Despite evidence of local glycinergic circuits in the mature cerebellar nuclei the result of their activation remains unknown. Here, using whole cell recordings in rat cerebellar slices we demonstrated that after postnatal day 17 (>P17) glycinergic IPSCs can be readily evoked in large deep cerebellar nuclear neurons (DCNs), in the same way as in neonatal DCNs (P7-P10). Spontaneous glycinergic IPSCs were very rare but direct presynaptic depolarization by superfusion with elevated potassium concentration or application of 4-aminopyridine consistently evoked strychnine sensitive IPSCs. Glycinergic IPSCs showed fast kinetics in >P17 DCNs while were significantly slower in neonatal DCNs. Immuno-histochemical investigations using a specific marker for glycinergic fibers and terminals showed low density of immuno-fluorescent puncta, putative glycinergic boutons surrounding P18-P23 DCNs, in agreement with the rare spontaneous synaptic activity. But putative glycinergic boutons were present in critical areas for the control of spike generation. In contrast to adult and neonatal DCNs, glycinergic IPSCs could not be induced in juvenile DCNs (P13-P17) despite similar perisomatic immuno-staining pattern and expression of glycinergic receptors to >P17 DCNs. The latter results demonstrate substantial postnatal development of glycinergic cerebellar nuclei circuits. The cerebellum is involved in rapidly controlling ongoing movements. For that function, it is thought important the temporal and spatial precision of its output, which is carried to target structures by DCNs. The present study, by demonstrating fast glycinergic IPSCs in mature DCNs, points to the activation of glycinergic microcircuits as one of the possible mechanism involved in the spatio-temporal control of cerebellar output.
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http://dx.doi.org/10.1016/j.neuropharm.2007.12.005 | DOI Listing |
Int J Mol Sci
March 2024
Department of Anesthesiology, University Medical Center, Georg-August University, 37099 Göttingen, Germany.
The preBötzinger complex (preBötC) and the Bötzinger complex (BötC) are interconnected neural circuits that are involved in the regulation of breathing in mammals. Fast inhibitory neurotransmission is known to play an important role in the interaction of these two regions. Moreover, the corelease of glycine and GABA has been described in the respiratory network, but the contribution of the individual neurotransmitter in different pathways remains elusive.
View Article and Find Full Text PDFJ Physiol
September 2023
Institute of Pharmacology and Toxicology, University of Zurich, Zurich, Switzerland.
Glycine receptors (GlyRs), together with GABA receptors, mediate postsynaptic inhibition in most spinal cord and hindbrain neurons. In several CNS regions, GlyRs are also expressed in presynaptic terminals. Here, we analysed the effects of a phospho-deficient mutation (S346A) in GlyR α3 subunits on inhibitory synaptic transmission in superficial spinal dorsal horn neurons, where this subunit is abundantly expressed.
View Article and Find Full Text PDFJ Neurophysiol
December 2022
Department of Physiology and Anatomy, University of Texas Health Science Center, Fort Worth, Texas.
Front Neural Circuits
July 2022
School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle, Callaghan, NSW, Australia.
The incidence of pain symptoms such as allodynia are known to increase with age. Parvalbumin expressing interneurons (PVINs) within the dorsal horn (DH) of the spinal cord play an important role in allodynia whereby their inhibitory connections prevent innocuous touch information from exciting nociceptive pathways. Here we ask whether the functional properties of PVINs are altered by aging, comparing their functional properties in adult (3-7 month) and aged mice (23-28 month).
View Article and Find Full Text PDFFront Mol Neurosci
April 2022
School of Health and Behavioural Sciences, University of the Sunshine Coast, Maroochydore, QLD, Australia.
Glycine receptors (GlyRs) containing the α2 subunit govern cell fate, neuronal migration and synaptogenesis in the developing cortex and spinal cord. Rare missense variants and microdeletions in the X-linked GlyR α2 subunit gene () have been associated with human autism spectrum disorder (ASD), where they typically cause a via protein truncation, reduced cell-surface trafficking and/or reduced glycine sensitivity (e.g.
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