Spinal lamina I neurons that express neurokinin 1 receptors: morphological analysis

Cheunsuang, Ornsiri; Morris, Richard

doi:10.1016/s0306-4522(00)00035-x

Cited by 53 publications

(60 citation statements)

References 36 publications

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“…In recent studies in spinal cord slices, Cheunsuang and Morris (2000) and Cheunsuang et al (2002) classified NK1r-immunoreactive lamina I cells in rats into two main morphological classes, small fusiform neurons and large multipolar neurons, which may be consistent with the finding presented here. Detailed analysis of the large multipolar types was not presented, unfortunately, precluding further comparison with the present study.…”

Section: Relationship Between Morphology and Phenotypesupporting

confidence: 90%

Morphology and neurokinin 1 receptor expression of spinothalamic lamina I neurons in the rat spinal cord

Silva

Koninck

2005

J of Comparative Neurology

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Distinct morphological types of spinothalamic tract (STT) lamina I (LI) neurons have been identified in the cat and monkey spinal dorsal horn. Because these morphological types appear to differ in functional properties and receptor expression, we examined their distribution in the rat to test how their identification relates to earlier classification schemes. LI STT cells were retrogradely labeled with cholera toxin subunit b (CTb). Three types were recognized on the basis of cell body shape and proximal dendrites in the horizontal plane: fusiform, multipolar, and pyramidal. The relative distribution of these types was: 43, 26, and 28%, respectively, similar to that observed in the cat and monkey. 3D reconstructions were used to view each cell in all three major projection planes: horizontal, parasagittal, and transverse. Most LI STT neurons appeared fusiform in the parasagittal plane even though they belonged to different types based on their appearance in the horizontal plane, except in the most lateral portion of the dorsal horn, where LI curves ventrally. The proportion of STT neurons within LI was quantified by using the optical dissector method. To label all LI neurons, we used an anti-neuron-specific nuclear protein (NeuN) antibody. We found that approximately 9% of LI neurons projected to the thalamus. We also investigated neurokinin 1 receptor (NK-1r) expression in LI STT neurons. As in the monkey, most pyramidal STT neurons did not express NK-1r. These results provide further evidence that distinct morphological types of neurons differ in phenotype but not in their projection pattern.

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Section: Relationship Between Morphology and Phenotypesupporting

confidence: 90%

Morphology and neurokinin 1 receptor expression of spinothalamic lamina I neurons in the rat spinal cord

Silva

Koninck

2005

J of Comparative Neurology

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“…Given that most lamina I projection neurons (5% of all lamina I neurons) that express NK1 receptor do so at moderate to strong levels (Spike et al, 2003) we are more apt to be targeting this projection neuron population rather than the population of weakly NK1 receptor immunoreactive neurons (Cheunsuang and Morris, 2000) that are likely to be interneurons (Todd et al, 2005).…”

Section: Resultsmentioning

confidence: 99%

Disinhibition Opens the Gate to Pathological Pain Signaling in Superficial Neurokinin 1 Receptor-Expressing Neurons in Rat Spinal Cord

2006

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Blockade of local spinal cord inhibition mimics the behavioral hypersensitivity that manifests in chronic pain states. This suggests that there is a pathway capable of mediating allodynia/hyperalgesia that exists but is normally under strong inhibitory control. Lamina I and III neurokinin 1 (NK1) receptor expressing (NK1Rϩ) dorsal horn neurons, many of which are projection neurons, are required for the development of this hypersensitivity and are therefore likely to be a component of this proposed pathway. To investigate, whole-cell patch-clamp recordings were made from lamina I and III NK1Rϩ neurons in the spinal cord slice preparation with attached dorsal root. Excitatory postsynaptic currents were recorded in response to electrical stimulation of the dorsal root. Lamina I NK1Rϩ neurons were shown to receive high-threshold (A␦/C fiber) monosynaptic input, whereas lamina III NK1Rϩ neurons received low-threshold (A␤ fiber) monosynaptic input. In contrast, lamina I neurons lacking NK1 receptor (NK1RϪ) received polysynaptic A fiber input. Blockade of local GABAergic and glycinergic inhibition with bicuculline (10 M) and strychnine (300 nM), respectively, revealed significant A fiber input to lamina I NK1Rϩ neurons that was predominantly A␤ fiber mediated. This novel A fiber input was polysynaptic in nature and required NMDA receptor activity to be functional. In lamina I NK1RϪ and lamina III NK1Rϩ neurons, disinhibition enhanced control-evoked responses, and this was also NMDA receptor dependent. These disinhibition-induced changes, in particular the novel polysynaptic low-threshold input onto lamina I NK1Rϩ neurons, may be an underlying component of the hypersensitivity present in chronic pain states.

