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We have previously shown that attenuation of axoplasmic transport by application of vinblastine to the developing infraorbital nerve (ION) results in a loss of central vibrissae-related patterns that is not accompanied by changes in the receptive field sizes for the V primary afferents innervating the whisker follicles. The present study examines the relationship between the loss of central vibrissae-related patterns and alterations in the response properties of neurons in the V principal sensory nucleus (PrV) of adult rats that sustained application of vinblastine to the ION at birth. Absence of histochemically demonstrable vibrissae-related patterns in PrV resulted in only modest changes in the receptive fields and response properties of vibrissae-sensitive neurons in this nucleus that projected to the contralateral thalamus. Response latencies to electrical activation of the V ganglion were similar in treated and untreated animals. The mean receptive field size was significantly increased from 1.3 ± 0.7 vibrissae in controls to 1.7 ± 0.9 vibrissae in vinblastine-treated animals, and the percentage of cells yielding a tonic response to vibrissae deflection was markedly reduced (p < 0.01 for both measures). Phasically responding cells recorded in vinblastine-treated animals showed a significant reduction in the mean number of spikes per stimulus following deflection of the vibrissae in either the preferred or non-preferred direction relative to cells recorded in normal animals (p < 0.05). The present results indicate that disruption of the normal vibrissae-related aggregates of neurons in PrV by application of vinblastine to the ION has limited effects on the functional representation of the vibrissae in this nucleus. [ABSTRACT FROM AUTHOR]

Immunocytochemical and autoradiographic techniques were employed to determine the time course of expression of the serotonin (5-HT) transporter (SERT) on thalamocortical afferents in the rat's primary somatosensory cortex (S-I), and to correlate this expression to the transient vibrissae-related patterning of 5-HT immunostaining previously described. In additional in vivo and in vitro experiments, 5-HT and [sup 3]H-5-HT were applied directly to the cortices of untreated and 5,7-dihydroxytryptamine-treated (5,7-DHT) rats in order to determine the period during which SERT functions on thalamocortical axons to take up 5-HT. In postnatal rats, SERT immunohistochemistry revealed a somatotopic patterning in S-I that persisted until P-15, which is 6 days after the disappearance of the vibrissae-related 5-HT immunostaining. [sup 3]H-citalopram autoradiography revealed a vibrissae-related pattern in layer IV of S-I until at least P-30. Following destruction of raphe-cortical afferents with 5,7-DHT on the day of birth, this binding pattern remained visible until at least P-25, indicating that SERT located on thalamocortical axons is responsible for the [sup 3]H-citalopram patterning observed in S-I. Tissue from 5,7-DHT-treated rats that had 5-HT applied directly to their cortices revealed a normal vibrissae-related pattern of 5-HT immunostaining in S-I at P-7 and P-11 but only a faint pattern at P-13 and none at P-14. In addition, 3H-5-HT injected directly into S-I labeled layer IV barrels at P-6 and P-12 but not at P-18. The results of these experiments demonstrate that SERT is expressed by thalamocortical afferents and remains functional long after the vibrissae-related 5-HT immunostaining in cortex disappears. [ABSTRACT FROM AUTHOR]

Acetylcholinesterase (AChE) is transiently expressed by thalamocortical axons in the rat, and staining for this enzyme has been used extensively to study the development of thalamocortical projections. In the present study, patterns of AChE staining were compared in the trigeminal brainstem, thalami and primary somatosensory cortices of perinatal rats, mice, and hamsters. As previously reported, the ventral posteromedial nucleus (VPM) of rats showed dense AChE staining from P-0 at least through P-8. The ventral posterolateral nucleus (VPL) contained heavy AChE staining at least through P-60. In the cortex, there was also dense AChE staining which was organized somatotopically in patches similar to those observed with other methods such as cytochrome oxidase (CO) staining. However, by adulthood, AChE staining revealed a negative image of the CO staining pattern in lamina IV. In the mouse and hamster, there was dense AChE staining in VPL from P-0 through adulthood, but VPM was much less heavily stained for this enzyme. Moreover, the staining in VPL of mice was markedly reduced after transection of axons that travel to the thalamus in the medial lemniscus, suggesting that much of it was contained in these afferent fibers. In the cortices of both perinatal and adult mice and hamsters, AChE staining yielded a negative image of the somatotopically organized patches demonstrable with CO staining. This negative image was apparent by P-2 in the mouse and P-4 in the hamster. These results document a dramatic species difference with respect to the expression of AChE in the thalami and cortices of developing rodents. The differences between the patterns observed in rats vs mice and hamsters probably reflect the fact that cortical AChE in the latter species is not contained in thalamocortical afferents arising from either VPM or VPL. [ABSTRACT FROM AUTHOR]

Function of the Dlx gene family in regulating basal telencephalon development. There are four known vertebrate Dlx genes (Dlx-1,-2,-5 and-6) that are expressed in the primordia of several forebrain regions including the striatum. Dlx-1 and -2 are expressed only in the proliferating cells of the ventricular and subventricular zones. The Dlx-1&-2 mutation causes a severe problem in basal ganglia development. Preliminary results suggest a block in differentiation of the striatum which causes hypo-plasia of this structure. In a neocortical brain slice preparation which is cut tangential to the pial surface and apply it to the study of layer IV stellate neurones in somatosensory cortex of P18-P22 mice.

