ABSTRACT
Group I metabotropic glutamate receptors (mGluR1 and 5) have been implicated in long-term potentiation (LTP), a persistent increase of synaptic efficiency, in the central nervous system including the spinal trigeminal nucleus (Vsp). In the ascending pathway from the caudalis (Vc) to the oralis (Vo) subnuclus in Vsp, it has been shown that the activation of group I mGluRs (mGluR1 and 5) with their agonist (S)-3,5-dihydroxyphenylglycine (DHPG) produces a delayed type of LTP of excitatory synaptic transmission and this LTP was mediated by mGluR1. Further, this study attempts to pharmacologically characterize essential signaling components for the expression of DHPG-induced LTP. As a result, it is found that the group I mGluRs essentially use G protein-mediated activation of the phospholipase C (PLC) pathway to express the LTP. However, recruited signaling molecules following the activation of PLC are differentially involved in the expression of LTP: i.e. IP3 receptor, intracellular Ca(2+) rise, CaMKII and ERK function as positive regulators, whereas PKC as a negative regulator. Furthermore, both L-type voltage-dependent Ca(2+) channel and canonical transient receptor potential channel positively contribute to the expression of LTP. Taken together, these results suggest that signaling molecules recruited by the activation of group I mGluRs collaboratively or oppositely control the optimal expression of synaptic plasticity at excitatory synapses in the Vo.
Subject(s)
Long-Term Potentiation , Receptor, Metabotropic Glutamate 5/metabolism , Receptors, Metabotropic Glutamate/metabolism , Signal Transduction , Trigeminal Nucleus, Spinal/metabolism , Animals , Calcium Signaling , Excitatory Amino Acid Agonists/pharmacology , Excitatory Postsynaptic Potentials , Female , Glycine/analogs & derivatives , Glycine/pharmacology , Intracellular Signaling Peptides and Proteins/metabolism , Male , Rats , Rats, Sprague-Dawley , Receptor, Metabotropic Glutamate 5/agonists , Receptors, Metabotropic Glutamate/agonists , Resorcinols/pharmacologyABSTRACT
To analyze the synaptic characteristics of axon terminals originated from the tooth pulp in the trigeminal nucleus oralis, labeling of tooth pulp afferents with wheat-germ agglutinin conjugated horseradish peroxidase and morphometric analysis with electron microscopic photographs were performed. The results obtained from 23 labeled endings were as follows. All of the labeled boutons contained clear and round synaptic vesicles (dia. 45~55 nm). 3 (13.64%) out of 23 labeled endings have 20~105 dense cored vesicles and do not make synaptic contacts with p-endings. But remaining 20 labeled endings (86.36%) almost do not have dense cored vesicles and 12 of them make synaptic contacts with p-endings. The mean number of synaptic contacts was 2.61+/-2.06 and the postsynaptic profiles were usually middle or distal dendrite and dendritic spine (1.74+/-1.36) rather than soma or proximal dendrite. The mean number of synaptic contacts with pendings was 0.87+/-1.01. And the frequency of the synaptic triads were 0.39+/-0.58. The vesicle density was 993.23+/-267.41/mum(2). The volume of labeled bouton was 3.54+/-2.20 mum(3) and highly correlated (P < 0.01) with surface area (11.78+/-4.92 mum(2), r = 0.95), total apposed surface area (2.90+/-1.56 mum(2), r=0.72), total active zone area (0.61+/-0.37 mum(2), r = 0.82), mitochondrial volume (0.75+/-0.53 mum(3), r = 0.94), the number of synaptic vesicles (2621.30+/-1473.61, r= 0.91) and the number of synaptic contacts (r = 0.76). These results suggest that there are two groups of tooth pulp afferent terminals according to the presence of dense cored vesicles in the trigeminal nucleus oralis. And the sensory processing mechanism of each groups may be different. And the "size principle" of Pierce & Mendell (1993) is also applicable to these terminals.
