First Report of Laurel Wilt, Caused by Raffaelea lauricola, on Sassafras (Sassafras albidum) in Alabama.

Laurel wilt, caused by Raffaelea lauricola, a fungal symbiont of the redbay ambrosia beetle, Xyleborus glabratus, is responsible for extensive mortality of native redbays (Persea borbonia and P. palustris) in the coastal plains of the southeastern United States (1). The wilt also affects the more widespread sassafras, Sassafras albidum, particularly in areas where diseased redbays are common and populations of X. glabratus are high. Because sassafras stems were thought to lack chemicals that are attractive to the beetle, and sassafras tends to be widely scattered in forests, it was believed that the advance of the laurel wilt epidemic front might slow once it reached the edge of the natural range of redbay, which is restricted to the coastal plains of the Gulf and Atlantic Coasts (2). In July and August of 2011, wilt-like symptoms (i.e., wilted and dead leaves, and streaks of black discoloration in the xylem) were observed on 1 to 10 sassafras trees (15 to 23 cm diameter; 6 to 9 m height) at each of three locations, which were approximately 6 km from one another in Marengo Co., Alabama. Samples of the discolored wood from five trees were plated on malt agar amended with cycloheximide and streptomycin (CSMA), and a fungus morphologically identical to R. lauricola was isolated from each tree (1). For confirmation, a portion of the large subunit (28S) of the rDNA region of three of the isolates was sequenced (3); in each case, the sequence matched exactly that of other isolates of R. lauricola (EU123077) from the United States. Symptomatic trees were found at all three sites when revisited in April 2012, and approximately 20 sassafras trees in various stages of wilt were observed at one location, where only one diseased tree had been noted in 2011. Bolts were cut from the main stem of a symptomatic tree, and eggs, larvae, and adults of X. glabratus were commonly found in tunnels, and R. lauricola was isolated from the discolored xylem. Three container-grown sassafras saplings (mean height 193 cm, mean diameter 2.1 cm at groundline) were inoculated as previously described (1) with conidia (~600,000) from an isolate of R. lauricola. Three additional sassafras saplings were inoculated with sterile, deionized water, and all plants were placed in a growth chamber at 25°C with a 15-h photoperiod. Inoculated plants began to exhibit wilt symptoms within 14 days, and at 30 days all inoculated plants were dead and xylem discoloration was observed. Control plants appeared healthy and did not exhibit xylem discoloration. Pieces of sapwood from 15 cm above the inoculation points were plated on CSMA, and R. lauricola was recovered from all wilted plants but not from control plants. This is the first record of laurel wilt in Alabama and is significant because the disease appears to be spreading on sassafras in an area where redbays have not been recorded (see http://www.floraofalabama.org ). The nearest previously documented case of laurel wilt is on redbay and sassafras in Jackson Co., Mississippi (4), approximately 160 km to the south. The exact source of the introduction of X. glabratus and R. lauricola into Marengo Co. is not known. The vector may have been transported into the area with storms, moved with infested firewood, or shipped with infested timber by companies that supply mills in the area. References: (1) S. Fraedrich et al. Plant Dis. 92:215, 2008. (2) J. Hanula et al. Econ. Ent. 101:1276, 2008. (3) T. Harrington et al. Mycotaxon 111:337, 2010. (4) J. Riggins et al. Plant Dis. 95:1479, 2011.

Susceptibility to Laurel Wilt and Disease Incidence in Two Rare Plant Species, Pondberry and Pondspice.

