scholarly journals EFFECTS OF ARTIFICIAL HYPOINSULINEMIA ON SYNAPTIC ACTIVITY AND PLASTICITY OF GLUTAMATERGIC NEUROTRANSMISSION IN CULTURE OF HIPPOCAMPAL NEURONS

2021 ◽  
Vol 67 (4) ◽  
pp. 3-11
Author(s):  
M.S. Shypshyna ◽  
◽  
K.I. Kuznetsov ◽  
S.A. Fedulova ◽  
M.S. Veselovsky ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Glutamate Release ◽  
Synaptic Activity ◽  
Short Term ◽  
Short Term Plasticity ◽  
Whole Cell Patch Clamp ◽  
Pulse Ratio ◽  
Coefficients Of Variation ◽  
Cultured Hippocampal Neurons

We investigated the effect of chronic hypoinsulinemia on the level of synaptic activity and short-term plasticity in cultured hippocampal neurons. Hypoinsulinemia was induced by culturing mature (16-20 days in vitro) rat’s hippocampal neurons without insulin for 1, 2, and 4 days. The control insulin concentration was 100 nM. Spontaneous and evoked glutamatergic excitatory postsynaptic currents (sEPSC and eEPSC, respectively) in these neurons were analyzed using the whole-cell patch-clamp method and the method of local electrical stimulation of individual axon. Hypoinsulinemia during the 1st, 2nd and 4th days led to significantly reduction of the mean sEPSC’s frequency to 49.9 ± 15.8% (n = 6), 8.5 ± 7.7% (n = 6) and 16.6 ± 5.2% (n = 8) respectively, relative to control. Also, there was a decrease of the average sEPSC’s amplitudes to 52.6 ± 5.5% (n = 6), 36.6 ± 5.8% (n = 6) and 43.9 ± 8.4% (n = 8), respectively, relative to control. Quantal analysis of the sEPSC’s amplitudes showed a decrease of multivesicular glutamate release at the synapses under such conditions. Hypoinsulinemia caused a shift in the direction of short-term plasticity in glutamatergic hippocampal synapses from potentiation to depression. The paired-pulse ratio decreased from 1.83 ± 0.25 in the control to 0.59 ± 0.07, 0.77 ± 0.07, and 0.80 ± 0.06 after the 1st, 2nd, and 4th days under cultivation without insulin. Accordingly, the ratio of the coefficients of variation of eEPSC’s amplitudes (CV2/ CV1) increased from 0.82 ± 0.07 to 1.30 ± 0.28, 1.52 ± 0.27, and 1.61 ± 0.24. The presented results indicate a significant reduction of synaptic activity and decrease in the probability of multivesicular release of glutamate at the synapses of cultured hippocampal neurons under hypoinsulinemia.

A Simple Depletion Model of the Readily Releasable Pool of Synaptic Vesicles Cannot Account for Paired-Pulse Depression

2007 ◽  
Vol 97 (1) ◽  
pp. 948-950 ◽  
Author(s):  
Jane M. Sullivan
Keyword(s):  
Synaptic Vesicles ◽  
Hippocampal Neurons ◽  
Synaptic Activity ◽  
Excitatory Synapses ◽  
Short Term ◽  
Paired Pulse ◽  
Short Term Plasticity ◽  
Releasable Pool ◽  
Readily Releasable Pool ◽  
Paired Pulse Depression

Paired-pulse depression (PPD) is a form of short-term plasticity that plays a central role in processing of synaptic activity and is manifest as a decrease in the size of the response to the second of two closely timed stimuli. Despite mounting evidence to the contrary, PPD is still commonly thought to reflect depletion of the pool of synaptic vesicles available for release in response to the second stimulus. Here it is shown that PPD cannot be accounted for by depletion at excitatory synapses made by hippocampal neurons because PPD is unaffected by changes in the fraction of the readily releasable pool (RRP) released by the first of a pair of pulses.

scholarly journals The Role of NMDA Receptor Subtypes in Short-Term Plasticity in the Rat Entorhinal Cortex

2008 ◽  
Vol 2008 ◽  
pp. 1-13 ◽  
Author(s):  
Sophie E. L. Chamberlain ◽  
Jian Yang ◽  
Roland S. G. Jones
Keyword(s):  
Entorhinal Cortex ◽  
Glutamate Release ◽  
Receptor Subtypes ◽  
Short Term ◽  
Low Frequencies ◽  
Short Term Plasticity ◽  
Whole Cell Patch Clamp ◽  
Layer V ◽  
Presynaptic Nmda Receptors

We have previously shown that spontaneous release of glutamate in the entorhinal cortex (EC) is tonically facilitated via activation of presynaptic NMDA receptors (NMDAr) containing the NR2B subunit. Here we show that the same receptors mediate short-term plasticity manifested by frequency-dependent facilitation of evoked glutamate release at these synapses. Whole-cell patch-clamp recordings were made from layer V pyramidal neurones in rat EC slices. Evoked excitatory postsynaptic currents showed strong facilitation at relatively low frequencies (3 Hz) of activation. Facilitation was abolished by an NR2B-selective blocker (Ro 25-6981), but unaffected by NR2A-selective antagonists (Zn2+, NVP-AAM077). In contrast, postsynaptic NMDAr-mediated responses could be reduced by subunit-selective concentrations of all three antagonists. The data suggest that NMDAr involved in presynaptic plasticity in layer V are exclusively NR1/NR2B diheteromers, whilst postsynaptically they are probably a mixture of NR1/NR2A, NR1/NR2B diheteromers and NR1/NR2A/NR2B triheteromeric receptors.

