Evoked inhibitory postsynaptic currents in the dynamics of development of cultured hippocampal neurons of rats

1999 ◽  
Vol 31 (5) ◽  
pp. 304-309 ◽  
Author(s):  
E. V. Isaeva ◽  
V. G. Sidorenko ◽  
S. A. Fedulova ◽  
N. S. Veselovskii
Keyword(s):  
Hippocampal Neurons ◽  
Inhibitory Postsynaptic Currents ◽  
Postsynaptic Currents ◽  
Cultured Hippocampal Neurons

Distributions of interevent intervals for miniature inhibitory and excitatory postsynaptic currents in cultured hippocampal neurons

2000 ◽  
Vol 32 (3) ◽  
pp. 158-160
Author(s):  
M. A. Chvanov ◽  
Ya. A. Boychuk ◽  
I. V. Melnick ◽  
P. V. Belan ◽  
P. G. Kostyuk
Keyword(s):  
Hippocampal Neurons ◽  
Excitatory Postsynaptic Currents ◽  
Postsynaptic Currents ◽  
Cultured Hippocampal Neurons

Effects of volatile anesthetics on the kinetics of inhibitory postsynaptic currents in cultured rat hippocampal neurons

1993 ◽  
Vol 70 (4) ◽  
pp. 1339-1349 ◽  
Author(s):  
M. V. Jones ◽  
N. L. Harrison
Keyword(s):  
Charge Transfer ◽  
Gabaa Receptor ◽  
Hippocampal Neurons ◽  
Slow Component ◽  
Volatile Anesthetics ◽  
Fast Component ◽  
Synaptic Inhibition ◽  
Inhibitory Postsynaptic Currents ◽  
Postsynaptic Currents ◽  
Kinetics Of

1. The effects of the volatile anesthetics enflurane, halothane, and isoflurane on gamma-aminobutyric acid (GABA) receptor-mediated inhibitory postsynaptic currents (IPSCs) were studied in cultured rat hippocampal neurons. The experimental concentrations of anesthetics were measured directly using gas chromatography. All three anesthetics increased the overall duration of IPSCs, measured as the time to half-decay (T1/2). Clinically effective concentrations of anesthetics [between 0.5 and 1.5 times MAC (minimum alveolar concentration)] produced between 100 and 400% increases in T1/2. These effects were fully reversible, and did not involve alterations in the reversal potential for the IPSC (EIPSC). 2. The decay of the IPSC was fitted as a sum of two exponential functions, yielding a fast component (tau fast = 20 ms), and a slow component (tau slow = 77 ms), such that the fast component accounted for 79% of the IPSC amplitude and 52% of the total charge transfer. All three anesthetics produced concentration-related increases in the amplitude and charge transfer of the slow component, while simultaneously decreasing the amplitude and charge transfer of the fast component. Thus T1/2 approximated tau fast under control conditions, but approximated tau slow in the presence of the anesthetics. 3. Varying the calcium chelating agents in the recording pipettes had no effect on the quality or magnitude of alterations in IPSC kinetics produced by halothane, suggesting that variations in intracellular calcium levels are not required for the effect of halothane on the time course of the IPSC. 4. The (+)-stereoisomer of isoflurane produced greater increases in the duration of the IPSC than the (-)-isomer when applied at approximately equal concentrations, suggesting that there is a structurally selective site of interaction for isoflurane that modulates the GABAA receptor. 5. These results suggest that the previously shown abilities of volatile anesthetics to potentiate responses to exogenously applied GABA and to prolong the duration of GABA-mediated synaptic inhibition may be due to an alteration in the gating kinetics of the GABAA receptor/channel complex. Prolongation of synaptic inhibition in the CNS is consistent with the physiological effects that accompany anesthesia and may contribute to the mechanism of anesthetic action.

scholarly journals Distinct Functions of Endophilin Isoforms in Synaptic Vesicle Endocytosis

