Disease relevance of Trigeminal Nuclei

• Serotonin inhibits trigeminal nucleus activity evoked by craniovascular stimulation through a 5HT1B/1D receptor: a central action in migraine [1]?
• However, we could not detect KCC2 messenger RNA expression in the dorsal root ganglion and mesencephalic trigeminal nucleus, where primary sensory neurons show depolarizing responses to GABA, suggesting that the absence of KCC2 is necessary for this phenomenon [2].
• The reduction of the expression of Fos-like immunoreactivity by exogenous morphine speaks in favour of an opioidergic link in the modulation of orofacial pain in the trigeminal nuclei [3].
• We attribute the resolution of orofacial dyskinesias with a cervical lesion to the interconnections between the orofacial area and cervical spine via the trigeminal nucleus (which has fibers descending as far caudally as C6), as well as to resetting of cortical maps [4].

High impact information on Trigeminal Nuclei

• Opiate analgesics inhibit substance P release from rat trigeminal nucleus [5].
• In a transgenic mouse line (Tg8) deficient for the gene encoding monoamine oxidase A (MAOA), we show that the primary somatosensory cortex (S1) lacks the characteristic barrel-like clustering of layer IV neurons, whereas normal pattern formation exists in the thalamus and the trigeminal nuclei [6].
• The 5-HT(1B/1D) agonist, naratriptan, was microinjected into the ventrolateral periaqueductal gray (vlPAG), and activity in the trigeminal nucleus caudalis (TNC) was monitored [7].
• A vibrissa-related pattern began to emerge in trigeminal nucleus principalis and subnucleus interpolaris (Spl) by embryonic day (E-) 19 and appeared fully developed by the day of birth (P-0) [8].
• Anterograde tracing studies reveal that the rod domain in VPM is innervated by fibers arising in the contra- and ipsilateral principal trigeminal nucleus, while the matrix domain (and calbindin-positive domains in adjacent nuclei) are innervated by fibers arising in the caudal nucleus of the spinal trigeminal complex [9].

Chemical compound and disease context of Trigeminal Nuclei

• Effect of a serotonin agonist (sumatriptan) on the peptidergic innervation of the rat cerebral dura mater and on the expression of c-fos in the caudal trigeminal nucleus in an experimental migraine model [10].
• Migraine pain-relay centers, including the trigeminal ganglion, trigeminal nucleus caudalis, and thalamus, contain glutamate-positive neurons, and glutamate activates the trigeminal nucleus caudalis [11].

Biological context of Trigeminal Nuclei

• As little information is available on the chemistry of synaptic transmission in trigeminal brain stem nuclei, an iontophoretic study was done on the effects of glutamate and substance P on single neurons in trigeminal nuclei oralis and caudalis in cats anesthetized with chloralose and paralyzed [12].
• To better understand estrogens modulation on pain processes, we examined changes in 5-HT and CGRP innervations of trigeminal nucleus caudalis (TNC) in ArKO, ArKO-E2 and WT groups sacrificed during the interphase [13].
• We conclude that there are sex-related differences in the ORL(1)-receptor gene expression in the trigeminal nucleus caudalis, which appear to be determined in part by estrogen levels [14].
• Nociceptive stimulation induces glutamate receptor down-regulation in the trigeminal nucleus [15].
• Substance P and neurokinin A variations throughout the rat estrous cycle; comparison with ovariectomized and male rats: II. Trigeminal nucleus and cervical spinal cord [16].

Anatomical context of Trigeminal Nuclei

• Electrical stimulation evoked significant increases in the (median) numbers of Fos-positive cells in laminae I and IIo of the superficial dorsal horn of C1, C2 and C3 cervical spinal cord (88, 92 and 18 cells, respectively) and of the trigeminal nucleus caudalis (TNC) (81 cells) [17].
• Whole-cell patch-clamp recordings were made from neurons in the trigeminal nucleus caudalis and trigeminal ganglion, in vitro, to investigate the cellular actions of the endogenous cannabinoid, anandamide [18].
• C-fos, an indicator of neuronal activation, was assessed within the trigeminal nucleus caudalis (TNC), area postrema. lateral reticular and solitary tract nuclei 2 h after intracisternal injection of capsaicin [19].
• Inhibition of nociceptive dural input in the trigeminal nucleus caudalis by somatostatin receptor blockade in the posterior hypothalamus [20].
• Vagus nerve stimulation in awake rats reduces formalin-induced nociceptive behaviour and fos-immunoreactivity in trigeminal nucleus caudalis [21].

Associations of Trigeminal Nuclei with chemical compounds

• Studies in the preceding paper demonstrated that the amplitude of the masseteric reflex in behaving cats is augmented by pharmacological manipulations that increase norepinephrine (NE) tone in the motor trigeminal nucleus (MoV) through exogenous means [22].
• Stimulation of the SSS results in Fos expression in the superfical laminae of the trigeminal nucleus caudalis and in the dorsal horn of C1 and C2 [23].
• The effects of intraperitoneal injected lipopolysaccharides (LPS) on behavior and c-fos expression in the trigeminal nucleus caudalis layer I, II (TNC I,II) elicited by intracisternally applied capsaicin were studied [24].
• Glutamate activation of neurons within trigeminal nucleus caudalis increases adrenocorticotropin in the cat [25].
• 1. In cats anaesthetized with urethane, extracellular micro-electrode recordings were made in the marginal layer of the trigeminal nucleus caudalis between the level of the obex and the Cl rootlets [26].

Gene context of Trigeminal Nuclei

• This E-cadherin expressing area of the spinal cord extended to part of the trigeminal nucleus in the medulla [27].
• Motor nuclei, including oculomotor, facial, and trigeminal nuclei, were also endothelin-converting enzyme-immunoreactive [28].
• Peripheral innervation patterns of proprioceptive afferents from dorsal root ganglia and the mesencephalic trigeminal nucleus were assessed in trkC-deficient mice using immunohistochemistry for protein gene product 9.5 and parvalbumin [29].
• Expression of pituitary adenylate cyclase-activating polypeptide (PACAP) in the mesencephalic trigeminal nucleus of the rat after transsection of the masseteric nerve [30].
• Addicsin transcripts were also extremely abundant in trigeminal neurons such as the principal trigeminal nucleus, mesencephalic trigeminal nucleus and motor trigeminal nucleus [31].

Analytical, diagnostic and therapeutic context of Trigeminal Nuclei

• 2. Bradykinin microinjections in different sites surrounding the Pa5 compromising the external cuneate nucleus, the trigeminal nucleus, the lateral and ventral spinal trigeminal tract and the dorsal trigeminal tract rostral and caudal to the Pa5 did not elicit significant pressor responses [32].
• In rabbits and rats under urethane anesthesia, a systematic survey was made of the caudal trigeminal nucleus, using glass coated tungsten microelectrodes [33].
• In this study, we describe the light microscopic distribution of CGRP immunoreactivity (IR) within the feline trigeminal ganglion and trigeminal nucleus of normal adult subjects and in subjects 10 and 30 days following complete retrogasserian rhizotomy [34].
• Rhodamine-labeled microspheres were injected into the motor trigeminal nucleus and True Blue was deposited into lumbar segments of the spinal cord [35].
• In addition, an intravenous injection of chlorpromazine (8 mg/kg) was found to increase the amplitude of monosynaptic masseteric reflex EMG activity evoked by stimulations of the mesencephalic trigeminal nucleus [36].

References