Laurel wilt, caused by Raffaelea lauricola, has been responsible for extensive losses of redbay (Persea borbonia) in South Carolina and Georgia since 2003. Symptoms of the disease have been noted in other species of the Lauraceae such as the federally endangered pondberry (Lindera melissifolia) and the threatened pondspice (Litsea aestivalis). Pondberry and pondspice seedlings were inoculated with R. lauricola from redbay, and both species proved highly susceptible to laurel wilt. Field assessments found substantial mortality of pondberry and pondspice, but in many cases the losses were not attributable to laurel wilt. R. lauricola was isolated from only 4 of 29 symptomatic pondberry plants at one site, but the fungus was not recovered from three plants at another site. R. lauricola was isolated from one of two symptomatic pondspice plants at one site, and from five of 11 plants at another site, but not from any plant at a third site. Insect bore holes, similar to those produced by Xyleborus glabratus (the vector of laurel wilt), were found in some pondberry and pondspice stems, but adults were not found. Damage caused by Xylosandrus compactus was found in pondberry stems, but this ambrosia beetle does not appear to be a vector of R. lauricola. Xyleborinus saxeseni adults were found in a dying pondspice with laurel wilt, and R. lauricola was recovered from two of three adults. Isolates of R. lauricola from pondberry, pondspice, and X. saxeseni had rDNA sequences that were identical to previously characterized isolates, and inoculation tests confirmed that they were pathogenic to redbay. Because pondberry and pondspice tend to be shrubby plants with small stem diameters, these species may not be frequently attacked by X. glabratus unless in close proximity to larger diameter redbay.

First Report of Laurel Wilt Disease Caused by Raffaelea lauricola on Camphor in Florida and Georgia.

Laurel wilt is a recently described (1) vascular disease of redbay (Persea borbonia (L.) Spreng) and other plants in the family Lauraceae. The wilt is caused by Raffaelea lauricola, a fungus vectored by the nonnative redbay ambrosia beetle (Xyleborus glabratus Eichhoff) (1,2). Since 2003, laurel wilt has caused widespread mortality of redbay in Georgia, South Carolina, and Florida (1) and has recently been found on avocado in Florida (4). Since June of 2007, wilted shoots and branch dieback have been observed in several camphor trees (Cinnamomum camphora (L.) Sieb.) in residential areas of McIntosh and Glynn counties in Georgia and Baker County in Florida. Symptomatic camphor trees ranged from 4.5 to 12 m high and occurred in areas where redbay mortality due to laurel wilt has been frequently observed during the last 2 to 3 years. In some camphor trees, only the smaller branches (<2 cm in diameter) were wilting or dead, whereas in other trees (e.g., Baker County, Florida), the larger branches and substantial portions of the crown were also symptomatic. Rapid wilt that affects entire trees that is usually observed in redbay, has not been observed in camphor. Some camphor trees in residential areas of Jekyll Island, Georgia (Glynn County), where extensive wilt of redbay has occurred, have exhibited only localized wilt of some shoots or branches and other camphors remain asymptomatic. Removal of bark from wilted branch sections revealed black-to-brownish staining in the sapwood, characteristic of laurel wilt. Although no evidence of ambrosia beetles was observed on these samples, more extensive surveys are needed to determine the role of this vector in laurel wilt of camphor. Wood chips from symptomatic areas of branches were surface sterilized and plated on cycloheximide-streptomycin malt agar as previously described (1,4) and R. lauricola was routinely isolated. Small subunit (18S) sequences from rDNA were amplified by PCR and sequenced using primers NS1 and NS4 (3). BLASTn searches revealed homology to R. lauricola C2203 (GenBank Accession No. EU123076, 100% similarity, e-value of 0.0, and a total score of 1,886). The small subunit rDNA sequence for this isolate has been deposited into GenBank ( http://www.ncbi.nlm.nih.gov/Genbank/index.html ) and has been assigned Accession No. EU 853303. The presence of laurel wilt in camphor provides an opportunity to understand the pathogen distribution and possible resistance mechanisms in this host, which could have implications for efforts to remediate the impacts of the disease in redbay and other species in the Lauraceae in the southeastern United States. References: (1) S. W Fraedrich et al. Plant Dis. 92:215, 2008. (2) T. C. Harrington et al. Mycotaxon 104:399, 2008. (3) M. A. Innis et al. PCR Protocols, A Guide to Methods and Applications. Academic Press. San Diego, CA, 1990. (4) A. E. Mayfield, III et al. Plant Dis. 92:976, 2008.

