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Staggered Development of GABAergic and Glycinergic Transmission in the MNTB
Abstract
Maturation of some brain stem and spinal inhibitory systems is characterized by a shift from GABAergic to glycinergic transmission. Little is known about how this transition is expressed in terms of individual axonal inputs and synaptic sites. We have explored this issue in the rat medial nucleus of the trapezoid body (MNTB). Synaptic responses at postnatal days 5-7 (P5-P7) were small, slow, and primarily mediated by GABA(A) receptors. By P8-P12, an additional, faster glycinergic component emerged. At these ages, GABA(A), glycine, or both types of receptors mediated transmission, even at single synaptic sites. Thereafter, glycinergic development greatly accelerated. By P25, evoked inhibitory postsynaptic currents (IPSCs) were 10 times briefer and 100 times larger than those measured in the youngest group, suggesting a proliferation of synaptic inputs activating fast-kinetic receptors. Glycinergic miniature IPSCs (mIPSCs) increased markedly in size and decay rate with age. GABAergic mIPSCs also accelerated, but declined slightly in amplitude. Overall, the efficacy of GABAergic inputs showed little maturation between P5 and P20. Although gramicidin perforated-patch recordings revealed that GABA or glycine depolarized P5-P7 cells but hyperpolarized P14-P15 cells, the young depolarizing inputs were not suprathreshold. In addition, vesicle-release properties of inhibitory axons also matured: GABAergic responses in immature rats were highly asynchronous, while in older rats, precise, phasic glycinergic IPSCs could transmit even with 500-Hz stimuli. Thus development of inhibition is characterized by coordinated modifications to transmitter systems, vesicle release kinetics, Cl- gradients, receptor properties, and numbers of synaptic inputs. The apparent switch in GABA/glycine transmission was predominantly due to enhanced glycinergic function.
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“By adulthood, both transmitters are inhibitory, activating their cognate chloride permeable ligand-gated ion channels, and hyperpolarizing their postsynaptic targets.48”
From Synaptic and circuit functions of multitransmitter neurons in the mammalian brain (2023) · cites this paper as [48]
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Petralia, R. S., & Wenthold, R. J. (2008) · Springer eBooks · doi:10.1007/978-3-540-29678-2_3957 · Cited by 7
Metadata
- Authors
- Awatramani, G. B., Turecek, R., & Trussell, L. O.
- Affiliations
- Oregon Health & Science University (US)
- Venue
- Journal of Neurophysiology
- Publisher
- American Physiological Society
- Published
- 2005-02
- Volume
- 93
- Issue
- 2
- Pages
- 819-828
- ISSN
- 0022-3077 (ISSN-L)
- 1522-1598
- OpenAlex
- W2025066952
- Cited by
- 138
- References
- 63
- Citations by year
- 2026: 2 · 2025: 5 · 2023: 4 · 2022: 3 · 2021: 3 · 2020: 2 · 2019: 10 · 2018: 7 · 2017: 6 · 2016: 6 · 2015: 6 · 2014: 14 · 2013: 11 · 2012: 3
- FWCI
- 1.52
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neurophysiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Deafness and Other Communication Disorders (DC04450, R01DC004450)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Keywords
- medial nucleus of the trapezoid body, GABAergic neurotransmission, glycinergic transmission, inhibitory postsynaptic currents, miniature IPSCs, synapse maturation, GABAA receptor, glycine receptor, chloride gradient, postnatal development
- MeSH terms
- Age Factors, Animals, Brain Stem, gamma-Aminobutyric Acid, Glycine, Synaptic Transmission, Receptors, GABA-A, Rats, Wistar, Receptors, Glycine, Rats, GABA-A Receptor Agonists, In Vitro Techniques
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