Abstract The one-to-one correspondence of whiskers to barrels in layer IV of rodent somatosensory cortex can be demonstrated by a precise match between columns of heavy 2-deoxyglucose (2DG) label in layer IV barrels and other layers which correspond to stimulated whiskers. While there is specificity of peripheral-to-central mapping, the extent to which integration and/or modulation are generated by circuitry within or interactions between the barrel-defined whisker columns is not clear. Following stimulation of selected whiskers, large cells at the layer IV-V boundary throughout the barrel field are heavily labeled by 2-deoxyglucose (2DG) at high resolution. Many of these cells are outside the barrel columns of the stimulated whiskers. Further, the number of cells labeled is not directly related to the number of activated barrel columns. These neurons are not labeled in animals anesthetized before 2DG injection and are not as heavily labeled in barrel fields of somnolent animals. Most of the heavily labeled neurons immunolabel for glutamate decarboxylase (GAD) and are presumed to be inhibitory, while a smaller number of labeled neurons, presumed to be excitatory, immunolabel for glutamate (Glu). Similar populations of large, heavily 2DG-labeled neurons are found in other cortical areas. These relatively few neurons are exceptionally active and may modulate integrative functions of cerebral cortex. [ABSTRACT FROM AUTHOR]

Abstract Single cell recording, receptive field analysis, and microejection techniques were used to evaluate the effects of neuropeptide Y (NPY) type 2 (Y2) receptor activation on the responses of vibrissae-sensitive ventral posteromedial thalamic (VPM) neurons. Activation of this receptor with the C-terminal fragment, NPY\[13-36] had no significant effect on responses evoked by deflection of principal or surround vibrissae or electrical stimulation of the trigeminal principal sensory nucleus. However, it did significantly decrease ( p 0.01) responses evoked by electrical stimulation of subnucleus interpolaris (SpI) by a mean ( standard error) of- 31.0 8.7%). The finding that responses to surround vibrissa stimulation were not significantly decreased by a manipulation that did significantly attenuate SpI- evoked responses suggests that this nucleus is not the sole source of surround vibrissae input to VPM neurons. [ABSTRACT FROM AUTHOR]

Previous experiments from this laboratory have indicated that transection of the infraorbital nerve (ION, the trigeminal \[V] branch that supplies the mystacial vibrissae follicles) at birth and in adulthood has markedly different effects on galanin immunoreactivity in the V brainstem complex. Adult nerve transection increases galanin immunoreactivity in the superficial layers of V subnucleus caudalis (SpC) only, while neonatal nerve transection results in increased galanin expression in vibrissae-related primary afferents throughout the V brainstem complex. The present study describes the distribution of binding sites for this peptide in the mature and developing V ganglion and brainstem complex and determines the effects of neonatal and adult ION damage and the associated changes in galanin levels upon their distribution and density. Galanin binding sites are densely distributed in all V brainstem subnuclei and are particularly dense in V subnucleus interpolaris and the superficial layers of SpC. They are present at birth (P-0) and their distribution is similar to that in adult animals. Transection of the ION in adulthood and examination of brainstem 7 days later indicated marked reductions in the density of galanin binding sites in the V brainstem complex. With the exception of the superficial laminae of SpC, the same reduction in density remained apparent in rats that survived 45 days after nerve cuts. Transection of the ION on P-0 resulted in no change in the density of galanin binding sites in the brainstem after either 7 or 60 days survival. These results indicate that densely distributed galanin binding sites are present in the V brainstem complex of both neonatal and adult rats, that they are located in regions not innervated by galanin-positive axons, and that their density is not significantly influenced by large lesion-induced changes in the primary afferent content of their natural ligand. [ABSTRACT FROM AUTHOR]

Two experiments were carried out to evaluate the relative contributions of thalamocortical and raphe-cortical fibers to the transient somatotopically organized pattern of serotonin (5-HT) immunoreactivity that appears in the primary somatosensory cortex (SI) of rats during the first 2 weeks of life. In the first experiment, the specific 5-HT uptake inhibitors, fluoxetine and paroxetine, were administered systemically, animals were killed 3, 6, or 12 h later, and cortices evaluated for 5-HT immunoreactivity. Fluoxetine treatment had no appreciable effect on the density of 5-HT immunoreactivity in the cortex. Paroxetine treatment caused a reduction in 5-HT immunoreactivity which was maximal 6 h after administration. Examination of the cortices of these animals revealed a loss of very fine dust-like 5-HT immunoreactivity, but a vibrissae-related pattern remained visible in thicker fibers. In a second experiment, raphe-cortical fibers were destroyed by systemic administration of 5,7-dihydroxytryptamine on the day of birth. Six days after this manipulation, 5-HT was applied directly to the cortex in vivo and the animals were then killed and cortices processed to demonstrate 5-HT immunoreactivity. The cortices of these rats revealed a fine dust-like immunoreactivity organized in a somatotopic pattern, but only very few 5-HT-positive axons. The results of these experiments suggest that both raphe-cortical axons and thalamocortical fibers contribute to the patterned 5-HT immunoreactivity observed in SI of perinatal rats. [ABSTRACT FROM AUTHOR]