ArticleJournal of neurophysiology2011
Peripheral nerve damage does not alter release properties of developing central trigeminal afferents.
Article in Journal of neurophysiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Neonatal sensory nerve injury-induced synaptic plasticity in the trigeminal principal sensory nucleus.Experimental neurology · 2016Review
- Sensory Activity-Dependent and Sensory Activity-Independent Properties of the Developing Rodent Trigeminal Principal Nucleus.Developmental neuroscience · 2016Review
- Functional significance of cortical NMDA receptors in somatosensory information processing.Journal of neurophysiology · 2013Article
- Astrocytes promote peripheral nerve injury-induced reactive synaptogenesis in the neonatal CNS.Journal of neurophysiology · 2011Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The infraorbital branch of the trigeminal nerve (ION) is essential in whisker-specific neural patterning ("barrelettes") in the principal nucleus of the trigeminal nerve (PrV). The barrelettes are formed by the ION terminal arbors, somata, and dendrites of the PrV cells; they are abolished after neonatal damage to the ION. Physiological studies show that disruption of the barrelettes is accompanied by conversion of functional synapses into silent synapses in the PrV. In this study, we used whole cell recordings with a paired-pulse stimulation protocol and MK-801 blocking rate to estimate the presynaptic release probability (Pr) of ION central trigeminal afferent terminals in the PrV. We investigated Pr during postnatal development, following neonatal ION damage, and determined whether conversion of functional synapses into silent synapses after peripheral denervation results from changes in Pr. The paired-pulse ratio (PPR) was quite variable ranging from 40% (paired-pulse depression) to 175% (paired-pulse facilitation). The results from paired-pulse protocol were confirmed by MK-801 blocking rate experiments. The nonuniform PPRs did not show target cell specificity and developmental regulation. The distribution of PPRs fit nicely to Gaussian function with a peak at ∼ 100%. In addition, neonatal ION transections did not alter the distribution pattern of PPR in their central terminals, suggesting that the conversion from functional synapses into silent synapses in the peripherally denervated PrV is not caused by changes in the Pr.
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