Hippocampal long-term potentiation is not accompanied by presynaptic spike broadening, unlike synaptic potentiation by K+ channel blockers

Estradiol synthesis depends on the activity of aromatase, the enzyme that specifically and irreversibly converts testosterone to estradiol in steroidogenesis. Aromatase is expressed and is active in the hippocampus, a brain region related to learning and memory. Dynamics of spines and spine synapses, including expression of presynaptic and postsynaptic proteins, are controlled by hippocampus-derived estradiol in female rodents, but not in male rodents. This also holds true for long-term potentiation. Inhibition of aromatase, either pharmacologically or by genetic approaches, results in a decrease in synapse density and synaptic potentiation in female animals and in neonatal hippocampal cultures that originate from females. The consistency of the findings in rodents and in perinatal primary hippocampal cultures points to sex-specific differentiation processes during embryonic development, which underlie sex-dependent differences in neurosteroid action in the hippocampus.

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Ineffectiveness of organic calcium channel blockers in antagonizing long-term potentiation

Brain Research ◽

10.1016/0006-8993(86)90781-x ◽

1986 ◽

Vol 379 (2) ◽

pp. 275-285 ◽

Cited By ~ 33

Author(s):

Jeffrey S. Taube ◽

Philip A. Schwartzkroin

Keyword(s):

Calcium Channel ◽

Calcium Channel Blockers ◽

Long Term Potentiation ◽

Channel Blockers ◽

Term Potentiation

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Mechanism of long-term potentiation of transmitter release induced by adrenaline in bullfrog sympathetic ganglia.

The Journal of General Physiology ◽

10.1085/jgp.87.5.775 ◽

1986 ◽

Vol 87 (5) ◽

pp. 775-793 ◽

Cited By ~ 15

Author(s):

E Kumamoto ◽

K Kuba

Keyword(s):

Transmitter Release ◽

Long Term Potentiation ◽

Sympathetic Ganglia ◽

Presynaptic Terminal ◽

Synaptic Delay ◽

K Channel ◽

Term Potentiation ◽

Relative Change ◽

Theoretical Considerations

A mechanism of the long-term potentiation of transmitter release induced by adrenaline (ALTP) was studied by recording intracellularly the fast excitatory postsynaptic potentials (fast EPSPs). The ALTP was produced during the blockade of K+ channels at the presynaptic terminals by tetraethylammonium (TEA). The synaptic delay, possibly reflecting a relative change in the duration of an action potential at the presynaptic terminal, was not changed during the course of the ALTP. By contrast, it was significantly lengthened by TEA and other K+ channel inhibitors (4-aminopyridine and Cs+) that markedly enhanced the evoked release of transmitter. The magnitude of facilitation of the fast EPSP, induced by a conditional stimulus to the preganglionic nerve, was decreased during the generation of the ALTP, but was unchanged during the potentiation of transmitter release caused by TEA. These results, together with theoretical considerations applying the residual Ca2+ hypothesis to the facilitation, suggest that the enhancement of transmitter release during the ALTP is not caused by an increased Ca2+ influx during a presynaptic impulse owing to the blockade of K+ channel or the modulation of Ca2+ channel, but presumably is induced by a rise in the basal level of free Ca2+ in the presynaptic terminal.

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Group III metabotropic glutamate receptors gate long-term potentiation and synaptic tagging/capture in rat hippocampal area CA2

eLife ◽

10.7554/elife.55344 ◽

2020 ◽

Vol 9 ◽

Cited By ~ 1

Author(s):

Ananya Dasgupta ◽

Yu Jia Lim ◽

Krishna Kumar ◽

Nimmi Baby ◽

Ka Lam Karen Pang ◽

...

Keyword(s):

