scholarly journals The norepinephrine transporter regulates dopamine-dependent synaptic plasticity in the mouse dorsal hippocampus

2019 ◽  
Author(s):  
Alex Sonneborn ◽  
Robert W. Greene
Keyword(s):  
Dorsal Hippocampus ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Norepinephrine Transporter ◽  
Receptor Activation ◽  
Attentional Processes ◽  
Term Potentiation ◽  
Plausible Mechanism ◽  
Presynaptic Nmda Receptors ◽  
Highly Correlated

AbstractThe rodent dorsal hippocampus is essential for episodic memory consolidation, a process dependent on dopamine D1-like receptor activation. It was previously thought that the ventral tegmental area provided the only supply of dopamine to dorsal hippocampus, but several recent studies have established the locus coeruleus (LC) as a second major source. However, the mechanism for LC-dependent dopamine release has never been explored. Our data identify norepinephrine transporter reversal as one plausible mechanism by demonstrating that transporter blockade can reduce dopamine-dependent long-term potentiation in hippocampal slices. We also suggest that presynaptic NMDA receptors on LC terminals may initiate this norepinephrine transporter reversal. Furthermore, as dopamine and norepinephrine should be co-released from the LC, we show that they act together to enhance synaptic strength. Since LC activity is highly correlated with attentional processes and memory, these experiments provide insight into how selective attention influences memory formation at the synaptic and circuit levels.

Adenosine Acting on A1 Receptors Protects NO-Triggered Rebound Potentiation and LTP in Rat Hippocampal Slices

2002 ◽  
Vol 87 (4) ◽  
pp. 1781-1789 ◽  
Author(s):  
Christelle L. M. Bon ◽  
John Garthwaite
Keyword(s):  
Synaptic Transmission ◽  
Nmda Receptors ◽  
Hippocampal Slices ◽  
Nmda Antagonist ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
No Donor ◽  
No Formation ◽  
Term Potentiation ◽  
Synthase Inhibitor

Exposure of hippocampal slices to nitric oxide (NO) results in a depression of CA1 synaptic transmission. Under 0.2-Hz stimulation, washout of NO leads to a persistent potentiation that depends on N-methyl-d-aspartate (NMDA) receptors and endogenous NO formation and that occludes tetanus-induced long-term potentiation (LTP). The experiments were initially aimed at determining the relationship between the NO-induced synaptic depression and rebound potentiation. The adenosine A1 antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) partially inhibited the depression produced by the NO donor diethylamine NONOate (300 μM). It also led to a complete block of both the rebound potentiation and the subsequent tetanus-induced LTP. LTP was preserved in the presence of DPCPX if the stimulation frequency was reduced to 0.033 Hz or if the NO application was omitted. The NO-triggered rebound potentiation was restored if the experiment (DPCPX followed by exogenous NO) was conducted in the presence of an NMDA antagonist. The restored potentiation was completely blocked by the NO synthase inhibitor,l-nitroarginine. It is concluded that the NO-induced depression is partially mediated by increased release of endogenous adenosine acting on A1 receptors. Moreover, tonic A1 receptor activation by adenosine protects LTP and the rebound potentiation from being disabled by untimely NMDA receptor activity. Hence, the NO-induced depression and rebound potentiation are linked in the sense that the depression helps to preserve the capacity of the synapses to undergo potentiation. Finally, the results give the first example of exogenous NO eliciting an enduring potentiation of hippocampal synaptic transmission that is dependent on endogenous NO formation, but not on NMDA receptors.

