Locomotor activity correlates with modifications of hippocampal mossy fibre synaptic transmission

Neuropeptides control rhythmic behaviors, but the timing and location of their release within circuits is unknown. Here, imaging in the brain shows that synaptic neuropeptide release by Drosophila clock neurons is diurnal, peaking at times of day that were not anticipated by prior electrical and Ca2+ data. Furthermore, hours before peak synaptic neuropeptide release, neuropeptide release occurs at the soma, a neuronal compartment that has not been implicated in peptidergic transmission. The timing disparity between release at the soma and terminals results from independent and compartmentalized mechanisms for daily rhythmic release: consistent with conventional electrical activity–triggered synaptic transmission, terminals require Ca2+ influx, while somatic neuropeptide release is triggered by the biochemical signal IP3. Upon disrupting the somatic mechanism, the rhythm of terminal release and locomotor activity period are unaffected, but the number of flies with rhythmic behavior and sleep–wake balance are reduced. These results support the conclusion that somatic neuropeptide release controls specific features of clock neuron–dependent behaviors. Thus, compartment-specific mechanisms within individual clock neurons produce temporally and spatially partitioned neuropeptide release to expand the peptidergic connectome underlying daily rhythmic behaviors.

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Microglia‐derived purines modulate mossy fibre synaptic transmission and plasticity through P2X 4 and A 1 receptors

European Journal of Neuroscience ◽

10.1111/ejn.13191 ◽

2016 ◽

Vol 43 (10) ◽

pp. 1366-1378 ◽

Cited By ~ 12

Author(s):

Jimmy George ◽

Rodrigo A. Cunha ◽

Christophe Mulle ◽

Thierry Amédée

Keyword(s):

Synaptic Transmission ◽

Mossy Fibre

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Heterogeneous Electrotonic Coupling and Synchronization of Rhythmic Bursting Activity in Mouse Hb9 Interneurons

Journal of Neurophysiology ◽

10.1152/jn.00338.2007 ◽

2007 ◽

Vol 98 (4) ◽

pp. 2370-2381 ◽

Cited By ~ 41

Author(s):

J. M. Wilson ◽

A. I. Cowan ◽

R. M. Brownstone

Keyword(s):

Spinal Cord ◽

Locomotor Activity ◽

Synaptic Transmission ◽

Calcium Imaging ◽

Channel Blockers ◽

Electrotonic Coupling ◽

Photon Excitation ◽

Wide Range ◽

Fast Chemical ◽

Bursting Activity

The neurons and mechanisms involved in mammalian spinal cord networks that produce rhythmic locomotor activity remain largely undefined. Hb9 interneurons, a small population of discretely localized interneurons in the mouse spinal cord, are conditionally bursting neurons. Here we applied potassium channel blockers with the aim of increasing neuronal excitability and observed that under these conditions, postnatal Hb9 interneurons exhibited bursts of action potentials with underlying voltage-independent spikelets. The bursts were insensitive to antagonists to fast chemical synaptic transmission, and the bursting and spikelets were blocked by tetrodotoxin. Calcium imaging studies using 2-photon excitation in spinal cord slices revealed that clustered Hb9 interneurons exhibited synchronous and occasional asynchronous, calcium transients that were also insensitive to fast synaptic transmission blockade. All transients were blocked by the gap junction blocker carbenoxolone. Paired whole cell patch-clamp recordings of Hb9 interneurons in the late postnatal mouse revealed common chemical synaptic inputs but no evidence of current transfer (i.e., electrotonic coupling) between the neurons. However, Hb9 and a previously defined population of non-Hb9 interneurons were electrotonically coupled. In the absence of fast chemical transmission in the whole spinal cord preparation, 2-photon excitation calcium imaging revealed bursting activity of Hb9 interneurons synchronous with rhythmic ventral root output. Thus Hb9 interneurons are both endogenous bursters and rhythmically active within a heterogeneous electrotonically coupled network. A network with these properties could produce the wide range of stable rhythms necessary for locomotor activity.

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Regulation of synaptic transmission in the mossy fibre-granule cell pathway of rat cerebellum by metabotropic glutamate receptors

Neuropharmacology ◽

10.1016/s0028-3908(99)00003-9 ◽

1999 ◽

Vol 38 (6) ◽

pp. 805-815 ◽

Cited By ~ 12

Author(s):

P Vetter ◽

J Garthwaite ◽

A.M Batchelor

Keyword(s):

Synaptic Transmission ◽

Glutamate Receptors ◽

Granule Cell ◽

Metabotropic Glutamate Receptors ◽

Mossy Fibre ◽

Metabotropic Glutamate ◽

Rat Cerebellum

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Independently Regulated Multi-compartment Neuropeptide Release from a Clock Neuron Controls Circadian Behavior

10.1101/2020.07.24.219725 ◽

2020 ◽

Author(s):

Markus K. Klose ◽

Marcel P. Bruchez ◽

David L. Deitcher ◽

Edwin S. Levitan

Keyword(s):

Locomotor Activity ◽

Circadian Rhythms ◽

Synaptic Transmission ◽

Electrical Activity ◽

Action Potentials ◽

Single Neuron ◽

Neuropeptide Release ◽

Circadian Behavior ◽

The Brain ◽

Neuronal Compartments

Neuropeptides control many behaviors, including circadian rhythms. However, because monitoring neuropeptide release in the brain is challenging, analysis of peptidergic circuits often has relied on monitoring surrogates in the soma based on the paradigm that synaptic transmission is mediated exclusively by Ca2+ influx induced by propagating action potentials. Here live imaging demonstrates that neuropeptide release by Drosophila small ventrolateral (s-LNv) clock neurons does not conform to this paradigm. First, neuropeptide release from terminals peaks hours after sunrise, which was not evident from electrical and Ca2+ data. Second, inconsistent with global release by propagating action potentials, release from terminals is preceded by hours by release from the soma, a compartment not usually considered in peptidergic transmission. The timing of release from the two neuronal compartments reflects different mechanisms: terminals require Ca2+ influx, as expected with coupling to electrical activity, while somatic release is based on intracellular IP3 signaling. Upon cell specific disruption of the somatic mechanism, daily neuropeptide release from terminals remains rhythmic and the period of daily locomotor activity is unaffected, but behavioral rhythmicity is reduced. Thus, rhythmic bouts of anatomically, mechanistically and temporally distinct release from a single neuron control neuropeptide dependent features of circadian behavior.

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