What question did this study set out to answer?

To determine how norepinephrine and selective adrenergic receptor agonists and antagonists modulate long-term synaptic plasticity and frequency-response dynamics in hippocampal CA1 synapses.

June 1, 1997Journal of Neurophysiology

Noradrenergic Regulation of Synaptic Plasticity in the Hippocampal CA1 Region

View Full Paper

Ask AI

Bookmark

Authors

HKHiroshi Katsuki YIYukitoshi Izumi CZCharles F. Zorumski

Discussion

Member takes

Overview

Ex vivo study reveals norepinephrine promotes synaptic potentiation and blocks depression in rat hippocampal slices, indicating receptor-specific modulation of memory-related plasticity.

Key Points

To determine how norepinephrine and selective adrenergic receptor agonists and antagonists modulate long-term synaptic plasticity and frequency-response dynamics in hippocampal CA1 synapses.
Assessed synaptic efficacy in rat hippocampal CA1 slices stimulated at frequencies ranging from 1 to 30 Hz as well as theta-burst stimulation.
Treated slices with norepinephrine (10 µM) to examine its effects on the induction of long-term potentiation, long-term depression, and depotentiation.
Applied selective adrenergic antagonists (timolol, phentolamine) and agonists (isoproterenol, phenylephrine) to differentiate the roles of beta- and alpha1-adrenergic receptors.
Norepinephrine (10 µM) shifted the frequency-response curve toward potentiation, permitting long-term potentiation induction at 10 Hz and inhibiting long-term depression at 1 to 3 Hz.
Facilitation of potentiation at 10 Hz and blockade of depression at 1 Hz were mediated by beta-adrenergic receptors, being blocked by timolol and reproduced by isoproterenol.
Norepinephrine prevented the reversal of established potentiation (depotentiation) triggered by 1-Hz stimulation, an action requiring coactivation of both alpha1- and beta-adrenergic receptors.

Cite This Study

Katsuki et al. (1997) studied this question.

synapsesocial.com/papers/6a15fc8dbdb7c25666524fe4 https://doi.org/10.1152/jn.1997.77.6.3013

View Full Paper

Ask AI

Bookmark

June 1, 1997Journal of Neurophysiology

Noradrenergic Regulation of Synaptic Plasticity in the Hippocampal CA1 Region

View Full Paper

Ask AI

Bookmark

Authors

HKHiroshi Katsuki YIYukitoshi Izumi CZCharles F. Zorumski

Discussion

Member takes

Overview

Ex vivo study reveals norepinephrine promotes synaptic potentiation and blocks depression in rat hippocampal slices, indicating receptor-specific modulation of memory-related plasticity.

Key Points

To determine how norepinephrine and selective adrenergic receptor agonists and antagonists modulate long-term synaptic plasticity and frequency-response dynamics in hippocampal CA1 synapses.
Assessed synaptic efficacy in rat hippocampal CA1 slices stimulated at frequencies ranging from 1 to 30 Hz as well as theta-burst stimulation.
Treated slices with norepinephrine (10 µM) to examine its effects on the induction of long-term potentiation, long-term depression, and depotentiation.
Applied selective adrenergic antagonists (timolol, phentolamine) and agonists (isoproterenol, phenylephrine) to differentiate the roles of beta- and alpha1-adrenergic receptors.
Norepinephrine (10 µM) shifted the frequency-response curve toward potentiation, permitting long-term potentiation induction at 10 Hz and inhibiting long-term depression at 1 to 3 Hz.
Facilitation of potentiation at 10 Hz and blockade of depression at 1 Hz were mediated by beta-adrenergic receptors, being blocked by timolol and reproduced by isoproterenol.
Norepinephrine prevented the reversal of established potentiation (depotentiation) triggered by 1-Hz stimulation, an action requiring coactivation of both alpha1- and beta-adrenergic receptors.

Cite This Study

Katsuki et al. (1997) studied this question.

synapsesocial.com/papers/6a15fc8dbdb7c25666524fe4 https://doi.org/10.1152/jn.1997.77.6.3013

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

View Full Paper

Ask AI

Bookmark