Cell-Permeable Scavengers of Superoxide Prevent Long-Term Potentiation in Hippocampal Area CA1

1998 ◽  
Vol 80 (1) ◽  
pp. 452-457 ◽  
Author(s):  
Eric Klann
Keyword(s):  
Nmda Receptor ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Manganese Porphyrin ◽  
Area Ca1 ◽  
Term Potentiation ◽  
Hippocampal Area ◽  
Nmda Receptor Activation

Klann, Eric. Cell-permeable scavengers of superoxide prevent long-term potentiation in hippocampal area CA1. J. Neurophysiol. 80: 452–457, 1998. Long-term potentiation (LTP) in hippocampal area CA1 is generally dependent on N-methyl-d-aspartate (NMDA) receptor activation. Reactive oxygen species (ROS), including superoxide, are produced in response to NMDA receptor activation in a number of brain regions, including the hipppocampus. In this study, two cell-permeable manganese porphyrin compounds that mimic superoxide dismutase (SOD) were used to determine whether production of superoxide is required for the induction of LTP in area CA1 of rat hippocampal slices. Incubation of hippocampal slices with either Mn(III) tetrakis (4-benzoic acid) porphyrin (MnTBAP) or Mn(III) tetrakis (1-methyl-4-pyridyl) porphyrin (MnTMPyP) prevented the induction of LTP. Incubation of slices with either light-inactivated MnTBAP or light-inactivated MnTMPyP had no effect on induction of LTP. Neither MnTBAP nor MnTMPyP was able to reverse preestablished LTP. These observations suggest that production of superoxide occurs in response to LTP-inducing stimulation and that superoxide is necessary for the induction of LTP.

Homeostatic plasticity induced by brief activity deprivation enhances long-term potentiation in the mature rat hippocampus

2014 ◽  
Vol 112 (11) ◽  
pp. 3012-3022 ◽  
Author(s):  
A. Félix-Oliveira ◽  
R. B. Dias ◽  
M. Colino-Oliveira ◽  
D. M. Rombo ◽  
A. M. Sebastião
Keyword(s):  
Synaptic Transmission ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Relative Strength ◽  
Homeostatic Plasticity ◽  
Hebbian Plasticity ◽  
Term Potentiation ◽  
Acute Hippocampal Slices

Different forms of plasticity occur concomitantly in the nervous system. Whereas homeostatic plasticity monitors and maintains neuronal activity within a functional range, Hebbian changes such as long-term potentiation (LTP) modify the relative strength of specific synapses after discrete changes in activity and are thought to provide the cellular basis for learning and memory. Here, we assessed whether homeostatic plasticity could influence subsequent LTP in acute hippocampal slices that had been briefly deprived of activity by blocking action potential generation and N-methyl-d-aspartate (NMDA) receptor activation for 3 h. Activity deprivation enhanced the frequency and the amplitude of spontaneous miniature excitatory postsynaptic currents and enhanced basal synaptic transmission in the absence of significant changes in intrinsic excitability. Changes in the threshold for Hebbian plasticity were evaluated by inducing LTP with stimulation protocols of increasing strength. We found that activity-deprived slices consistently showed higher LTP magnitude compared with control conditions even when using subthreshold theta-burst stimulation. Enhanced LTP in activity-deprived slices was also observed when picrotoxin was used to prevent the modulation of GABAergic transmission. Finally, we observed that consecutive LTP inductions attained a higher magnitude of facilitation in activity-deprived slices, suggesting that the homeostatic plasticity mechanisms triggered by a brief period of neuronal silencing can both lower the threshold and raise the ceiling for Hebbian modifications. We conclude that even brief periods of altered activity are able to shape subsequent synaptic transmission and Hebbian plasticity in fully developed hippocampal circuits.

