Neurotransmitter segregation: Functional and plastic implications

Sámano, Cynthia; Cifuentes, Fredi; Morales, M.A.

doi:10.1016/j.pneurobio.2012.04.004

Cited by 22 publications

(23 citation statements)

References 123 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…26, based on growing evidence that neurons in several brain regions can synthesize and segregate neurotransmitters, their synthesizing enzymes, or associated vesicular transporters to different populations of synaptic vesicles in the same terminals, or sort these molecules to different axon processes (El Mestikawy et al 2011; Samano et al 2012; Vaaga et al 2014). This makes it possible for terminals to co-release (or co-transmit) neurotransmitters onto the same or different targets (Saunders et al 2015).…”

Section: Discussionmentioning

confidence: 99%

“…This makes it possible for terminals to co-release (or co-transmit) neurotransmitters onto the same or different targets (Saunders et al 2015). In addition, the sorting of these molecules is also subject to plasticity (see Samano et al 2012), which may also contribute to observations of activity-dependent changes in expression levels (De Gois et al 2005). While presently unknown for TC and CC projections in the auditory forebrain, these findings suggest that some neurons may possess the machinery needed to route transmitters and other molecules to different terminal processes in a dynamic manner.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Differential maturation of vesicular glutamate and GABA transporter expression in the mouse auditory forebrain during the first weeks of hearing

et al. 2015

View full text Add to dashboard Cite

Vesicular transporter proteins are an essential component of the presynaptic machinery that regulates neurotransmitter storage and release. They also provide a key point of control for homeostatic signaling pathways that maintain balanced excitation and inhibition following changes in activity levels, including the onset of sensory experience. To advance understanding of their roles in the developing auditory forebrain, we tracked the expression of the vesicular transporters of glutamate (VGluT1, VGluT2) and GABA (VGAT) in primary auditory cortex (A1) and medial geniculate body (MGB) of developing mice (P7, P11, P14, P21, adult) before and after ear canal opening (~P11–P13). RNA sequencing, in situ hybridization, and immunohistochemistry were combined to track changes in transporter expression and document regional patterns of transcript and protein localization. Overall, vesicular transporter expression changed the most between P7 and P21. The expression patterns and maturational trajectories of each marker varied by brain region, cortical layer, and MGB subdivision. VGluT1 expression was highest in A1, moderate in MGB, and increased with age in both regions. VGluT2 mRNA levels were low in A1 at all ages, but high in MGB, where adult levels were reached by P14. VGluT2 immunoreactivity was prominent in both regions. VGluT1+ and VGluT2+ transcripts were co-expressed in MGB and A1 somata, but co-localization of immunoreactive puncta was not detected. In A1, VGAT mRNA levels were relatively stable from P7 to adult, while immunoreactivity increased steadily. VGAT+ transcripts were rare in MGB neurons, whereas VGAT immunoreactivity was robust at all ages. Morphological changes in immunoreactive puncta were found in two regions after ear canal opening. In the ventral MGB, a decrease in VGluT2 puncta density was accompanied by an increase in puncta size. In A1, peri-somatic VGAT and VGluT1 terminals became prominent around the neuronal somata. Overall, the observed changes in gene and protein expression, regional architecture, and morphology relate to—and to some extent may enable— the emergence of mature sound-evoked activity patterns. In that regard, the findings of this study expand our understanding of the presynaptic mechanisms that regulate critical period formation associated with experience-dependent refinement of sound processing in auditory forebrain circuits.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Differential maturation of vesicular glutamate and GABA transporter expression in the mouse auditory forebrain during the first weeks of hearing

et al. 2015

View full text Add to dashboard Cite

show abstract

“…Homosynaptic plasticity can also involve interactions of multiple transmitters as the same neuron may contain multiple cotransmitters. For instance, neuropeptides can potentiate the PSPs elicited by a classic transmitter contained in the same neuron (e.g., Fox and Lloyd 2001;Koh and Weiss 2005;Sámano et al 2012). Also, the same neuron can contain multiple classic transmitters.…”

mentioning

confidence: 99%

PKC-mediated GABAergic enhancement of dopaminergic responses: implication for short-term potentiation at a dual-transmitter synapse

