scholarly journals Long-term potentiation of excitatory synaptic transmission in the rat hippocampus: the role of inhibitory processes

1982 ◽  
Vol 329 (1) ◽  
pp. 541-552 ◽  
Author(s):  
H. L. Haas ◽  
G. Rose
Keyword(s):  
Synaptic Transmission ◽  
Long Term Potentiation ◽  
Excitatory Synaptic Transmission ◽  
Rat Hippocampus ◽  
Inhibitory Processes ◽  
Term Potentiation

Orphanin FQ inhibits synaptic transmission and long-term potentiation in rat hippocampus

Hippocampus ◽  
1997 ◽  
Vol 7 (1) ◽  
pp. 88-94 ◽  
Author(s):  
Tzu-Ping Yu ◽  
Jeffrey Fein ◽  
Tien Phan ◽  
Christopher J. Evans ◽  
Cui-Wei Xie
Keyword(s):  
Synaptic Transmission ◽  
Long Term Potentiation ◽  
Rat Hippocampus ◽  
Orphanin Fq ◽  
Term Potentiation

scholarly journals Learning-induced modulation of the effect of neuroglial transmission on synaptic plasticity

2018 ◽  
Vol 119 (6) ◽  
pp. 2373-2379 ◽  
Author(s):  
Luna Jammal ◽  
Ben Whalley ◽  
Edi Barkai
Keyword(s):  
Synaptic Transmission ◽  
Gap Junctions ◽  
Piriform Cortex ◽  
Rule Learning ◽  
Long Term Potentiation ◽  
Synaptic Inhibition ◽  
Term Potentiation ◽  
Term Maintenance

Training rats in a complex olfactory discrimination task results in acquisition of “rule learning” (learning how to learn), a term describing the capability to perform the task superbly. Such rule learning results in strengthening of both excitatory and inhibitory synaptic connections between neurons in the piriform cortex. Moreover, intrinsic excitability is also enhanced throughout the pyramidal neuron population. Surprisingly, the cortical network retains its stability under these long-term modifications. In particular, the susceptibility for long-term potentiation (LTP) induction, while decreased for a short time window, returns to almost its pretraining value, although significant strengthening of AMPA receptor-mediated glutamatergic transmission remains. Such network balance is essential for maintaining the single-cell modifications that underlie long-term memory while preventing hyperexcitability that would result in runaway synaptic activity. However, the mechanisms underlying the long-term maintenance of such balance have yet to be described. In this study, we explored the role of astrocyte-mediated gliotransmission in long-term maintenance of learning-induced modifications in susceptibility for LTP induction and control of the strength of synaptic inhibition. We show that blocking connexin 43 hemichannels, which form gap junctions between astrocytes, decreases significantly the ability to induce LTP by stimulating the excitatory connections between piriform cortex pyramidal neurons after learning only. In parallel, spontaneous miniature inhibitory postsynaptic current amplitude is reduced in neurons from trained rats only, to the level of prelearning. Thus gliotransmission has a key role in maintaining learning-induced cortical stability by a wide-ranged control on synaptic transmission and plasticity. NEW & NOTEWORTHY We explore the role of astrocyte-mediated gliotransmission in maintenance of olfactory discrimination learning-induced modifications. We show that blocking gap junctions between astrocytes decreases significantly the ability to induce long-term potentiation in the piriform cortex after learning only. In parallel, synaptic inhibition is reduced in neurons from trained rats only, to the level of prelearning. Thus gliotransmission has a key role in maintaining learning-induced cortical stability by a wide-ranged control on synaptic transmission and plasticity.

scholarly journals Synaptic memory requires CaMKII

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Wucheng Tao ◽  
Joel Lee ◽  
Xiumin Chen ◽  
Javier Díaz-Alonso ◽  
Jing Zhou ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Learning And Memory ◽  
Long Term Potentiation ◽  
Cellular Model ◽  
Term Potentiation

Long-term potentiation (LTP) is arguably the most compelling cellular model for learning and memory. While the mechanisms underlying the induction of LTP ('learning') are well understood, the maintenance of LTP ('memory') has remained contentious over the last 20 years. Here, we find that CaMKII contributes to synaptic transmission and is required LTP maintenance. Acute inhibition of CaMKII erases LTP and transient inhibition of CaMKII enhances subsequent LTP. These findings strongly support the role of CaMKII as a molecular storage devise.

