IADR Abstract Archives
GABAergic interneurons in the trigeminal subnucleus caudalis after unilateral tooth pulp injury.
Keywords: GABA, trigeminal, nociception
Glutamate and GABA are respectively excitatory and inhibitory neurotransmitters in the central nervous system. Moreover, glutamate is the substrate of the enzyme glutamate decarboxylase (GAD) for GABA synthesis. Primary afferent neurons innervating the tooth pulp terminate on projection neurons in the most superficial laminae of the trigeminal subnucleus caudalis (Vc). These neurons transmit nociceptive messages to brainstem and/or thalamus as well as local interneurons. NMDA receptor activation increases intracellular Ca2+ which it is known to play a key role in CNS neuroplasticity. Our laboratory have studied the role of neurons immunoreactive (IR) for calbindin and calretinin, both calcium buffers proteins that act regulating intracellular calcium homeostasis and nitrergic neurons (Canzobre et al. SAIO 2006 and 2009). In this study we analyze GABAergic interneurons that through pre- and post-synaptic inhibition, or acting over other interneurons of Vc, modulate primary afferents of the nociceptive trigeminal pathway. Objetives: evaluate changes in the expression of GAD-6 and examining the relationship between IR GAD-6 synaptic terminals, and other neuronal subtypes in the Vc, after unilateral tooth pulp injury. Materials: In adult female Wistar rats were exposed the mesial pulp chamber of the left mandibular first molar. We have examined the distribution of GAD-6 at different levels of the ipsi and contralateral Vc, in each animal group, by immunofluorescent double-staining and NADPH histochemistry. Results: Our results provide morphological evidence that the GAD-6 axon terminals establish a crown-like synaptic network over local neurons of the Vc. On the other hand, we observed an increase in GABAergic axonal plexus in the superficial laminae of the ipsilateral nucleus after the 4th postoperative day. Conclusions: This study shows us that GABAergic neurons could be activated during tooth pulp inflammation and establishment of nociceptive stimuli, suggesting a control of painful afferent stimuli in the Vc. Grant: UBACyT O 014
Glutamate and GABA are respectively excitatory and inhibitory neurotransmitters in the central nervous system. Moreover, glutamate is the substrate of the enzyme glutamate decarboxylase (GAD) for GABA synthesis. Primary afferent neurons innervating the tooth pulp terminate on projection neurons in the most superficial laminae of the trigeminal subnucleus caudalis (Vc). These neurons transmit nociceptive messages to brainstem and/or thalamus as well as local interneurons. NMDA receptor activation increases intracellular Ca2+ which it is known to play a key role in CNS neuroplasticity. Our laboratory have studied the role of neurons immunoreactive (IR) for calbindin and calretinin, both calcium buffers proteins that act regulating intracellular calcium homeostasis and nitrergic neurons (Canzobre et al. SAIO 2006 and 2009). In this study we analyze GABAergic interneurons that through pre- and post-synaptic inhibition, or acting over other interneurons of Vc, modulate primary afferents of the nociceptive trigeminal pathway. Objetives: evaluate changes in the expression of GAD-6 and examining the relationship between IR GAD-6 synaptic terminals, and other neuronal subtypes in the Vc, after unilateral tooth pulp injury. Materials: In adult female Wistar rats were exposed the mesial pulp chamber of the left mandibular first molar. We have examined the distribution of GAD-6 at different levels of the ipsi and contralateral Vc, in each animal group, by immunofluorescent double-staining and NADPH histochemistry. Results: Our results provide morphological evidence that the GAD-6 axon terminals establish a crown-like synaptic network over local neurons of the Vc. On the other hand, we observed an increase in GABAergic axonal plexus in the superficial laminae of the ipsilateral nucleus after the 4th postoperative day. Conclusions: This study shows us that GABAergic neurons could be activated during tooth pulp inflammation and establishment of nociceptive stimuli, suggesting a control of painful afferent stimuli in the Vc. Grant: UBACyT O 014