Spontaneous miniature IPSPs recorded with whole-cell clamp were unaffected by tiagabine. Pentobarbital sodium, in contrast, increased the decay time constant of both evoked and spontaneous GABAA-mediated currents. 4. Tiagabine (25 microM) inhibited spontaneous and evoked epileptiform bursting induced by increasing the extracellular potassium concentration to 8 mM. 5. We conclude that GABA uptake plays a significant role in determining the time course of evoked IPSPs and also limits the likelihood that GABAB receptors are activated.

scholarly journals Differences in Time Course of ACh and GABA Modulation of Excitatory Synaptic Potentials in Slices of Rat Hippocampus

2001 ◽  
Vol 86 (4) ◽  
pp. 1792-1802 ◽  
Author(s):  
Michael E. Hasselmo ◽  
Brian P. Fehlau
Keyword(s):  
Presynaptic Inhibition ◽  
Acetylcholine Receptors ◽  
Time Course ◽  
Onset Time ◽  
Afferent Input ◽  
Muscarinic Acetylcholine Receptors ◽  
Time Constants ◽  
Synaptic Potentials ◽  
Extracellular Potentials

Activation of muscarinic receptors and GABABreceptors causes presynaptic inhibition of glutamatergic synaptic potentials at excitatory feedback connections in cortical structures. These effects may regulate dynamics in cortical structures, with presynaptic inhibition allowing extrinsic afferent input to dominate during encoding, while the absence of presynaptic inhibition allows stronger excitatory feedback during retrieval or consolidation. However, proposals for a functional role of such modulatory effects strongly depend on the time course of these modulatory effects; how rapidly can they turn off and on? In brain slice preparations of hippocampal region CA1, we have explored the time course of suppression of extracellularly recorded synaptic potentials after pressure pulse application of acetylcholine and GABA. Acetylcholine causes suppression of extracellular potentials with onset time constants between 1 and 2 s, and decay constants ranging between 10 and 20 s, even with very brief injection pulses. GABA causes suppression of extracellular potentials with onset time constants between 0.2 and 0.7 s, and decay time constants that decrease to values shorter than 2 s for very brief injection pulses. These techniques do not give an exact measure of the physiological time course in vivo, but they give a notion of the relative time course of the two modulators. The slow changes due to activation of muscarinic acetylcholine receptors may alter the dynamics of cortical circuits over longer intervals (e.g., between different stages of waking and sleep), setting dynamics appropriate for encoding versus consolidation processes. The faster changes in synaptic potentials caused by GABA could cause changes within each cycle of the theta rhythm, rapidly switching between encoding and retrieval dynamics during exploration.

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