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Jifeng Zhang ◽  
Minghui Tan ◽  
Yichen Yin ◽  
Bingyu Ren ◽  
Nannan Jiang ◽  
...  
Keyword(s):  
Rna Interference ◽  
Synaptic Vesicle ◽  
Hippocampal Neurons ◽  
Electrophysiological Recording ◽  
Excitatory Postsynaptic Currents ◽  
Postsynaptic Currents ◽  
Functional Differences ◽  
Cultured Hippocampal Neurons ◽  
Recording Techniques

Endophilin isoforms perform distinct characteristics in their interactions with N-type Ca2+channels and dynamin. However, precise functional differences for the endophilin isoforms on synaptic vesicle (SV) endocytosis remain unknown. By coupling RNA interference and electrophysiological recording techniques in cultured rat hippocampal neurons, we investigated the functional differences of three isoforms of endophilin in SV endocytosis. The results showed that the amplitude of normalized evoked excitatory postsynaptic currents in endophilin1 knockdown neurons decreased significantly for both single train and multiple train stimulations. Similar results were found using endophilin2 knockdown neurons, whereas endophilin3 siRNA exhibited no change compared with control neurons. Endophilin1 and endophilin2 affected SV endocytosis, but the effect of endophilin1 and endophilin2 double knockdown was not different from that of either knockdown alone. This result suggested that endophilin1 and endophilin2 functioned together but not independently during SV endocytosis. Taken together, our results indicate that SV endocytosis is sustained by endophilin1 and endophilin2 isoforms, but not by endophilin3, in primary cultured hippocampal neurons.

scholarly journals Immunoglobulins from amyotrophic lateral sclerosis patients enhance the frequency of glycine-mediated spontaneous inhibitory postsynaptic currents in rat hypoglossal motoneurons

2007 ◽  
Vol 59 (4) ◽  
pp. 251-255 ◽  
Author(s):  
P.R. Andjus
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Hippocampal Neurons ◽  
Spontaneous Release ◽  
Hypoglossal Motoneurons ◽  
Inhibitory Postsynaptic Currents ◽  
Postsynaptic Currents ◽  
Als Patients ◽  
Brain Stem Slices ◽  
Ca2 Channels ◽  
Lateral Sclerosis

Amyotrophic lateral sclerosis (ALS) is a devastating, still incurable neurological disorder affecting upper and lower motoneurons. Passive transfer of the disease occurs when immunoglobulins from ALS patients are injected into experimental animals. It is suggested that ALS IgGs cause excitotoxicity by acting on voltage-gated Ca2+ channels. We reported previously that ALS IgGs increase spontaneous release of glutamate in hippocampal neurons. Since these cells are not normally affected in ALS, we here studied the effect of ALS IgGs on hypoglossal motoneurons in rat brain-stem slices. The frequency of spontaneous glycine-mediated inhibitory postsynaptic currents (sIPSCs) was augmented, but not that of miniature ones (mIPSCs), thus pointing to an indirect effect on release.

scholarly journals Agonist-Dependent Postsynaptic Effects of Opioids on Miniature Excitatory Postsynaptic Currents in Cultured Hippocampal Neurons

2007 ◽  
Vol 97 (2) ◽  
pp. 1485-1494 ◽  
Author(s):  
Dezhi Liao ◽  
Olga O. Grigoriants ◽  
Horace H. Loh ◽  
Ping-Yee Law
Keyword(s):  
Hippocampal Neurons ◽  
Chronic Treatment ◽  
Green Fluorescence Protein ◽  
Cell Types ◽  
Excitatory Synapses ◽  
Excitatory Postsynaptic Currents ◽  
Knock Out ◽  
Postsynaptic Currents ◽  
Knock Out Mice ◽  
Cultured Hippocampal Neurons

