Animal models of migraine and experimental techniques used to examine trigeminal sensory processing

Abstract

BackgroundMigraine is a common debilitating condition whose main attributes are severe recurrent headaches with accompanying sensitivity to light and sound, nausea and vomiting. Migraine-related pain is a major cause of its accompanying disability and can encumber almost every aspect of daily life.Main bodyAdvancements in our understanding of the neurobiology of migraine headache have come in large from basic science research utilizing small animal models of migraine-related pain. In this current review, we aim to describe several commonly utilized preclinical models of migraine. We will discuss the diverse array of methodologies for triggering and measuring migraine-related pain phenotypes and highlight briefly specific advantages and limitations therein. Finally, we will address potential future challenges/opportunities to refine existing and develop novel preclinical models of migraine that move beyond migraine-related pain and expand into alternate migraine-related phenotypes.ConclusionSeveral well validated animal models of pain relevant for headache exist, the researcher should consider the advantages and limitations of each model before selecting the most appropriate to answer the specific research question. Further, we should continually strive to refine existing and generate new animal and non-animal models that have the ability to advance our understanding of head pain as well as non-pain symptoms of primary headache disorders.

Hemokinin-1 Gene Expression Is Upregulated in Trigeminal Ganglia in an Inflammatory Orofacial Pain Model: Potential Role in Peripheral Sensitization

“…Satellite glial cells (SGC) and resident macrophages in the TG, as well as astrocytes and microglia in the central nervous system, are also activated in the process and contribute to the sensitization. There is growing evidence that the cross-talk between neurons and glial cells has a prominent modulatory role on nociceptive transmission under physiological and pathophysiological conditions [1][2][3][4][5][6].…”

Neurotransmitter and tryptophan metabolite concentration changes in the complete Freund’s adjuvant model of orofacial pain

“…Although the pathomechanism of orofacial pain and headache disorders, is not fully understood [1], the activation and sensitization of the trigeminovascular system (TS) probably takes part in the evolution of symptoms [2][3][4]. The pathomechanism of these disorders may be further investigated by using animal models with the activation of nociceptive pathways of the TS [1,3,5]. The administration of inflammation-inducing substances to the orofacial area can evoke the above-described activation/sensitization of the primary and secondary trigeminal neurons during pain processing [6,7].…”

Neurotransmitter and tryptophan metabolite concentration changes in the Complete Freund’s adjuvant model of orofacial pain

“…Although the pathomechanism of orofacial pain and headache disorders, including migraine, is not fully understood [1], the activation and sensitization of the trigeminovascular system (TS) probably takes part in the evolution of symptoms [2][3][4]. The pathomechanism of these disorders may be further investigated by using animal models with the activation of nociceptive pathways of the TS [1,3,5]. The administration of inflammation-inducing substances to the orofacial area can evoke the above-described activation/sensitization of the primary and secondary trigeminal neurons during pain processing [6,7].…”