Interaction Between Tetanus Long-Term Potentiation and Hypoxia-Induced Potentiation in the Rat Hippocampus

1997 ◽  
Vol 78 (5) ◽  
pp. 2475-2482 ◽  
Author(s):  
M. Lyubkin ◽  
D. M. Durand ◽  
M. A. Haxhiu
Keyword(s):  
Synaptic Transmission ◽  
Long Term Potentiation ◽  
Rat Hippocampus ◽  
Magnesium Concentration ◽  
High Frequency Stimulation ◽  
Excitatory Postsynaptic Potential ◽  
Synaptic Specificity ◽  
Term Potentiation ◽  
Neuronal Processing

Lyubkin, M., D. M. Durand, and M. A. Haxhiu. Interaction between tetanus long-term potentiation and hypoxia-induced potentiation in the rat hippocampus. J. Neurophysiol. 78: 2475–2482, 1997. The interaction between tetanus-induced long-term potentiation (LTP) and hypoxia-induced potentiation was investigated by performing extracellular recordings in the CA1 region of rat hippocampus using a two-pathway design. Hippocampal slices were placed in an interface chamber containing artificial cerebrospinal fluid (ACSF) solution with high magnesium concentration. Hypoxia was induced by replacing the 5% CO2-95% O2 gas mixture with 5% CO2-95% N2 for 2 min. Tetanus-LTP was induced with 1-s, 100-Hz current pulses. Significant hypoxia-induced potentiation of the slope of the dendritic excitatory postsynaptic potential (EPSP) was found in ACSF containing 2 mM of magnesium 2, 27 ± 10% (mean ± SE; n = 16; P < 0.01) with no change in the mean amplitude of the presynaptic volley. All experiments in which a stable control baseline was obtained were used for data analysis. The data show that short episodes (2 min) of hypoxia can induce LTP of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-mediated synaptic transmission. The present study demonstrated that after tetanus-LTP, 33 ± 3% ( n = 10; P < 0.01), hypoxia further potentiated the field EPSP slopes by a mean value of 16 ± 5% ( n = 10; P < 0.05). Moreover, using a two-pathway design, we showed that hypoxia produced similar potentiation in both the control [19 ± 5%; n = 10; P < 0.01) and tetanus-induced LTP pathway, and the total potentiation produced by a combination of tetanus then hypoxia, 63 ± 13% ( n = 10; p < 0.01), was significantly larger ( P < 0.01) than hypoxia alone. These data suggest that hypoxia-induced potentiation is additive with tetanus-LTP. Occlusion experiments were performed to verify whether the mechanisms responsible for hypoxia-induced potentiation are independent of preexisting synaptic levels induced by high-frequency stimulation. Hypoxia produced significant potentiation (23 ± 7%; n = 7; P < 0.05) after successful occlusion of the LTP pathway. Therefore, because the magnitude of hypoxia-induced potentiation is both independent of preexisting synaptic levels and also additive, synaptic specificity associated with LTP is preserved. The magnitude of tetanus-LTP induced 20 min after hypoxia (15 ± 4%; n = 10) was significantly smaller ( P < 0.01) relative to LTP after normoxic conditions (33 ± 3%; n = 10). Additionally, hypoxia blocked the transient, robust potentiation occurring during the early phase of LTP induction. This study suggests that although hypoxia modifies neuronal processing by general excitation, synaptic specificity associated with tetanus-LTP still is preserved. However, hypoxia can disrupt neuronal processing by inhibiting new modification of synaptic transmission.

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