Glycine regulation of synaptic NMDA receptors in hippocampal neurons

1996 ◽  
Vol 76 (5) ◽  
pp. 3415-3424 ◽  
Author(s):  
K. S. Wilcox ◽  
R. M. Fitzsimonds ◽  
B. Johnson ◽  
M. A. Dichter
Keyword(s):  
Nmda Receptor ◽  
Nmda Receptors ◽  
Hippocampal Neurons ◽  
Time Course ◽  
Hippocampal Slices ◽  
Maximal Effect ◽  
Patch Clamp Technique ◽  
Whole Cell Patch Clamp ◽  
Dissociated Cell Culture ◽  
Cultured Hippocampal Neurons

1. Although glycine has been identified as a required coagonist with glutamate at N-methyl-D-aspartate (NMDA) receptors, the understanding of glycine's role in excitatory synaptic neurotransmission is quite limited. In the present study, we used the whole cell patch-clamp technique to examine the ability of glycine to regulate current flow through synaptic NMDA receptors at excitatory synapses between cultured hippocampal neurons and in acutely isolated hippocampal slices. 2. These studies demonstrate that the glycine modulatory site on the synaptic NMDA receptor is not saturated under baseline conditions and that increased glycine concentrations can markedly increased NMDA-receptor-mediated excitatory postsynaptic currents (EPSCs) in hippocampal neurons in both dissociated cell culture and in slice. Saturation of the maximal effect of glycine takes place at different concentrations for different cells in culture, suggesting the presence of heterogenous NMDA receptor subunit compositions. 3. Bath-applied glycine had no effect on the time course of EPSCs in either brain slice or culture, indicating that desensitization of the NMDA receptor is not prevented by glycine over the time course of an EPSC. 4. When extracellular glycine concentration is high, all miniature EPSCs recorded in the cultured hippocampal neurons contained NMDA components, indicating that segregation of non-NMDA receptors at individual synaptic boutons does not occur.

NO inhibits supraoptic oxytocin and vasopressin neurons via activation of GABAergic synaptic inputs

2001 ◽  
Vol 280 (6) ◽  
pp. R1815-R1822 ◽  
Author(s):  
Javier E. Stern ◽  
Mike Ludwig
Keyword(s):  
Neuronal Excitability ◽  
Cell Types ◽  
Synaptic Activity ◽  
No Donor ◽  
Whole Cell Patch Clamp ◽  
Electrophysiological Recordings ◽  
Neuronal Types ◽  
Vasopressin Neurons

To study modulatory actions of nitric oxide (NO) on GABAergic synaptic activity in hypothalamic magnocellular neurons in the supraoptic nucleus (SON), in vitro and in vivo electrophysiological recordings were obtained from identified oxytocin and vasopressin neurons. Whole cell patch-clamp recordings were obtained in vitro from immunochemically identified oxytocin and vasopressin neurons. GABAergic synaptic activity was assessed in vitro by measuring GABAA miniature inhibitory postsynaptic currents (mIPSCs). The NO donor and precursor sodium nitroprusside (SNP) and l-arginine, respectively, increased the frequency and amplitude of GABAA mIPSCs in both cell types ( P ≤ 0.001). Retrodialysis of SNP (50 mM) onto the SON in vivo inhibited the activity of both neuronal types ( P ≤ 0.002), an effect that was reduced by retrodialysis of the GABAA-receptor antagonist bicuculline (2 mM, P≤ 0.001). Neurons activated by intravenous infusion of 2 M NaCl were still strongly inhibited by SNP. These results suggest that NO inhibition of neuronal excitability in oxytocin and vasopressin neurons involves pre- and postsynaptic potentiation of GABAergic synaptic activity in the SON.

Extracellular adenosine 5′-triphosphate-evoked glutamate release in cultured hippocampal neurons

1992 ◽  
Vol 134 (2) ◽  
pp. 215-218 ◽  
Author(s):  
Kazuhide Inoue ◽  
Ken Nakazawa ◽  
Kannosuke Fujimori ◽  
Tomokazu Watano ◽  
Akira Takanaka
Keyword(s):  
Hippocampal Neurons ◽  
Glutamate Release ◽  
Extracellular Adenosine ◽  
Cultured Hippocampal Neurons
Sign in / Sign up

Export Citation Format

Share Document