Cells of origin of the trigeminohypothalamic tract in the rat

Malick, Amy; Burstein, Rami

doi:10.1002/(sici)1096-9861(19981012)400:1<125::aid-cne9>3.0.co;2-b

Cited by 139 publications

(87 citation statements)

References 141 publications

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“…It has been proposed that these disorders are probably caused by an abnormality in the region of the hypothalamus, with subsequent disinhibition of the trigeminal-autonomic reflex that leads to trigeminovascular and cranial autonomic activation [35]. The precise pathway is not known, although the direct hypothalamic-trigeminal connection is an attractive candidate [36].…”

Section: The Hypothalamus and The Putative Mechanisms Of Nociceptionmentioning

confidence: 85%

Functional and structural neuroimaging in trigeminal autonomic cephalalgias

Matharu

May²

2008

Current Science Inc

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The trigeminal autonomic cephalalgias (TACs) are a group of primary headache disorders characterized by unilateral trigeminal distribution pain that occurs in association with ipsilateral cranial autonomic features. They include cluster headache, paroxysmal hemicrania, and short-lasting unilateral neuralgiform headache with conjunctival injection and tearing. Until recently, primary headache disorders, including the TACs, were widely considered to be caused by peripheral mechanisms such as vascular changes or neurogenic inflammation. Developments in neuroimaging are revolutionizing our understanding of the pathophysiology of primary headache syndromes. Functional imaging studies have demonstrated hypothalamic activation in all the TACs. Furthermore, neuroimaging studies using voxel-based morphometry and magnetic resonance spectroscopy techniques have demonstrated structural and biochemical alterations, respectively, in the hypothalamus of patients with cluster headache. These studies suggest that the hypothalamus plays a crucial role in the pathophysiology of TACs, thereby supporting the notion that these disorders are primarily due to central rather than peripheral mechanisms.

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Section: The Hypothalamus and The Putative Mechanisms Of Nociceptionmentioning

confidence: 85%

Functional and structural neuroimaging in trigeminal autonomic cephalalgias

Matharu

May²

2008

Current Science Inc

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“…24 The LH also appears to be a target for some direct nociceptive inputs from the spinal and medullary dorsal horn. [25][26][27] Furthermore, nociceptive signals originated from innervation territory of the trigeminal nerve reach and the hypothalamus through both the direct trigeminohypothalamic tract and the indirect reticulohypothalamic tract. This suggests that highly prioritized painful signals are transferred in parallel channels to ensure that this critical information reaches the hypothalamus.…”

Section: Discussionmentioning

confidence: 99%

“…This suggests that highly prioritized painful signals are transferred in parallel channels to ensure that this critical information reaches the hypothalamus. 26,27 Particularly, the unilateral inflammation of the masseter, a model of orofacial deep tissue injury, induces Fos protein expression in the neurons located into the caudal ventrolateral medulla, lateral reticular nucleus, and nucleus tractus solitarius that project to the parabrachial nucleus and lateral hypothalamus. 11 The appearance of Fos-IR cells in the CEA and LH in this and other studies 11,13 may be due to the fact that these areas receive information through nociceptive pathways, such as the spino(trigemino)parabrachiohypothalamic, 9 the spinohypothalamic, 25 and the spino(trigemino)pontoamygdaloid tract.…”

Section: Discussionmentioning

confidence: 99%

Tooth Movement Activates the Central Amygdala and the Lateral Hypothalamus by the Magnitude of the Force Applied

Novaes

Rocha

Leite–Panissi

2010

The Angle Orthodontist

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Objective: To determine if the magnitude of the force used to induce incisor tooth movement promotes distinct activation in cells in the central amygdala (CEA) and lateral hypothalamus (LH) of rats. Also, the effect of morphine on Fos immunoreactivity (Fos-IR) was investigated in these nuclei. Materials and Methods: Adult male rats were anesthetized and divided into six groups: only anesthetized (control), without orthodontic appliance (OA), OA but without force, OA activated with 30g or 70g, OA with 70g in animals pretreated with morphine (2 mg/kg, intraperitoneal). Three hours after the onset of the experiment the rats were reanesthetized and perfused with 4% paraformaldehyde. The brains were removed and fixed, and sections containing CEA and LH were processed for Fos protein immunohistochemistry. Results:The results show that in the control group, the intramuscular injection of a ketamine/ xylazine mixture did not induce Fos-IR cells in the CEA or in the LH. Again, the without force group showed a little Fos-IR. However, in the 70g group the Fos-IR was the biggest observed (P Ͻ .05, Tukey) in the CEA and LH compared with the other groups. In the 30g group, the Fos-IR did not differ from the control group, the without OA group, and the without force group. Furthermore, pretreatment with morphine in the 70g group reduced Fos-IR in these regions. Conclusions: Tooth movement promotes Fos-IR in the CEA and LH according to the magnitude of the force applied. (Angle Orthod. 2010;80:111-115.)

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“…The observed defective control of trigeminal excitability therefore may be due to alterations of descending central pathways. The hypothalamus is discussed in the literature to be the main cerebral structure in terms of modulation of the trigeminovascular nociceptive system and autonomic pathways [23,24]. These observations are supported by recent structural and imaging studies that show change within the hypothalamic gray in CH patients [2,3].…”

Section: Discussionmentioning

confidence: 89%

The electrophysiology of cluster headache

Holle

Obermann²,

Katsarava

2009

Current Science Inc

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Cluster headache (CH) is a neurovascular headache disease characterized by recurrent, strictly unilateral, severe pain attacks. Despite its typical clinical features, including circadian rhythm of the attacks and ipsilateral autonomic dysfunction, the underlying pathophysiology of CH is still unclear. Electrophysiological data point to central disinhibition of the trigeminal nociceptive system as one of the key mechanisms of CH pain. Therefore, altered habituation pattern and changes within trigeminal-facial neuronal circuits due to central sensitization seem to be involved. One biochemical correlate is probably represented in dysfunctions of serotonergic raphe nuclei-hypothalamic pathways. Structural and functional imaging data show an alteration of hypothalamic structures in CH patients, supporting the hypothesis that the hypothalamus, according to its function as a circadian pacemaker, plays a pivotal role in CH pathology. Cortical and brainstem reflexes are reviewed to illuminate the pathophysiology of CH.

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Cells of origin of the trigeminohypothalamic tract in the rat

Cited by 139 publications

References 141 publications

Functional and structural neuroimaging in trigeminal autonomic cephalalgias

Functional and structural neuroimaging in trigeminal autonomic cephalalgias

Tooth Movement Activates the Central Amygdala and the Lateral Hypothalamus by the Magnitude of the Force Applied

The electrophysiology of cluster headache

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