Synaptic Plasticity ◽

Glutamate Receptors ◽

Metabotropic Glutamate Receptors ◽

Long Term Potentiation ◽

Synaptic Potentiation ◽

Group Iii ◽

Metabotropic Glutamate ◽

Term Potentiation ◽

Hippocampal Area

Metabotropic glutamate receptors (mGluRs) play an important role in synaptic plasticity and memory and are largely classified based on amino acid sequence homology and pharmacological properties. Among group III metabotropic glutamate receptors, mGluR7 and mGluR4 show high relative expression in the rat hippocampal area CA2. Group III metabotropic glutamate receptors are known to down-regulate cAMP-dependent signaling pathways via the activation of Gi/o proteins. Here, we provide evidence that inhibition of group III mGluRs by specific antagonists permits an NMDA receptor- and protein synthesis-dependent long-lasting synaptic potentiation in the apparently long-term potentiation (LTP)-resistant Schaffer collateral (SC)-CA2 synapses. Moreover, long-lasting potentiation of these synapses transforms a transient synaptic potentiation of the entorhinal cortical (EC)-CA2 synapses into a stable long-lasting LTP, in accordance with the synaptic tagging/capture hypothesis (STC). Furthermore, this study also sheds light on the role of ERK/MAPK protein signaling and the downregulation of STEP protein in the group III mGluR inhibition-mediated plasticity in the hippocampal CA2 region, identifying them as critical molecular players. Thus, the regulation of group III mGluRs provides a conducive environment for the SC-CA2 synapses to respond to events that could lead to activity-dependent synaptic plasticity.

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Novel form of long-term potentiation produced by a K+channel blocker in the hippocampus

Nature ◽

10.1038/349067a0 ◽

1991 ◽

Vol 349 (6304) ◽

pp. 67-69 ◽

Cited By ~ 223

Author(s):

L. Aniksztejn ◽

Y. Ben-Ari

Keyword(s):

Channel Blocker ◽

Long Term Potentiation ◽

K Channel ◽

Term Potentiation

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Adenosine A1 Receptors Mediate Retinotectal Presynaptic Inhibition: Uncoupling by C-Kinase and Role in LTP During Regeneration

Journal of Neurophysiology ◽

10.1152/jn.1998.79.2.501 ◽

1998 ◽

Vol 79 (2) ◽

pp. 501-510 ◽

Cited By ~ 15

Author(s):

Chunyi Zhang ◽

John T. Schmidt

Keyword(s):

Presynaptic Inhibition ◽

Field Potential ◽

Long Term Potentiation ◽

Channel Blockers ◽

Adenosine A1 Receptors ◽

Kinase Activation ◽

Term Potentiation ◽

Adenosine A1 ◽

A1 Receptor

Zhang, Chunyi and John T. Schmidt. Adenosine A1 receptors mediate retinotectal presynaptic inhibition: uncoupling by C-kinase and role in LTP during regeneration. J. Neurophysiol. 79: 501–510, 1998. Presynaptic adenosine receptors inhibit transmitter release at many synapses and are known to exist on retinotectal terminals. In this paper we show that adenosine decreases retinotectal field potentials by ∼30% and investigate the mechanism. First, as judged by the effects of specific calcium channel blockers, retinotectal transmission was mediated almost exclusively by N-type calcium channels, which are known to be modulated by adenosine A1 receptors. Transmission was completely blocked by either ω-Conotoxin GVIA (−100%, N-type blocker) or ω-Conotoxin MVIIC (−99%, N-, P- and Q-type blocker) and was not significantly affected by ω-Agatoxin IVA [+1.7 ± 9.3% (SE), P-,Q-type blocker], but was augmented slightly by nifedipine(+9.3 ± 2.1%, L-type blocker). Second, the adenosine inhibition was presynaptic, as indicated by a 43% increase in paired-pulse facilitation. Third, the selective A1 agonist cyclohexyl adenosine (CHA) at 50 nM caused a 21% decrease in amplitude and the selective A2 agonist N 6-[2-(3,5-dimethoxyphenyl)-2-(2-methylphenyl)-ethyl]adenosine (DPMA) at 100 nM caused a 24% increase. Fourth, the selective A1 antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) alone produced an increase in the field potential, suggesting a tonic inhibition mediated by endogenous adenosine. Fifth, pertussis toxin eliminated adenosine inhibition implicating Gi or Go protein coupling. Sixth, C-kinase activation eliminated the A1-mediated inhibition. In regenerating projections, adenosine also caused a decrease in transmission (−30 ± 12%), but after induction of long-term potentiation (LTP) via trains of stimuli or via treatment with the phosphatase inhibitor okadaic acid, the adenosine response was converted to an augmentation. Because LTP is associated with C-kinase activation, this is consistent with C-kinase uncoupling the A1 receptor from inhibiting N-type Ca2+ channels. This uncovers the A2-mediated augmentation as demonstrated in normals with DPMA. Such an effect could account in part for the LTP of immature synapses and the change from rapidly fatiguing to robust synaptic transmission.

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