scholarly journals Noradrenaline Release from Locus Coeruleus Terminals in the Hippocampus Enhances Excitation-Spike Coupling in CA1 Pyramidal Neurons Via β-Adrenoceptors

2020 ◽  
Vol 30 (12) ◽  
pp. 6135-6151 ◽  
Author(s):  
Travis J Bacon ◽  
Anthony E Pickering ◽  
Jack R Mellor
Keyword(s):  
Noradrenaline Release ◽  
Information Transfer ◽  
Pyramidal Neurons ◽  
Schaffer Collateral ◽  
Release Of Noradrenaline ◽  
Ca1 Pyramidal Neurons ◽  
Endogenous Noradrenaline ◽  
Memory Representations ◽  
Endogenous Release ◽  
Ca1 Pyramidal Neuron

Abstract Release of the neuromodulator noradrenaline signals salience during wakefulness, flagging novel or important experiences to reconfigure information processing and memory representations in the hippocampus. Noradrenaline is therefore expected to enhance hippocampal responses to synaptic input; however, noradrenergic agonists have been found to have mixed and sometimes contradictory effects on Schaffer collateral synapses and the resulting CA1 output. Here, we examine the effects of endogenous, optogenetically driven noradrenaline release on synaptic transmission and spike output in mouse hippocampal CA1 pyramidal neurons. We show that endogenous noradrenaline release enhances the probability of CA1 pyramidal neuron spiking without altering feedforward excitatory or inhibitory synaptic inputs in the Schaffer collateral pathway. β-adrenoceptors mediate this enhancement of excitation-spike coupling by reducing the charge required to initiate action potentials, consistent with noradrenergic modulation of voltage-gated potassium channels. Furthermore, we find the likely effective concentration of endogenously released noradrenaline is sub-micromolar. Surprisingly, although comparable concentrations of exogenous noradrenaline cause robust depression of slow afterhyperpolarization currents, endogenous release of noradrenaline does not, indicating that endogenous noradrenaline release is targeted to specific cellular locations. These findings provide a mechanism by which targeted endogenous release of noradrenaline can enhance information transfer in the hippocampus in response to salient events.

Release of noradrenaline from the rat tail artery induced by inhibition of the sodium pump in calcium-free solution

1981 ◽  
Vol 59 (4) ◽  
pp. 347-350 ◽  
Author(s):  
Vladimír Palatý
Keyword(s):  
Noradrenaline Release ◽  
Sodium Pump ◽  
Rat Tail Artery ◽  
Release Of Noradrenaline ◽  
Tail Artery ◽  
Storage Vesicles ◽  
Endogenous Noradrenaline ◽  
Electron Dense Core ◽  
Rat Tail ◽  
Isolated Rat

The release of noradrenaline from the isolated rat tail artery into Ca2+- and K-free, 1 mM ouabain containing solution was measured by means of radioenzymatic method. The rate of noradrenaline release increased gradually reaching a maximum of ca. 2.30 nmol∙g−1∙h−1 after 100 min. The enhancement of noradrenaline release could be inhibited by cocaine and phenoxybenzamine but not by desipramine. The rate of noradrenaline release could be approximately doubled by prior inhibition of monoamine oxidase with pargyline. The release was accompanied by a decline in the proportion of storage vesicles containing an electron-dense core. These observations indicate that, in the absence of external Ca2+, inhibition of the sodium pump causes nonexocytotic release of endogenous noradrenaline.

scholarly journals Selective muscarinic regulation of functional glutamatergic Schaffer collateral synapses in rat CA1 pyramidal neurons

2002 ◽  
Vol 545 (1) ◽  
pp. 51-63 ◽  
Author(s):  
David Fernández Sevilla ◽  
Carolina Cabezas ◽  
Amaranta N. Oshima Prada ◽  
Abel Sánchez‐Jiménez ◽  
Washington Buño
Keyword(s):  
Pyramidal Neurons ◽  
Schaffer Collateral ◽  
Ca1 Pyramidal Neurons

scholarly journals Astrocyte GluN2C NMDA receptors control basal synaptic strengths of hippocampal CA1 pyramidal neurons in the stratum radiatum

2021 ◽  
Author(s):  
Peter H. Chipman ◽  
Alejandra Pazo Fernandez ◽  
Chi Chung Alan Fung ◽  
Angelo Tedoldi ◽  
Atsushi Kawai ◽  
...  
Keyword(s):  
Pyramidal Neurons ◽  
Strength Distribution ◽  
Stratum Radiatum ◽  
Appreciable Change ◽  
Ca1 Pyramidal Neurons ◽  
Hippocampal Ca1 ◽  
Exact Function ◽  
Change In The Mean ◽  
Circuit Function ◽  
Ca1 Pyramidal Neuron

