Pharmacological analysis of excitatory and inhibitory synaptic transmission in horizontal brainstem slices preserving three subnuclei of spinal trigeminal nucleus

Han, Sang-Mi; Ahn, Dongbin; Youn, Dong‐ho

doi:10.1016/j.jneumeth.2007.08.011

Cited by 30 publications

(19 citation statements)

References 60 publications

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“…Alternatively, these temperature-sensitive and -insensitive, TRPV1Ϫ neurons may originate from central neurons creating a complex synaptic arrangement. Glutamate released in Vc may arise from interneurons (Kato et al 2009) comprising internuclear and -laminar connections (Hamba and Onimaru 1998;Han et al 2008;Onodera et al 2000) as well as descending pathways (Aicher et al 2012;Sato et al 2013). Knowledge of the degree of synaptic convergence of such afferent nerves is limited in Vc but the varied thermal and CAP responses could reflect these diverse sources (Zanotto et al 2007).…”

Section: Discussionmentioning

confidence: 99%

Physiological temperatures drive glutamate release onto trigeminal superficial dorsal horn neurons

Largent-Milnes

Hegarty

Aicher

et al. 2014

Journal of Neurophysiology

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Largentϩ , thermal, and chemical stimuli. The present study investigated the relationships among the spontaneous release of glutamate, temperature, and TRPV1 localization at synapses in the Vc. Spontaneous excitatory postsynaptic currents (sEPSCs) were recorded from Vc neurons (n ϭ 151) in horizontal brain-stem slices obtained from Sprague-Dawley rats. Neurons had basal sEPSC rates that fell into two distinct frequency categories: High (Ն10 Hz) or Low (Ͻ10 Hz) at 35°C. Of all recorded neurons, those with High basal release rates (67%) at near-physiological temperatures greatly reduced their sEPSC rate when cooled to 30°C without amplitude changes. Such responses persisted during blockade of action potentials indicating that the High rate of glutamate release arises from presynaptic thermal mechanisms. Neurons with Low basal frequencies (33%) showed minor thermal changes in sEPSC rate that were abolished after addition of TTX, suggesting these responses were indirect and required local circuits. Activation of TRPV1 with capsaicin (100 nM) increased miniature EPSC (mEPSC) frequency in 70% of neurons, but half of these neurons had Low basal mEPSC rates and no temperature sensitivity. Our evidence indicates that normal temperatures (35-37°C) drive spontaneous excitatory synaptic activity within superficial Vc by a mechanism independent of presynaptic action potentials. Thus thermally sensitive inputs on superficial Vc neurons may tonically activate these neurons without afferent stimulation.trigeminal nucleus caudalis; temperature; TRPV1; spontaneous release; electrophysiology

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Section: Discussionmentioning

confidence: 99%

Physiological temperatures drive glutamate release onto trigeminal superficial dorsal horn neurons

Largent-Milnes

Hegarty

Aicher

et al. 2014

Journal of Neurophysiology

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“…The somatotopic and functional distribution of primary afferent inputs to the trigeminal spinal nucleus [1] allows microglia to be studied at a variety of locations (Sp5C; Sp5I/Sp5C boundary; Sp5O) specific to unique and well-characterized sensory pathways [62,191]. It is also possible to ask questions concerning intra-or inter-nuclear signaling [63] and the pathological significance of microglia involvement in its modulation. Such studies may offer clues to potentially multiple roles for microglia in nociceptive modulation, not just in trigeminal but also spinal neuropathic pain.…”

Section: Discussionmentioning

confidence: 99%

“…Do the inflammatory reactions in the different regions represent different activating processes, or merely reflect anatomical differences? Unlike the spinal cord, the trigeminal system appears unique in its degree of intra-and intersubnuclear signaling [63]. Further studies of this signaling network may allow a functional dissection of injury-specific neuropathies that is not possible in spinal pain models and may reveal mechanisms of central sensitization specific to the trigeminal system [1,64].…”