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“…Axons and dendrites showed classical features (19) and were discriminated as follows. Dendrites arose from the neuron soma and tapered gradually; they branched typically into two, and these second-order dendrites were reduced in diameter.…”

Section: Methodsmentioning

confidence: 99%

Orexin A Preferentially Excites Glucose-Sensitive Neurons in the Lateral Hypothalamus of the Rat In Vitro

Liu

Morris²,

Spiller³

et al. 2001

Diabetes

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Falls in blood glucose induce hunger and initiate feeding. The lateral hypothalamic area (LHA) contains glucose-sensitive neurons (GSNs) and orexin neurons, both of which are stimulated by falling blood glucose and are implicated in hypoglycemia-induced feeding. We combined intracellular electrophysiological recording with fluorescein labeling of GSNs to determine their neuroanatomic and functional relationships with orexin neurons. Orexin A (1 mol/l) caused a 500% increase (P < 0.01) in spontaneous firing rate and rapid and lasting depolarization that was tetrodotoxin-resistant and thus a direct postsynaptic effect. Orexin A altered the intrinsic neuronal properties of GSNs, consistent with increased excitability. Confocal microscopy showed that GSNs were intimately related to orexin neurons: orexin-immunoreactive axons were frequently entwined around GSN dendrites, establishing close and putatively synaptic contacts. Orexin-cell axons also passed in close proximity to glucose-responsive neurons, which are inhibited by low glucose, but orexin A caused smaller depolarization than on GSNs and only a 200% increase in spontaneous firing rate (P < 0.05 vs. GSN). We conclude that GSNs are specific target neurons for orexin A and suggest that they may mediate, at least in part, the acute appetite-stimulating effect of orexin A. Orexin neurons may regulate GSNs so as to control the onset and termination of hypoglycemiainduced feeding. Diabetes 50:2431-2437, 2001 R educed availability of glucose, the brain's main metabolic fuel, causes intense hunger (1). The lateral hypothalamic area (LHA) is crucial to the hyperphagia induced by hypoglycemia and glucoprivation, as this feeding response is abolished by LHA lesions (1). The LHA neuronal systems that drive glucoprivic feeding are unknown, but promising candidates include the glucose-sensing neurons and orexin (hypocretin) neurons that are prominent in this region.Glucose-sensing neurons, which alter their firing behavior in response to changes in ambient glucose concentration, are found in the hypothalamus and in several other central nervous system regions (2). Glucose-sensitive neurons (GSNs) are inhibited by rising glucose concentrations but excited when glucose falls, whereas glucose-responsive neurons (GRNs) are stimulated as glucose rises and are inhibited by hypoglycemia (3,4). GSNs are particularly abundant in the LHA, where they account for 30 -40% of all neurons (3,5). These cells are stimulated directly by low glucose in vitro (3,6) but are also regulated indirectly in vivo, being inhibited by rising glucose levels in the hindbrain and viscera and by gastric distension (1,7). These indirect signals are presumed to be relayed to the LHA from the nucleus of the solitary tract (NTS) in the medulla, which contains glucose-sensing neurons and also receives vagal afferents from visceral glucose sensors and gastric stretch receptors (7). In view of these properties, lateral hypothalamic GSNs are assumed to participate in triggering and controlling glucoprivic feeding...

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Spinal lamina I neurons that express neurokinin 1 receptors: morphological analysis

Cited by 53 publications

References 36 publications

Morphology and neurokinin 1 receptor expression of spinothalamic lamina I neurons in the rat spinal cord

Morphology and neurokinin 1 receptor expression of spinothalamic lamina I neurons in the rat spinal cord

Disinhibition Opens the Gate to Pathological Pain Signaling in Superficial Neurokinin 1 Receptor-Expressing Neurons in Rat Spinal Cord

Orexin A Preferentially Excites Glucose-Sensitive Neurons in the Lateral Hypothalamus of the Rat In Vitro

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