Expression of polysialylated NCAM but not L1 or N-cadherin by regenerating adult mouse optic fibers in vitro.

This study asks if there might be irreversible maturational changes in adult neurons that limit their capacity to regenerate. Retina from adult and embryonic mouse were placed in culture on laminin substrates so that regenerating adult optic fibers could be compared to growing embryonic fibers. Several cell adhesion molecules (CAMs) known to mediate the growth of embryonic neurites on astrocytes were assayed by immunocytochemistry: L1, N-cadherin, and NCAM. Thy 1.2, a potential CAM with inhibitory activity, was also examined. As in vivo, embryonic fibers were found to express both L1 and N-cadherin. In contrast, regenerating adult fibers had no detectable amounts of either of these CAMs. N-Cadherin is normally down regulated during development so its absence in adult fibers suggests it can not be reexpressed during regeneration. L1 is normally found in the proximal regions of adult optic fibers so its absence indicates it is not expressed or transported in regenerating fibers. Adult regenerating fibers expressed high levels of Thy 1.2, which was undetectable in embryonic optic fibers. Thy 1.2 is normally found in mature fibers, indicating this phenotypic feature is preserved during regeneration. Both adult and embryonic fibers showed strong reactivity for NCAM, which in vivo is normally found in embryonic and at lower levels in adult fibers. Surprisingly, both embryonic and regenerating adult fibers expressed high levels of polysialic acid, which is normally absent in adult fibers. NCAM may be one of few CAMs available to adult optic fibers for regeneration on astrocytes.

Antisperm antibodies and male subfertility.

The outcome of treatment for couples with male immunological infertility must be considered in conjunction with the risks, costs and time to success involved. Reversible factors should be treated. Steroid treatment is a good option but its failure in two-thirds of patients should add impetus to attempts to predict responders before or soon after starting treatment. The treatment options are not mutually exclusive [48]. The success of IUI may be enhanced further by new sperm preparation techniques. If severe immunological infertility exists or other infertility factors are present, IVF or ICSI may be considered from the outset.

Estimates of stability of daily wandering behavior among cognitively impaired long-term care residents.

Direct observation and time-study techniques were used with a sample of 25 ambulatory, cognitively impaired subjects drawn from two long-term care settings to evaluate wandering behavior. The purposes of this study were (a) to describe the 24-hour distribution of wandering and direct ambulating cycles, (b) to examine the stability of wandering behavior over a 3-day interval, (c) to evaluate whether wandering during a 2-hour epoch is representative of that of a 24-hour day, and (d) to evaluate whether large-scale integrated (LSI) activity meters can substitute as an index or proxy for direct observation in the study of wandering behavior. Subjects displayed a daily average of 20.1 cycles encompassing 43.9 minutes of wandering ambulation and 28.8 cycles encompassing 40.4 minutes of direct ambulation. Wandering behavior was present in all subjects. However, wandering was highly variable from subject to subject. For a given subject, wandering was only moderately stable over a 3-day interval, but more so than direct ambulation. Similarly, a standard 2-hour epoch was moderately representative of daily wandering ambulation, but more so than for direct ambulation. Finally, LSI meters, when applied at the ankle and worn over longer (24-hr) rather than shorter (2-hr) intervals, are a promising means to index wandering behavior.

The neurite-promoting effect of laminin is mediated by different mechanisms in embryonic and adult regenerating mouse optic axons in vitro.