Experience-dependent plasticity is a key feature of brain synapses for which neuronal N-Methyl-D-Aspartate receptors (NMDARs) play a major role, from developmental circuit refinement to learning and memory. Astrocytes also express NMDARs although their exact function has remained controversial. Here we identify a circuit function for GluN2C NMDAR, a subtype highly expressed in astrocytes, in layer-specific tuning of synaptic strengths in mouse hippocampal CA1 pyramidal neurons. Interfering with astrocyte NMDAR or GluN2C NMDAR activity reduces the range of presynaptic strength distribution specifically in the stratum radiatum inputs without an appreciable change in the mean presynaptic strength. Mathematical modeling shows that narrowing of the width of presynaptic release probability distribution compromises the expression of long-term synaptic plasticity. Our findings suggest a novel feedback signaling system that uses astrocyte GluN2C NMDARs to adjust basal synaptic weight distribution of Schaffer collateral inputs, which in turn impacts computations performed by the CA1 pyramidal neuron.

scholarly journals α5 Subunit-containing GABAA receptors mediate a slowly decaying inhibitory synaptic current in CA1 pyramidal neurons following Schaffer collateral activation

2010 ◽  
Vol 58 (3) ◽  
pp. 668-675 ◽  
Author(s):  
Mariana Vargas-Caballero ◽  
Loren J. Martin ◽  
Michael W. Salter ◽  
Beverley A. Orser ◽  
Ole Paulsen
Keyword(s):  
Gabaa Receptors ◽  
Pyramidal Neurons ◽  
Synaptic Current ◽  
Schaffer Collateral ◽  
Ca1 Pyramidal Neurons

Long-lasting potentiation and depression without presynaptic activity

1996 ◽  
Vol 75 (5) ◽  
pp. 2157-2160 ◽  
Author(s):  
D. Neveu ◽  
R. S. Zucker
Keyword(s):  
Pyramidal Neurons ◽  
Long Term Potentiation ◽  
Long Term Depression ◽  
Biochemical Processes ◽  
Common Features ◽  
Ca1 Pyramidal Neurons ◽  
Term Potentiation ◽  
Necessary And Sufficient ◽  
Ca1 Pyramidal Neuron

1. Long-term potentiation (LTP) and long-term depression (LTD) require a rise in intracellular Ca2+ concentration ([Ca2+]i) in the postsynaptic CA1 pyramidal neuron to activate Ca-dependent biochemical processes. This rise in [Ca2+]i is a necessary trigger for the induction of LTP and LTD, but it is unclear if concurrent presynaptic activity is required for their induction or expression. 2. We used photolysis of the caged-Ca2+ compound nitr-5 to elevate postsynaptic [Ca2+]i. Long-lasting potentiation (LLP) and long-lasting depression (LLD) were obtained in the absence of presynaptic activity. 3. Because LLP and LLD share common features with LTP and LTD induced by presynaptic stimulation these results show that a rise in [Ca2+]i in the postsynaptic CA1 pyramidal neurons is necessary and sufficient for the induction and expression of LTP and LTD, and that concurrent presynaptic activity is not required.

Correlation Between Noradrenaline Fluxes, Metabolism and Compartmentalisation in Human Platelets

1982 ◽  
Vol 48 (01) ◽  
pp. 062-066 ◽  
Author(s):  
Chantal Legrand ◽  
Véronique Dubernard ◽  
Philippe Meyer
Keyword(s):  
Noradrenaline Release ◽  
Human Platelets ◽  
Release Of Noradrenaline ◽  
Storage Pool ◽  
Platelet Storage ◽  
Efflux Of Noradrenaline ◽  
Preferential Localization

Summary(3H) noradrenaline was taken up by human platelets and partially converted into sulfoconjugated noradrenaline. This uptake was inhibited by drugs which have been previously shown to impair the uptake of 5-HT (ouabain, chlorimipramine) or the storage of 5-HT (tyramine, reserpine) by platelets. In addition, tyramine and reserpine stimulated the formation of sulfoconjugated noradrenaline. The efflux of noradrenaline from platelets was measured in parallel and was found to be directly related to the proportion of non metabolized to metabolized noradrenaline in the cells. Unlike tyramine, which induced a similar release of noradrenaline and 5-HT, reserpine was less effective at inducing noradrenaline release than 5-HT release. This study indicates a preferential localization of noradrenaline in the granular pool of human platelets with the existence of an extragranular sulfoconjugated pool which is increased when the granular storage of noradrenaline is impaired. Studies of noradrenaline fluxes and metabolism may be useful in the understanding of both acquired and inherited platelet storage pool defects.

Sign in / Sign up

Export Citation Format

Share Document