PMID- 2996924
OWN - NLM
STAT- MEDLINE
DCOM- 19851213
LR  - 20190721
IS  - 0014-4819 (Print)
IS  - 0014-4819 (Linking)
VI  - 60
IP  - 2
DP  - 1985
TI  - An electrophysiological characterization of inhibitions and postsynaptic 
      potentials in rat hippocampal CA3 neurones in vitro.
PG  - 299-308
AB  - Inhibitory processes in the CA3 region of the rat hippocampal slice were studied 
      extracellularly using paired stimuli and with intracellular impalements of 
      pyramidal neurones. As with mossy fibre (MF) or commissural (COMM) conditioning 
      stimuli (Kehl and McLennan 1983), activation of the perforant path (PP) input 
      caused a long-lasting inhibition of test orthodromic population spikes (PSs) 
      evoked by shocks delivered to the fimbria. That at least a portion of this 
      orthodromically-evoked inhibition reflected postsynaptic events was shown by the 
      reduction both of the amplitude of antidromic PSs and the firing rate of 
      spontaneously active single units. Experiments in which the extracellular 
      concentration of chloride was reduced indicated that only an early component of 
      the inhibition was due to a conductance for that anion. The existence of two 
      inhibitory mechanisms distinguishable extracellularly by their sensitivity to 
      bicuculline and manipulation of extracellular ion concentrations was correlated 
      intracellularly with two hyperpolarising peaks occurring approximately 20 and 150 
      ms following MF, COMM or PP stimuli. The later hyperpolarisation had an 
      equilibrium potential 20-25 mV more negative than the early IPSP, was unaffected 
      by manipulations of extra- or intracellular concentrations of chloride and was 
      associated with a decrease of membrane resistance suggesting that a potassium 
      conductance was involved in its generation. The fact that it was recorded in the 
      absence of any preceding depolarisation, was blocked by drugs acting 
      presynaptically to cause disinhibition (Kehl and McLennan 1985) and, like the 
      early inhibition, was reversibly reduced by hypoxia suggested that the late 
      inhibition/hyperpolarisation was a synaptic phenomenon rather than an intrinsic 
      membrane event. Because the late inhibition/IPSP could be shown to have a lower 
      threshold for activation vis-a-vis the chloride- dependent early inhibition, it 
      is possible that two distinct populations of interneurones mediate these two 
      synaptic events.
FAU - Kehl, S J
AU  - Kehl SJ
FAU - McLennan, H
AU  - McLennan H
LA  - eng
PT  - Journal Article
PL  - Germany
TA  - Exp Brain Res
JT  - Experimental brain research
JID - 0043312
RN  - 56-12-2 (gamma-Aminobutyric Acid)
RN  - RWP5GA015D (Potassium)
SB  - IM
MH  - Animals
MH  - Evoked Potentials
MH  - Hippocampus/*physiology
MH  - In Vitro Techniques
MH  - Interneurons/physiology
MH  - Membrane Potentials
MH  - Neural Inhibition
MH  - Neural Pathways/physiology
MH  - Potassium/physiology
MH  - Rats
MH  - Synapses/physiology
MH  - Synaptic Transmission
MH  - gamma-Aminobutyric Acid/physiology
EDAT- 1985/01/01 00:00
MHDA- 1985/01/01 00:01
CRDT- 1985/01/01 00:00
PHST- 1985/01/01 00:00 [pubmed]
PHST- 1985/01/01 00:01 [medline]
PHST- 1985/01/01 00:00 [entrez]
AID - 10.1007/BF00235924 [doi]
PST - ppublish
SO  - Exp Brain Res. 1985;60(2):299-308. doi: 10.1007/BF00235924.