Caffeine-Mediated Presynaptic Long-Term Potentiation in Hippocampal CA1 Pyramidal Neurons

2003 ◽  
Vol 89 (6) ◽  
pp. 3029-3038 ◽  
Author(s):  
Eduardo D. Martín ◽  
Washington Buño
Keyword(s):  
Nmda Receptors ◽  
Glutamate Release ◽  
Ryanodine Receptors ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Cellular Mechanisms ◽  
Pipette Solution ◽  
Term Potentiation

We report a new form of long-term potentiation (LTP) in Schaffer collateral (SC)-CA1 pyramidal neuron synapses that originates presynaptically and does not require N-methyl-d-aspartate (NMDA) receptor activation nor increases in postsynaptic-free Ca2+. Using rat hippocampal slices, application of a brief “pulse” of caffeine in the bath evoked a nondecremental LTP (CAFLTP) of SC excitatory postsynaptic currents. An increased probability of transmitter release paralleled the CAFLTP, suggesting that it originated presynaptically. The P1 adenosine receptor antagonist 8-cyclopentyltheophylline and the P2 purinoreceptor antagonists suramin and piridoxal-5′-phosphate-azophenyl 2′,4′-disulphonate blocked the CAFLTP. Inhibition of Ca2+ release from caffeine/ryanodine stores by bath-applied ryanodine inhibited the CAFLTP, but ryanodine in the pipette solution was ineffective, suggesting a presynaptic effect of ryanodine. Previous induction of the “classical” LTP did not prevent the CAFLTP, suggesting that the LTP and the CAFLTP have different underlying cellular mechanisms. The CAFLTP is insensitive to the block of NMDA receptors by 2-amino-5-phosphonopentanoic acid and to Ca2+ chelation with intracellular 1,2-bis (2-aminophenoxy) ethane- N,N,N′ ,N′-tetraacetic acid, indicating that neither postsynaptic NMDA receptors nor increases in cytosolic-free Ca2+ participate in the CAFLTP. We conclude that the CAFLTP requires the interaction of caffeine with presynaptic P1, P2 purinoreceptors, and ryanodine receptors and is caused by an increased probability of glutamate release at SC terminals.

scholarly journals The Specific Role of cGMP in Hippocampal LTP

1998 ◽  
Vol 5 (3) ◽  
pp. 231-245 ◽  
Author(s):  
Hyeon Son ◽  
Yun-Fei Lu ◽  
Min Zhuo ◽  
Ottavio Arancio ◽  
Eric R. Kandel ◽  
...  
Keyword(s):  
Hippocampal Slices ◽  
Soluble Guanylyl Cyclase ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Stratum Radiatum ◽  
Tetanic Stimulation ◽  
Ca1 Region ◽  
Term Potentiation ◽  
Dependent Protein

Previous results have suggested that cGMP is involved in hippocampal long-term potentiation (LTP), perhaps as the presynaptic effector of a retrograde messenger. However, other studies have failed to replicate some of those results, making the role of cGMP uncertain. We therefore reexamined this question and identified several variables that can affect the contribution of cGMP. First, brief perfusion with 8-Br–cGMP before weak tetanic stimulation produced long-lasting potentiation in the CA1 region of hippocampal slices, but more prolonged perfusion with 8-Br–cGMP before the tetanus did not produce long-lasting potentiation. Second, the activity-dependent long-lasting potentiation by cGMP analogs was reduced when NMDA receptors were completely blocked, indicating that NMDA receptor activation contributes to, but is not required for, the potentiation. The amount of reduction of the potentiation differed with different protocols, and in some cases could be complete. Third, LTP produced by strong tetanic stimulation in the stratum radiatum of CA1 (which expresses eNOS) was blocked by inhibitors of soluble guanylyl cyclase or cGMP-dependent protein kinase, but LTP in the stratum oriens (which does not express eNOS) was not. The results of these experiments should help to explain some of the discrepant findings from previous studies, and, in addition, may provide insights into the mechanisms and functional role of the cGMP-dependent component of LTP.

receptor activation is required for the induction of both early and late phases of long-term potentiation in rat hippocampal slices

1989 ◽  
Vol 96 (1) ◽  
pp. 96-101 ◽  
Author(s):  
Klaus G. Reymann ◽  
Herbert K. Matthies ◽  
Karin Schulzeck ◽  
Hansjürgen Matthies
Keyword(s):  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Term Potentiation
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