Section: Microglia Respond To Inflammatory Insultmentioning

confidence: 99%

Painful Neuron-Microglia Interactions in the Trigeminal Sensory System

Davies¹,

Kim²,

Oh³

2010

TOPAINJ

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Abstract:The trigeminal sensory system is unique in its innervation of structures specific to the orofacial area. Nociceptive trigeminal afferents are known to synapse with second-order neurons in the trigeminal subnucleus caudalis (Sp5C) in the brain stem. The activity of neurons within the Sp5C is responsible for the relay of nociceptive signals to higher brain centers. Recent evidence suggests that central sensitization may be fundamental to many trigeminal-specific painful neuropathies, including trigeminal neuralgia and migraine.Glia within the Sp5C are emerging as prime suspects in trigeminal central sensitization. In particular, microglial activation has been implicated in the development of neuropathic pain. It is possible that activated microglia release factors that alter the activity of second-order neurons or the synaptic activity of peripheral terminals within the Sp5C.Microglial activation has been characterized by changes in morphology, expression of membrane receptors and ion channels, as well as alterations to cytokine and chemokine release. In addition, microglia have been studied in brain slice and dissociated culture where activation is characterized by changes to P2X receptor and potassium channel membrane currents. However, little is known about resting and activated microglial membrane properties in the Sp5C and, furthermore, how these properties are affected following trigeminal nerve injury. This review summarizes the anatomical and pathophysiological importance of the Sp5C and focuses on recent studies on neurons and microglia in the trigeminal sensory system. The final part of the review aims to link important aspects of microglial membrane physiology with their potential role in chronic trigeminal pain conditions.

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“…Horizontal brainstem slices Institutional Animal Care and Use Committee of School of Dentistry, Kyungpook National University, that accepts National Institutes of Health (USA) guide for the Care and Use of Laboratory Animals, approved all the experimental procedures [8]. Male/female Sprague-Dawley rats (2-19-day-old) were deeply anesthetized by urethane (1.5 g/kg, i.p.)…”

Section: Methodsmentioning

confidence: 99%

“…Vsp comprises three subnuclei, that is, oralis (Vo), interpolais (Vi) and caudalis (Vc) in rostrocaudal direction [6], which are interconnected by excitatory and inhibitory synaptic transmission [7][8][9]. Of the intersubnuclear connections, an ascending transmission from Vc to Vo plays an important role in the orofacial nociceptive transmission in the trigeminal system [10][11][12][13][14][15].…”

Section: Introductionmentioning

confidence: 99%

N-methyl-D-aspartate-dependent long-term potentiation of excitatory transmission in trigeminal subnucleus oralis

Youn

2008

NeuroReport

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This study for the first time demonstrates early developmental changes of passive/active membrane properties, and long-term potentiation (LTP) of excitatory synaptic transmission at spinal trigeminal subnucleus caudalis (Vc)-to-oralis (Vo) synapses. During postnatal development, the probability of Vo neurons with monosynaptic excitatory postsynaptic currents (EPSCs) upon Vc stimulation significantly increased, whereas the input resistances of Vo neurons and the latencies of monosynaptic EPSCs significantly decreased. Application of a 'pairing' protocol that comprises 2 Hz-conditioning stimulation of Vc with postsynaptic depolarization of Vo neuron to +30 mV generated LTP of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor-mediated monosynaptic EPSC amplitude in more than 70% of Vo neurons. The induction of LTP required the activation of N-methyl-D-aspartate receptor, but its magnitudes had correlation neither with postnatal ages nor with baseline EPSC amplitudes.

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Pharmacological analysis of excitatory and inhibitory synaptic transmission in horizontal brainstem slices preserving three subnuclei of spinal trigeminal nucleus

Cited by 30 publications

References 60 publications

Physiological temperatures drive glutamate release onto trigeminal superficial dorsal horn neurons

Physiological temperatures drive glutamate release onto trigeminal superficial dorsal horn neurons

Painful Neuron-Microglia Interactions in the Trigeminal Sensory System

N-methyl-D-aspartate-dependent long-term potentiation of excitatory transmission in trigeminal subnucleus oralis

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