Abstract:Heme oxygenase (HO)/carbon monoxide (CO) and nitric oxide synthase (NOS)/nitric oxide (NO) systems are involved in sensory information processing. The present study was undertaken to examine the distribution of HO-2 and NOS in the spinal trigeminal nucleus (STN) of the rat, using histochemistry and immunohistochemistry. Nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) staining was found that NADPH-d activity was more prominent in the nucleus caudalis (Vc) and the dorsomedial subdivision of the … Show more
“…In the present study, we described the distribution of NADPH-d without determining which isoforms of NOS were involved. Our results agree with those from other studies (Kolesár et al, 2006; Fan et al, 2008, 2009a). It should also be noted that most of the Vc neurons involved in orofacial nociception do not synthesize NO under normal conditions, but are modulated by NO, which diffuses from adjacent NOS-positive neurons (Yeo, 2002).…”
Melatonin and nitric oxide (NO) are involved in orofacial signal processing in the trigeminal sensory system. The aim of the present study was to examine the distribution of melatonin 1a-receptor (MT1) and its colocalization with nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) in the spinal trigeminal nucleus (STN), the trigeminal ganglion (TG), and the mesencephalic trigeminal nucleus (MTN) in the rat, using histochemistry and immunohistochemistry. Our results show that MT1-positive neurons are widely distributed in the TG and the subnucleus caudalis of the STN. Furthermore, we found that MT1 colocalizes with NADPH-d throughout the TG and MTN, most extensively in the TG. The distribution pattern of MT1 and its colocalization with NADPH-d indicate that melatonin might play an important role in the trigeminal sensory system, which could be responsible for the regulation of NO levels.
“…In the present study, we described the distribution of NADPH-d without determining which isoforms of NOS were involved. Our results agree with those from other studies (Kolesár et al, 2006; Fan et al, 2008, 2009a). It should also be noted that most of the Vc neurons involved in orofacial nociception do not synthesize NO under normal conditions, but are modulated by NO, which diffuses from adjacent NOS-positive neurons (Yeo, 2002).…”
Melatonin and nitric oxide (NO) are involved in orofacial signal processing in the trigeminal sensory system. The aim of the present study was to examine the distribution of melatonin 1a-receptor (MT1) and its colocalization with nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) in the spinal trigeminal nucleus (STN), the trigeminal ganglion (TG), and the mesencephalic trigeminal nucleus (MTN) in the rat, using histochemistry and immunohistochemistry. Our results show that MT1-positive neurons are widely distributed in the TG and the subnucleus caudalis of the STN. Furthermore, we found that MT1 colocalizes with NADPH-d throughout the TG and MTN, most extensively in the TG. The distribution pattern of MT1 and its colocalization with NADPH-d indicate that melatonin might play an important role in the trigeminal sensory system, which could be responsible for the regulation of NO levels.
“…The different degrees of intensity of OD, observed in this study with both techniques, could be considered as a relative parameter of the expression or activity of the enzyme NOS in neurons, as was previously considered by other authors (Kolesár et al,2006; Fan et al,2009). The values of OD were obtained according to the formula: OD = log (256/mean gray), and data were collected in an Excel (Microsoft) spreadsheet.…”
Sensory information on facial structures, including teeth pulp, periodontium, and gingiva, is relayed in the trigeminal complex. Tooth pulp inflammation constitutes a common clinical problem, and this peripheral injury can induce neuroplastic changes in trigeminal nociceptive neurons. There is considerable evidence that the trigeminal subnucleus caudalis (Vc) is the principal relay for trigeminal nociceptive information as well as modulation of the painful stimuli. Glutamatergic primary afferents innervating the tooth pulp project to the most superficial laminae of the Vc. N-methyl-D-aspartate receptor stimulation leads to the activation of the enzyme nitric oxide synthase (NOS), which synthesizes the free radical nitric oxide (NO). This enzyme is expressed mainly in lamina II interneurons, and in a small number of cells in lamina I as well as in deep laminae projection neurons of Vc. In the present study, we analyzed the temporal changes in neuronal NOS (nNOS) in Vc local circuitries after unilateral intermediate molar pulp injury. Our results demonstrate that a peripheral dental pulp injury leads to neuroplastic changes in the relative amount and activity of nNOS enzyme. Moreover, after a period of time, the nitrergic system shifts to the initial values, independently of the persistence of inflammation in the pulp tissues.
“…Nitric oxide (NO) is also an endogenously produced gas that can act as a second messenger molecules, which is synthesized from L‐arginine via NO synthase (NOS). The colocalization of HO‐2 and NOS has been observed in the PNS (Hedlund et al,1997; Ho et al,1999; Battish et al,2000; Fan et al,2008) and some neurons in CNS (Vincent et al,1994; Snyder et al,1998; Fan et al,2009). This suggests that the products of the two enzymes, NO and CO, might act as cotransmitters in neuronal signaling transmission.…”
Section: Carbon Monoxide and Nitric Oxidementioning
confidence: 98%
“…HO‐2 is expressed abundantly in neuronal populations in spinal cord, midbrain, basal ganglia, thalamic regions, and brainstem (Vincent et al,1994; Dwyer et al,1995; Mancuso,2004; Fan et al,2008,2009), the activity of which is commonly considered when assessing neuronal activity of CO. Moreover, some investigators examine HO‐2 expression in the peripheral nervous system (PNS) of the guinea pig (Vollerthun et al,1996), the rat (Fan et al,2008), and man (Uddman et al,2004) and find numerous HO‐2‐immunoreactive cell bodies in the sensory ganglia, including trigeminal, cervical, and lumbar dorsal root ganglia.…”
Section: Biosynthesis and Heme Oxygenase Localization In The Nervous mentioning
Carbon monoxide (CO) has been recognized to act as an atypical neurotransmitter or neuromodulator in the nervous system and to be involved in a wide variety of neuronal activities. Several lines of evidence suggest that CO may play a role through multiple mechanisms in nociception processing. Differential regulation of a family of CO-generating enzymes, heme oxygenase (HO), contributes mainly to the complexity underlying the role of CO in nociception. This Mini-Review describes the latest evidence for the role of CO during normal sensory transmission and pathological pain conditions and discusses potential cellular mechanisms by which CO is involved in pathological pain.
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