Corelease of two fast neurotransmitters at a central synapse.

@article{Jonas1998CoreleaseOT,
  title={Corelease of two fast neurotransmitters at a central synapse.},
  author={Peter Jonas and Josef Bischofberger and J{\"u}rgen Sandk{\"u}hler},
  journal={Science},
  year={1998},
  volume={281 5375},
  pages={
          419-24
        }
}
It is widely accepted that individual neurons in the central nervous system release only a single fast transmitter. The possibility of corelease of fast neurotransmitters was examined by making paired recordings from synaptically connected neurons in spinal cord slices. Unitary inhibitory postsynaptic currents generated at interneuron-motoneuron synapses consisted of a strychnine-sensitive, glycine receptor-mediated component and a bicuculline-sensitive, gamma-aminobutyric acid (GABA)A receptor… 
View on PubMed
cbr.meduniwien.ac.at
813 Citations
Highly Influential Citations
84
Background Citations
407
Methods Citations
39
Results Citations
35

813 Citations

Synaptic corelease of ATP and GABA in cultured spinal neurons

Differential modulation of excitatory versus inhibitory components of this mixed cotransmission may help to explain changes in sensory message processing in the DH during mechanical hyperalgesia and neuropathic pain.

Interneuronal synapses formed by motor neurons appear to be glutamatergic

Using whole-cell patch clamp, it is shown that spontaneous excitatory postsynaptic currents of rat motor neurons in primary ventral horn cultures are entirely glutamatergic, although the cells respond to exogenous acetylcholine.

Target-Dependent Use of Coreleased Inhibitory Transmitters at Central Synapses

It is demonstrated that, in the vestibulocerebellum, Golgi cells contact both granule cells and unipolar brush cells, which are excitatory relay interneurons for vestibular afferences.

Distinct profiles of refilling of inhibitory neurotransmitters into presynaptic terminals projecting to spinal neurones in immature rats

Observations indicate that three types of vesicles coexist in single synaptic terminals, and that refilling of glycine into the synaptic vesicle predominantes over GABA after pretreatment with bafilomycin A1 in immature rats is indicated.

Postsynaptic Determinants of Inhibitory Transmission at Mixed GABAergic/Glycinergic Synapses

It is proposed that tunable glycinergic inhibition timecourse may optimize rate-coding circuits of the hindbrain whereas forebrain coding through oscillations and synchrony may benefit from the rigid yet diverse subunit combination of GABAA receptors.

GABA, Glycine, and Glutamate Co-Release at Developing Inhibitory Synapses

Evidence showing that inhibitory synapses co-release multiple inhibitory neurotransmitters, and that some classical inhibitorysynapses also release excitatory neurotransmiters is reviewed, with special attention to developmental plasticity.

Mammalian motor neurons corelease glutamate and acetylcholine at central synapses.

It is shown, using a multidisciplinary approach, that mammalian spinal MNs, in addition to acetylcholine, corelease glutamate to excites Renshaw cells and other MNs but not to excite muscles.

Cotransmission of acetylcholine and GABA

Monosynaptic GABAergic Signaling from Dentate to CA3 with a Pharmacological and Physiological Profile Typical of Mossy Fiber Synapses

Corelease of GABA/glycine in lamina-X of the spinal cord of neonatal rats

Miniature inhibitory postsynaptic currents were recorded in the presence of tetrodotoxin and kynurenic acid to block action potential-dependent transmitter release and glutamatergic transmissions, respectively, suggesting that &ggr;-amino-n-butyric acid and glycine can be coreleased from the same single synaptic vesicles, and that this corelease can be detected by the post Synaptic cell.
...

References

SHOWING 1-10 OF 29 REFERENCES

Submillisecond AMPA Receptor-Mediated Signaling at a Principal Neuron–Interneuron Synapse

Single-channel currents underlying glycinergic inhibitory postsynaptic responses in spinal neurons

Colocalization of GABA, glycine, and their receptors at synapses in the rat spinal cord

The results strongly support the idea that cotransmission by GABA and glycine occurs in the spinal cord.

Involvement of GABA and glycine in recurrent inhibition of spinal motoneurons.

The results suggest that both glycinergic and GABAergic mechanisms play a role in recurrent inhibition of motoneurons in the mammalian spinal cord and suggest that a major portion of the strychnine-resistant component of the IPSP is mediated by a GABAergic mechanism.

Synaptic actions of single interneurones mediating reciprocal Ia inhibition of motoneurones

The interneurones were found to produce unitary monosynapticIPSPs in those motoneurones in which disynaptic IPSPs are evoked by the group Ia afferents whichmonosynaptically excite the interneerones.

NMDA and non-NMDA receptors are co-localized at individual excitatory synapses in cultured rat hippocampus

It is shown that the majority of the excitatory synapses on a postsynaptic cell possess both kinds of receptor, although to different extents, which provides direct evidence for co-localization of glutamate-receptor subtypes at individual synapses and points to the possibility that long-term potentiation might be differentially expressed at each synapse according to the mix of receptor sub types at that synapse.

GABA and glycine in synaptic vesicles: storage and transport characteristics

The coupling of neurotransmitter receptors to ion channels in the brain.

The existence of both convergence and divergence in the action of neurotransmitters results in a remarkable diversity in neuronal signaling.

Unitary inhibitory synaptic potentials in the guinea‐pig hippocampus in vitro.

Mechanisms involved in the generation of synaptic inhibition have been investigated by making simultaneous intracellular recordings from pairs of neurones in the CA3 pyramidal cell field of guinea‐pig hippocampal slices and the recurrent nature of some hippocampal inhibition has been demonstrated by showing that activity in a single cell may initiate feed‐back i.p.s.s onto itself.

Desensitized states prolong GABAA channel responses to brief agonist pulses