Retinal explants from embryonic or adult mice were placed on laminin or merosin substrates and the outgrowth of optic fibers was assayed under serum-free conditions. Both substrates strongly promoted outgrowth. A blocking antibody to the beta1/beta3 integrin subunits completely blocked laminin-dependent growth of embryonic optic fibers but had no detectable effect on adult fibers. Similarly, a blocking antibody against the main neurite-promoting region within the globular domain of the E8 fragment of laminin inhibited growth of embryonic fibers but had no effect on adult optic fibers. The beta1 integrin subunit was identified immunohistochemically on both embryonic and adult fibers. These findings indicate that adult fibers have lost the beta1 function which dominates laminin-dependent growth in embryonic fibers but express a receptor for laminin-dependent growth that is not detectable in embryonic fibers. These findings suggest that there are intrinsic differences between embryonic and adult optic fibers that may have implications for regenerative failure in the central nervous system of adult mammals .

Heterotrimeric G protein activation rapidly inhibits outgrowth of optic axons from adult and embryonic mouse, and goldfish retinal explants.

Axons in the adult mammalian CNS normally do not regenerate following axotomy even though they retain the capacity for growth under certain experimental conditions. Although this implies that the regeneration of adult axons is under regulative control, very little is known about the signaling pathways "responsible" for this regulation. This study examines the possibility that a G protein signaling system exists in adult mouse optic fibers and that it functions to regulate axonal outgrowth. To induce the growth of optic fibers, retinas from adult mouse were placed in organotypic culture under serum free conditions and allowed to regenerate onto a laminin substrate. Heterotrimeric G proteins were stimulated by adding mastoparan (MST) to the medium while monitoring growing fibers with time lapse microscopy. Mastoparan treatment produced rapid growth cone collapse and axonal retraction which persisted while MST was present. Prior addition of pertussis toxin (PTX), which irreversibly inactivates the G proteins, G(o) and G (i),completely blocked the effect of MST, confirming that MST was acting through the PTX sensitive G proteins. Selective activation of G proteins in the growth cone by local application of MST with a micropipet was equally effective. For comparison, equivalent experiments were performed on embryonic day 15 retinal explants and on retinal explants from adult goldfish, which normally regenerate in vivo. MST similarly inhibited these axons and this effect was blocked by PTX. However, embryonic fibers were less reliably affected compared to goldfish or adult mouse, suggesting a developmentally regulated sensitivity. The presence of G-proteins in the mouse axons was further tested immunohistochemically using antibodies against G(o)/G(i). Positive staining was detected in the growth cones and shaft of adult and embryonic mouse optic fibers. These findings demonstrate that G protein activation inhibits axonal outgrowth and suggest that there may be a G protein signaling pathway that normally regulates this outgrowth. However, since this pathway appears to exist in both axons that can regenerate and those that normally do not, the presence of PTX-sensitive G proteins alone cannot account for regenerative failure. Regenerative failure may instead be explained as the selective or increased activation of this pathway in the adult mammalian CNS.

Differential effect of serum on laminin-dependent outgrowth of embryonic and adult mouse optic axons in vitro.

Laminin is an extracellular matrix molecule which promotes neurite outgrowth from a variety of neurons in culture. However, the reported effectiveness of laminin on neurite outgrowth from retinal ganglion cells in rat and that from chick have been contradictory. In chick, embryonic retinal ganglion cells show strong laminin-dependent neurite outgrowth which is lost during development. In contrast, in rat, laminin promotes neurite outgrowth from adult, but not embryonic retinal ganglion cells. We have reexamined the response of adult and embryonic mouse retinal ganglion cells to laminin in culture. We found, first, that both adult and embryonic retinal neurites respond to laminin with neurite outgrowth in serum-free medium. Second, we found that the addition of serum to the medium greatly inhibits the outgrowth of neurites from embryonic, but not adult, retinal explants. This inhibition appears specific for neurite outgrowth involving laminin receptors, since embryonic explants showed extensive neurite outgrowth in the presence of serum when astrocytes were used as a substrate. These developmental differences in the effect of serum on laminin-dependent neurite outgrowth may indicate maturational changes in surface molecules on optic fibers related to regenerative failure in the adult CNS.

