Ultrastructural and immunocytochemical characterization of primary afferent terminals in the rat cuneate nucleus

Abstract

The cuneate nucleus is a relay center for somatosensory information by receiving tactile and proprioceptive inputs from primary afferent fibers that ascend in the dorsal funiculus. The morphology, synaptic contacts, and neurochemical content of primary afferent terminals in the cuneate nucleus of rats were investigated by combining anterograde transport of horseradish peroxidase conjugated to wheat-germ agglutinin or to cholera toxin (injected in cervical dorsal root ganglia) with postembedding immunogold labeling for glutamate and GABA. Both tracers gave similar results. Two types of terminals were labeled: type I terminals were irregularly shaped, had a mean area of 4.0 microns 2, synapsed on several dendrites, and were contacted by other terminals, some of which were GABA positive. Type II terminals were dome-shaped, had a mean area of 2.18 microns 2, and made synaptic contact on a single dendrite. All the anterogradely labeled terminals (interpreted as endings of primary afferents) were enriched in glutamate but not in GABA. The finding that identified primary afferent terminals are enriched in glutamate with respect to other tissue profiles strongly suggests a neurotransmitter role for glutamate in this afferent pathway to the rat cuneate nucleus.

Chemotropic guidance facilitates axonal regeneration and synapse formation after spinal cord injury

“…Boutons in regenerated CTB-labeled axon terminals contained round rather than flattened synaptic vesicles, further suggesting an excitatory neurotransmitter phenotype 19. Four of the six regenerating axon terminals studied made synaptic contacts with multiple dendritic targets, a common feature for primary afferent projections to the gracile nucleus in intact rats 20, 21 (see below); the remaining two terminals made synaptic contact with single dendritic targets. Finally, CTB-containing regenerating axon terminals made synaptic contacts with dendritic rather than somal elements, a feature typical of the pre-injury ultrastructural phenotype20-22.…”

Primary afferent terminals that express presynaptic NR1 in rats are mainly from myelinated, mechanosensitive fibers

“…Presynaptic NMDA receptors in terminals of ascending dorsal column fibers are reported for the first time; they might colocalize with presynaptic kainate receptors, also present in the majority of primary afferent terminals to the gracile nucleus (Hwang et al, 2001b). because these terminals, like primary afferents to the dorsal horn, release glutamate (De Biasi et al, 1994), PIGRs in this nucleus are likely to function as autoreceptors. The common occurence of NR1 and other PIGRs in primary afferent terminals and their absence at another level of the somatosensory pathway, i.e., in the ventroposterior nucleus of the thalamus, as demonstrated here and by Hwang et al (2001b), suggest a special relation between PIGRs and terminals that undergo primary afferent depolarization (Lee et al, 2002).…”

Cuneothalamic relay neurons are postsynaptic to glycine-immunoreactive terminals in the rat cuneate nucleus

“…The occurrence of an axoaxonic synapse has been reported in previous studies (Clements et al, 1990;Fagg and Foster, 1983;Ljungdahl and Hökfelt, 1973;Lue et al, 1997c;Popratiloff et al, 1996;Todd et al, 1991). On the basis of its ultrastructural features described previously (De Biasi et al, 1994;Ellis and Rustioni, 1981;Lue et al, 1993Lue et al, , 1996Lue et al, , 1997a, it is suggested that the unlabelled terminal that is postsynaptic to the glycine-IR terminal, is derived from the primary afferents. Although, it has been reported in pharmacological studies that glycine depolarized the dorsal funiculus in slice preparation of the cuneate nucleus (Simmonds, 1978(Simmonds, , 1983, the application of strychnine, an antagonist of glycine, failed to suppress the presynaptic inhibition (Hill et al, 1976).…”