Axon and ganglion cell injury in rabbits after percutaneous trigeminal balloon compression.

New Zealand white rabbits were used to determine whether the changes in the Vth cranial nerve sensory root after compression were associated with the loss of a specific subclass of Vth cranial nerve ganglion cells, the disappearance of a distinct subset of primary afferent terminals in Vth cranial nerve nucleus caudalis, and/or injury to a specific axonal fiber type. There was no significant difference in the size of surviving ganglion cells after Vth cranial nerve compression, as measured 2 to 3 months after injury (P > 0.5, n = 4).

Patterning of local intracortical projections within the vibrissae representation of rat primary somatosensory cortex.

Anterograde and retrograde tracing with biotinylated dextran amine and Phaseolus vulgaris leukoagglutinin was used to assess projection patterns within the vibrissae representation of the rat's primary somatosensory cortex (S-I). Large and small injections of either tracer into the center of the vibrissae representation yielded dense anterograde and retrograde labelling throughout much of the tangential extent of the vibrissae representation within S-I. In all layers, the pattern and extent of retrograde and anterograde label was in rough congruence.

Long-term age-related consequences of forelimb damage upon expression of primary afferent phenotypes in the cervical dorsal horn.

Rats that sustained forelimb removal on either embryonic day 16 (E-16) or the day of birth (P-0), or transection of the brachial plexus in adulthood, had sections through the cervical dorsal horn stained for galanin, calcitonin gene-related peptide (CGRP), or the plant lectin Bandieria simplicifolia-I (BS-I) 35-50 days after these lesions. The results of these experiments demonstrated age-related differences in the effects of peripheral nerve damage upon the distributions of each of these three primary afferent markers in the dorsal horn. Damage to the brachial plexus in adulthood caused a significant increase in the density of galanin immunoreactivity in the medial portion of layers I and II and the appearance of galanin immunoreactivity in layers III and IV of the cervical dorsal horn.

Evidence for survival of the central arbors of trigeminal primary afferents after peripheral neonatal axotomy: experiments with galanin immunocytochemistry and Di-I labelling.

Studies employing axoplasmic transport techniques have suggested that the central arbors of vibrissae-related primary afferents are rapidly and permanently lost from the trigeminal (V) brainstem complex after transection of the intraorbital nerve (ION). The present study reexamined this issue using immunocytochemistry for galanin (GAL) and anterograde labelling with Di-I to evaluate V brainstem organization in rats that sustained damage to the ION or individual vibrissae follicles in infancy or adulthood. After adult nerve damage, GAL-positive fibers are increased in layers I and II of V subnucleus caudalis (SpC).

Lesion-induced changes in the central terminal distribution of galanin-immunoreactive axons in the dorsal column nuclei.

Rats that sustained forelimb removal on either embryonic day (E) 16, on the day of birth (P-0), or transection of the brachial plexus in adulthood had brainstem sections stained for galanin, calcitonin gene-related peptide (CGRP), or substance P (SP) at various intervals after these lesions were made. In normal adult rats, only a few galanin-immunoreactive fibers are present in the cuneate nucleus and most are located in its caudal portion. CGRP-positive axons are also sparse in the cuneate and are distributed mainly in the periphery of the nucleus.