Extension and regeneration of corticospinal axons after early spinal injury and the maintenance of corticospinal topography.

It has been established that neonatal corticospinal (CS) axons are able to grow around lesions of the spinal cord early in neonacy (Bernstein and Stelzner, J. Comp. Neurol. 221:382-400; Firkins, Bates, and Stelzner, Exp. Neurol., 120:1-15). To determine if these corticospinal axons include regenerating as well as late developing axons a double-labeling paradigm is used in which CS neurons are retrogradely labeled from the cervical spinal cord by injections of fast blue (FB) on Postnatal Day (PND) 2, 4, or 10. Two days later, the FB is aspirated along with the left dorsal funiculus and the right hemicord (CHR). As adults, the animals receive an injection of diamidino yellow (DY) or rhodamine into the spinal cord caudal to the lesion site. Thus, FB neurons are those that originally projected to the spinal cord before the lesion and which survived axotomy, DY neurons are those whose axons reached the spinal cord after the lesion, and double-labeled neurons (FB/DY) are cells which projected to the spinal cord prior to the lesion and regenerated a spinal axon postlesion. Animals FB injected on PND 2 have a widespread distribution of FB-labeled neurons in cortex, including areas outside of sensorimotor cortex. These animals also had both DY- and FB/DY-labeled cells within sensorimotor cortex, indicating that the population of axons growing caudal to neonatal spinal lesions consists of both late growing and regenerating axons. In animals FB injected on PND 10, the FB neurons were all located in sensorimotor cortex. Very few DY and no FB/DY neurons were present. We have also looked at the topography of the CS neurons which project caudal to early spinal lesions. Rat pups received a CHR on PND 0, 3, 6, or 12. As adults, horseradish peroxidase was injected into the cervical or lumbar enlargement of the spinal cord and the distribution of labeled cells in the cerebral cortex was plotted and compared to normal and lesioned adult controls. In all experimental animals, the distribution of retrogradely labeled cells was restricted to the area containing CS projection neurons in the normal animal. This is despite the fact that the number of CS projection neurons is greatly reduced from normal and the normal pathway for CS axonal outgrowth has been completely disrupted by the neonatal lesion.

Corticospinal tract plasticity and astroglial reactivity after cervical spinal injury in the postnatal rat.

We have investigated corticospinal (CS) axon growth around cervical spinal injury in the neonatal rat and related this growth to the astroglial reaction occurring at the lesion site. Rats received a high cervical overhemisection (left dorsal funiculotomy, right spinal hemisection) and a right cortical ablation on Postnatal Days (PNDs) 0, 3, 6, 12, and 21 to 24 (weanlings). In chronic operates the remaining CS projection from the left sensorimotor cortex was then assayed using wheat germ agglutinin-horseradish peroxidase as an anterograde tracer. In other operates the formation of the astroglial scar at the spinal lesion site was studied using a monoclonal antibody to glial fibrillary acidic protein. In PNDs 0-6 operates labeled axons extend through the intact left hemicord to bypass the lesion. The labeled axons travel to the edge of the lesion, cross the midline, and pass lateral to the lesion within the dorsal and intermediate gray and dorsal lateral white matter. Axons project bilaterally to normal areas of CS termination in PND 0 operates for a distance of 2.5 to 4 spinal segments caudal to the lesion which decreases to 1.5 to 2 segments in PND 6 operates. In PND 12 and weanling operates labeled fibers do not grow around the lesion but instead are retracted rostrally. There is an astrocytic reaction to injury at all ages by 3 days postoperatively (p.o.) that becomes greater with age and p.o. survival time. A more complicated cystic scar forms in 6-day and older operates. These data show that there is an age-related change in the ability of CS axons to grow around spinal injury which ends near the time CS elongation and gliogenesis is complete in the spinal cord.