Although chronic treatment with morphine is known to alter the function and morphology of excitatory synapses, the effects of other opioids on these synapses are not clear. Here we report distinct effects of several opioids (morphine, [d-ala2,me-phe4,gly5-ol]enkephalin (DAMGO), and etorphine) on miniature excitatory postsynaptic currents (mEPSCs) in cultured hippocampal neurons: 1) chronic treatment with morphine for >3 days decreased the amplitude, frequency, rise time and decay time of mEPSCs. In contrast, “internalizing” opioids such as etorphine and DAMGO increased the frequency of mEPSCs and had no significant effect on the amplitude and kinetics of mEPSCs. These results demonstrate that different opioids can have distinct effects on the function of excitatory synapses. 2) mu opioid receptor fused with green fluorescence protein (MOR-GFP) is clustered in dendritic spines in most hippocampal neurons but is concentrated in axon-like processes in striatal and corticostriatal nonspiny neurons. It suggests that MORs might mediate pre- or postsynaptic effects depending on cell types. 3) Neurons were cultured from MOR knock-out mice and were exogenously transfected with MOR-GFP. Chronic treatment with morphine suppressed mEPSCs only in neurons that contained postsynaptic MOR-GFP, indicating that opioids can modulate excitatory synaptic transmission postsynaptically. 4) Morphine acutely decreased mEPSC amplitude in neurons expressing exogenous MOR-GFP but had no effect on neurons expressing GFP. It indicates that the low level of endogenous MORs could only allow slow opioid-induced plasticity of excitatory synapses under normal conditions. 5) A theoretical model suggests that morphine might affect the function of spines by decreasing the electrotonic distance from synaptic inputs to the soma.

Gabapentin Increases a Tonic Inhibitory Conductance in Hippocampal Pyramidal Neurons

2006 ◽  
Vol 105 (2) ◽  
pp. 325-333 ◽  
Author(s):  
Victor Y. Cheng ◽  
Robert P. Bonin ◽  
Mary W. Chiu ◽  
J Glen Newell ◽  
John F. MacDonald ◽  
...  
Keyword(s):  
Gabaa Receptors ◽  
Hippocampal Neurons ◽  
Gabab Receptors ◽  
Gamma Aminobutyric Acid ◽  
Western Blots ◽  
Inhibitory Postsynaptic Currents ◽  
Postsynaptic Currents ◽  
Inhibitory Conductance ◽  
Tonic Current

Background The mechanisms underlying the therapeutic actions of gabapentin remain poorly understood. The chemical structure and behavioral properties of gabapentin strongly suggest actions on inhibitory neurotransmission mediated by gamma-aminobutyric acid (GABA); however, gabapentin does not directly modulate GABAA or GABAB receptors. Two distinct forms of GABAergic inhibition occur in the brain: postsynaptic conductance and a persistent tonic inhibitory conductance primarily generated by extrasynaptic GABAA receptors. The aim of this study was to determine whether gabapentin increased the tonic conductance in hippocampal neurons in vitro. As a positive control, the effects of vigabatrin, which irreversibly inhibits GABA transaminase, were also examined. Methods GABAA receptors in hippocampal neurons from embryonic mice were studied using whole cell patch clamp recordings. Miniature inhibitory postsynaptic currents and the tonic current were recorded from cultured neurons that were treated for 36-48 h with gabapentin, vigabatrin, or gabapentin and vigabatrin. To determine whether gabapentin increased the expression of GABAA receptors, Western blots were stained with antibodies selective for alpha1, alpha2, and alpha5 subunits. Results GABAA receptors were insensitive to the acute application of gabapentin, whereas chronic treatment increased the amplitude of the tonic current threefold (EC50 = 209 microm) but did not influence miniature inhibitory postsynaptic currents. Vigabatrin increased the tonic conductance, and the maximally effective concentration did not occlude the actions of gabapentin, which suggests that these compounds act by different mechanisms. Neither gabapentin nor vigabatrin increased the expression of GABAA receptors in the neurons. Conclusions Gabapentin increases a tonic inhibitory conductance in mammalian neurons. High-affinity GABAA receptors that generate the tonic conductance may detect small increases in the ambient concentration of neurotransmitter caused by gabapentin.

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