| 1. |
- Wang, YQ, et al.
(författare)
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Muscle-selective RUNX3 dependence of sensorimotor circuit development
- 2019
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Ingår i: Development (Cambridge, England). - : The Company of Biologists. - 1477-9129 .- 0950-1991. ; 146:20
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Tidskriftsartikel (refereegranskat)abstract
- The control of all our motor outputs requires constant monitoring by proprioceptive sensory neurons (PSNs) that convey continuous muscle sensory inputs to the spinal motor network. Yet, the molecular programs that control the establishment of this sensorimotor circuit remain largely unknown. The transcription factor RUNX3 is essential for the early steps of PSNs differentiation, making it difficult to study its role during later aspects of PSNs specification. Here, we conditionally inactivate Runx3 in PSNs after peripheral innervation and identify that RUNX3 is necessary for maintenance of cell identity of only a subgroup of PSNs, without discernable cell death. RUNX3 controls also the sensorimotor connection between PSNs and motor neurons at limb level, with muscle-by-muscle variable sensitivities to the loss of Runx3 that correlate with levels of RUNX3 in PSNs. Finally, we find that muscles and neurotrophin-3 signaling are necessary for maintenance of RUNX3 expression in PSNs. Hence, a transcriptional regulator critical for specifying a generic PSN type identity after neurogenesis, is later regulated by target muscle-derived signal to contribute to the specialized aspects of the sensorimotor connection selectivity.
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| 2. |
- Hascup, E. R., et al.
(författare)
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Sub-second measurements of glutamate and other neurotransmitter signaling using enzyme-based ceramic microelectrode arrays
- 2013
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Ingår i: Microelectrode Biosensors (Part II). - Totowa, NJ : Humana Press. - 9781627033695 - 9781627033701 ; , s. 179-199
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Konferensbidrag (refereegranskat)abstract
- We have set out to develop a novel, implantable microelectrode array that has the capabilities to detect neurotransmitters with enhanced sensitivity, selectivity, and temporal sampling capabilities compared to other current technologies. We have shown that this device maintains recording performance during chronic measurements of extracellular neurotransmitter levels for at least 7 days postimplantation, single-unit neuronal activity for as long as 6 months, and provides enhanced biocompatibility compared to current technologies. As we continue to refine and improve our recording capability, we are able to incorporate the chronic microelectrode array technology into multimodal experimental paradigms, such as behavioral testing, pharmacological intervention (local and systemic), or combined measurements of neurotransmitter levels and neuronal activity (local field potential). Furthermore, the improvements made with the microelectrode technology discussed in this chapter have the potential to conduct longitudinal analyses that can benefit a wide range of translational efforts, including studies on learning and memory, aging, neurodegenerative disease progression, and traumatic brain injury neuropathology.
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| 3. |
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| 4. |
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| 5. |
- Konradsson-Geuken, Asa, et al.
(författare)
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Second-by-second analysis of alpha 7 nicotine receptor regulation of glutamate release in the prefrontal cortex of awake rats.
- 2009
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Ingår i: Synapse. - : Wiley. - 0887-4476 .- 1098-2396. ; 63:12
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Tidskriftsartikel (refereegranskat)abstract
- These experiments utilized an enzyme-based microelectrode selective for the second-by-second detection of extracellular glutamate to reveal the alpha 7-based nicotinic modulation of glutamate release in the prefrontal cortex (PFC) of freely moving rats. Rats received intracortical infusions of the nonselective nicotinic agonist nicotine (12.0 mM, 1.0 microg/0.4 microl) or the selective alpha 7 agonist choline (2.0 mM/0.4 microl). The selectivity of drug-induced glutamate release was assessed in subgroups of animals pretreated with the alpha 7 antagonist, alpha-bungarotoxin (alpha-BGT, 10 microM), or kynurenine (10 microM) the precursor of the astrocyte-derived, negative allosteric alpha 7 modulator kynurenic acid. Local administration of nicotine increased glutamate signals (maximum amplitude = 4.3 +/- 0.6 microM) that were cleared to baseline levels in 493 +/- 80 seconds. Pretreatment with alpha-BGT or kynurenine attenuated nicotine-induced glutamate by 61% and 60%, respectively. Local administration of choline also increased glutamate signals (maximum amplitude = 6.3 +/- 0.9 microM). In contrast to nicotine-evoked glutamate release, choline-evoked signals were cleared more quickly (28 +/- 6 seconds) and pretreatment with alpha-BGT or kynurenine completely blocked the stimulated glutamate release. Using a method that reveals the temporal dynamics of in vivo glutamate release and clearance, these data indicate a nicotinic modulation of cortical glutamate release that is both alpha 7- and non-alpha 7-mediated. Furthermore, these data may also provide a mechanism underlying the recent focus on alpha 7 full and partial agonists as therapeutic agents in the treatment of cortically mediated cognitive deficits in schizophrenia.
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