The heavy neurofilament protein is expressed in regenerating adult but not embryonic mammalian optic fibers in vitro.

Axonal neurofilaments are composed of light (NF-L), medium (NF-M), and heavy (NF-H) subunits which are sequentially expressed during axonal development. In retina, NF-L and NF-M appear prenatally, followed postnatally by NF-H which occurs at about the time axons are reaching their target tissue. Phosphorylation of the NF-H protein occurs after it has first appeared in the axon. Phosphorylated NF-H is also downregulated in regenerating peripheral nerves. These observations lead to the hypothesis that NF-H stabilizes axons, thereby inhibiting their ability to grow. We have previously shown that adult mouse retinal ganglion cells (RGCs) can extend neurites in vitro and that these neurites reexpress the developmental protein GAP-43. Here we ask whether the expression of neurofilament proteins in the growing adult RGC axons involves the recapitulation of development. Adult mice which had a priming lesion of the optic nerve and Embryonic Day 15 mouse retinas were explanted onto laminin substrates and grown in culture. After 2-4 days the growing neurites were stained with a battery of monoclonal antibodies against differentially phosphorylated versions of the neurofilament subunits. Both adult and embryonic neurites were highly immunoreactive for NF-L and NF-M. Only the adult neurites stained with antibodies against phosphorylated NF-H. There was no immunoreactivity in the embryonic explants. This indicates that regrowing adult RGC axons maintain their adult cytoskeletal properties and can nevertheless regenerate.

Distribution of microtubule-associated proteins (MAPs) in adult and embryonic mouse retinal explants: presence of the embryonic map, MAP5/1B, in regenerating adult retinal axons.

Microtubule-associated proteins (MAPs) are developmentally regulated proteins involved in microtubule polymerization and stabilization. We have asked whether MAPs in regenerating adult mouse retinal ganglion cell axons recapitulate the pattern of MAPs seen during development. Adult and Embryonic Day 15 (E15) mouse retinal segments were explanted onto laminin-coated coverslips and allowed to extend neurites in serum-free medium. Using a variety of monoclonal antibodies (Mabs), we stained adult and E15 explant cultures for early (MAP5) and late (MAP1, MAP2, MAP2a+b, tau) MAPs. Optic neurites growing from E15 explants were strongly immunoreactive for MAP5. Labeling was absent for MAP1 and MAP2a+b. Mabs to MAP2 and tau lightly stained axons and cell bodies, probably due to MAP2c and juvenile tau which are found in developing neurons. In adult explant cultures, both perikarya and axons were immunoreactive for MAP1. MAP2 and MAP2a+b labeled perikarya and fibers within the explant, and tau stained axons on the substrate. MAP5 immunoreactivity was intense in the adult explant cultures, labeling axons extending over the substrate and perikarya and dendrites in the explant in a pattern similar to that seen in E15 explants. In summary, adult retinal explants maintain their adult complement of MAPs, in showing high levels of MAP1, tau immunoreactivity restricted to neurites on the substrate, and MAP2 segregated into neurites and perikarya within the explant. The exception is MAP5 for which the pattern of immunoreactivity is similar in adult and E15 retinal explants.

Everyday indicators of impaired cognition: development of a new screening scale.

Development of the Everyday Indicators of Impaired Cognition (EIIC) Scale to assess nursing home residents for performance errors in four domains of cognitive functioning is reported. The EIIC had strong content validity, with indices ranging from .7 to 1.0. Factor analyses of data from two independent samples (N = 198, N = 107) confirmed four factors: abstract thinking, judgement, language, and spatial skills. Cronbach's alpha for subscales ranged from .67 to .92; test-retest reliabilities ranged from .49 to .80 with higher reliabilities occurring when time of retest matched time of original testing. Overall EIIC scores correlated to the short Memory-Orientation-Concentration (MOC) test and the Mini-Mental Status Examination (MMSE) at values supporting convergent validity (r = .67 and -.74, respectively). Evidence for divergent validity is a small, negative, nonsignificant correlations (r = -.15, -.18) of the EIIC at Times 1 and 2 to the Bradburn Affect Balance Scale.