Svensson

Proekt

Jing

et al. 2014

Journal of Neurophysiology

View full text Add to dashboard Cite

Svensson E, Proekt A, Jing J, Weiss KR. PKC-mediated GABAergic enhancement of dopaminergic responses: implication for short-term potentiation at a dual-transmitter synapse. J Neurophysiol 112: 22-29, 2014. First published April 9, 2014 doi:10.1152/jn.00794.2013.-Transmitter-mediated homosynaptic potentiation is generally implemented by the same transmitter that mediates the excitatory postsynaptic potentials (EPSPs), e.g., glutamate. When a presynaptic neuron contains more than one transmitter, however, potentiation can in principle be implemented by a transmitter different from that which elicits the EPSPs. Neuron B20 in Aplysia contains both dopamine and GABA. Although only dopamine acts as the fast excitatory transmitter at the B20-to-B8 synapse, GABA increases the size of these dopaminergic EPSPs. We now provide evidence that repeated stimulation of B20 potentiates B20-evoked dopaminergic EPSPs in B8 apparently via a postsynaptic mechanism, and short-term potentiation of this synapse is critical for the establishment and maintenance of an egestive network state. We show that GABA can act postsynaptically to increase dopamine currents that are elicited by direct applications of dopamine to B8 and that dopamine is acting on a 5-HT 3 -like receptor. This potentiation is mediated by GABA B -like receptors as GABA B -receptor agonists and antagonists, respectively, mimicked and blocked the potentiating actions of GABA. The postsynaptic actions of GABA rely on a G protein-mediated activation of PKC. Our results suggest that the postsynaptic action of cotransmitter-mediated potentiation may contribute to the maintenance of the egestive state of Aplysia feeding network and, in more general terms, may participate in the plasticity of networks that mediate complex behaviors.

show abstract

“…This "modern version of Dale`s principle" claimed that neurons release the same set of transmitters from all of their axon processes, assuming that the identity of the transmitters expressed by neurons is unchanging. Nevertheless, recent discoveries [16,17,18] demonstrate that electrical activity can respecify neurotransmitter expression during development, but also in mature nervous system. The logical question that arises is what happens with postsynaptic receptors if the identity of presinaptically created neurotransmitter changes.…”

Section: Lost In Translationmentioning

confidence: 99%

Neurotransmitters in the central nervous system: Basic knowledge revisited

Lozic-Djuric¹

2015

Med podmladak

View full text Add to dashboard Cite

The chemistry within us This elegant experiment performed by Otto Loewi is considered to be the Rosetta stone of chemical transmission concept and has provided the first evidence that nerves do not influence the heart directly, but liberate specific chemical substances from their terminals. Today, when neurotransmitters are inseparable part of theories of how our brain works, it is difficult to understand that it took more than thirty years of scientific disputes between neurophysiologists and pharmacologists to prove that synaptic transmission is chemical rather than electrical. The great victory of pharmacologists in a war called "the war of sparks and soups" [2,3] happened in 1936, when Otto Loewi and Sir Henry Dale were awarded the Nobel Prize for establishing chemical synaptic transmission.Given the fact that acetylcholine was the first neurotransmitter to be discovered [4], it is not surprising that the classic criteria for neurotransmitters were based on the properties of this particular molecule.Although conventional definition describes a neurotransmitter as a substance that satisfies the following criteria [5,6]:1. It is synthesized and stored within the presynaptic neuron 2. It is released by nerve stimulation in a calcium-dependent manner 3. It binds to specific receptor(s) localized presinaptically or postsinaptically 4. Its exogenous application mimics the postsynaptic effect of presynaptic stimulation 5. Specific receptor antagonists block the effects of endogenous (synaptically released) or exogenous (externally applied) substance 6. Its action(s) can be terminated in enzyme-mediated way or by the cellular uptake mechanism, the increasing knowledge in the field of neuroscience has been continually modifying the understanding of the term "neurotransmitter". Nowadays, we are faced with at least two questions that may sound like a rather perplexing word game, but still need to be properly addressed: Are only neurotransmitters-neurotransmitters? Are neurotransmitters only neurotransmitters?

show abstract

Neurotransmitter segregation: Functional and plastic implications

Cited by 22 publications

References 123 publications

Differential maturation of vesicular glutamate and GABA transporter expression in the mouse auditory forebrain during the first weeks of hearing

Differential maturation of vesicular glutamate and GABA transporter expression in the mouse auditory forebrain during the first weeks of hearing

PKC-mediated GABAergic enhancement of dopaminergic responses: implication for short-term potentiation at a dual-transmitter synapse

Neurotransmitters in the central nervous system: Basic knowledge revisited

Contact Info

Product

Resources

About