TITLE:
5-HTr Expression in Primary Trigeminal Neuron Following Injury
AUTHORS:
Ombretta Mameli, Antonella Russo, Stefania Stanzani, Giovanni Tringali, Elio Insirello, Marcello Alessandro Caria, Pier Luigi De Riu
KEYWORDS:
Sensory Neurons Plasticity; Trigeminal Ganglia Neurons; Axotomy; Pre-Synaptic Deafferentation; 5-HT Receptors
JOURNAL NAME:
Journal of Behavioral and Brain Science,
Vol.2 No.4,
November
30,
2012
ABSTRACT: Trigeminal ganglia neurons significantly affect the amplitude and type of 5-HT receptor gene expression following activation of their axon terminals and sensitisation by painful stimuli. Moreover, these neurons significantly alter gene expression in cytoskeletal proteins following injury. The aim of the present study was to determine whether peripheral and/or central deafferenting lesions affect gene expression in serotonergic receptors that are involved in pain transmission. Adult rats were subjected to unilateral ablation of the facial sensory and motor cortices. Fifteen days after the surgery, degeneration of the cortico-trigeminal pathway was observed. Presynaptic deafferentation of the primary trigeminal neurons and central afferents of the contralateral ganglia was conducted. As a consequence of the excision of the meninges covering the ablated cortices, the peripheral axotomy of the trigeminal-vascular primary neurons of the ipsi-lateral side was induced. Serotonergic receptor (5-HT5A/5B/1B/1D/1F) gene expression was analysed in both sides of the trigeminal ganglia neurons. The results of the present study showed a significant increase in 5-HT5A/5B/1B/1D receptor gene expression in the primary sensory neurons of both ganglia, with the highest levels of expression noted in the ganglia contralateral to the lesion. 5-HT1F receptor expression, however, was more strongly expressed in the ganglia ipsilateral to the lesion. Our results also confirm that the adaptive response of primary trigeminal neurons to injury involves anatomical remodelling, as well as changes in receptor gene expression involved in sensory transmission. This may explain the distortion of sensory signals observed in trigeminal neuropathic states, and may lead to the development of novel pharmacological interventions.