Disruptive behavior in elderly nursing home residents: a survey of nursing staff.

A significant number of nursing home residents exhibit behavior disturbances that are disruptive to the living and working environment in the nursing home. The most common disruptive behaviors cited by licensed nursing personnel included hitting/slapping, verbally aggressive remarks, screaming, pacing, wandering, and repetitive verbal requests. Self-injurious behavior, property destruction, and hiding things were not mentioned. Many of the nursing strategies listed by nursing staff as being used to alleviate disruptive behaviors are traditional care activities, eg, talking to and counseling patients, touching, or altering care. However, chemical and physical restraints were also frequently listed.

A new endoscopic method for treatment of malignant oesophagobronchial fistulas.

A short malignant oesophagobronchial fistula which could not be sealed using adhesive agents was successfully treated using a new endoscopic technique. The procedure provided good palliation and the results withstood the test of time in the patient. The method, which is described in detail, provides a useful modification to existing methods.

Tracheal lipoma.

A 50 year old man was found to have a tracheal lipoma two years after first noticing symptoms.

Transganglionic transport of HRP from the circumvallate papilla of the rat.

To learn whether horseradish peroxidase (HRP) injections in gustatory papillae on the tongue can be used to study central topographical projections of taste buds and papillae, injections were made into the circumvallate papilla in rats. Labeled central projections after papilla injections were compared to projections after applying HRP to the cut glossopharyngeal nerve. Papilla injections result in HRP transport by afferent and efferent fibers of the glossopharyngeal nerve, and the pattern of central projections is similar to that after labeling the cut nerve. Projections include a separation in the brainstem of afferent, dorsally located fibers and efferent, ventrally located fibers. Afferent fibers project to the solitary nucleus and the trigeminal system. Efferent projections label muscle motorneurons in the nucleus ambiguus and the cells of origin of parasympathetic preganglionic fibers, which from the inferior salivatory nucleus. The parasympathetic neurons labeled after papilla projections are preganglionic fibers to Remak's ganglia in the tongue; post-ganglionic fibers of these ganglia are the secretomotor supply to the von Ebner's glands. In summary, injections of HRP into gustatory papillae reliably label central projections of the papilla and can be used for studies to discern topography in central projections of the taste system. Injections into the circumvallate papilla also have demonstrated that the parasympathetic neurons innervating von Ebner's glands are located in the inferior salivatory nucleus.

The organization of the neonatal rat's brainstem trigeminal complex and its role in the formation of central trigeminal patterns.

The present study delimits the relationship of primary trigeminal afferents to their targets, the brainstem trigeminal nuclei of the neonatal rat. Previously, the brainstem trigeminal complex of the rat has been subdivided on the basis of either cytoarchitectonics or patterns of succinic dehydrogenase activity into the principal sensory nucleus and the three subnuclei of the spinal trigeminal nucleus, oralis, interpolaris, and caudalis. In this paper, we demonstrate that each of these subdivisions can also be identified by its pattern of primary trigeminal afferents. In addition, we demonstrate that the terminations of these afferents are distributed in a punctate fashion which correlates with vibrissae-related patterns of histochemical staining. Further, vibrissae removal in the neonatal rat at any age studied results in a corresponding deafferentation of both the principal sensory nucleus and all subnuclei of the spinal trigeminal nucleus. This same procedure has a graded, age-dependent effect on the vibrissae-related pattern of cytochrome oxidase staining in somatosensory cortex. On this basis, we conclude that vibrissae-related pattern formation in the central trigeminal system can be best understood in terms of a single "sensitive" period for the entire system. We hypothesize that this is the period during which an interaction normally occurs between primary trigeminal afferents and target neurons of the principal sensory nucleus.