Neural damage in the rat thalamus after cortical infarcts.

Histopathologic changes in the thalamus of 23 rats after somatosensory cortical infarction produced by middle cerebral artery occlusion were examined using the Fink-Heimer silver staining method, immunohistochemistry with antibodies against glial fibrillary acidic protein and laminin, and conventional stains. Middle cerebral artery occlusion produced cortical infarcts in the lateral parietal region, with variable involvement of the frontoparietal parasagittal sensorimotor cortex. Within 3 days after occlusion, massive terminal degeneration but no neuronal changes were apparent in the ipsilateral thalamus. By 1 week after occlusion, abnormal neurons with darkly stained, shrunken nuclei and atrophic perikarya were present in the ipsilateral thalamic nuclei. These neurons were densely argyrophilic in Fink-Heimer sections. Rats with small lateral parietal cortical lesions had degenerating neurons limited to the medial ventroposteromedial nucleus. Large lesions involving the parasagittal sensorimotor cortex resulted in widespread neuronal damage in the ventroposteromedial, ventroposterolateral, intralaminar, and posterior nuclear regions but nowhere else. Immunoreactivity to laminin antibody decreased, and astrocytic proliferation was abundant in affected thalamic areas. These findings are consistent with retrograde neuronal degeneration due to thalamocortical fiber damage in ischemic cortical regions. Such lesions remote from the infarct may influence functional recovery in patients with stroke.     

Substance P innervation of the rat and cat thalamus. I. Distribution and relation to ascending spinal pathways.

An antiserum for substance P (SP) with minimal cross-reactivity for other tachykinins was employed to map the distribution of SP-positive nerve fibers and terminals in the thalamus of cats and rats with special emphasis on the innervation by these fibers of nuclei related to the somatosensory system. In both species SP innervation is predominantly along the midline, in medial and posterior thalamic regions, and sparser in sensory relays for specific modalities. Among the most densely innervated nuclei are the parafascicular, paraventricular, rhomboid, central medial and parts of mediodorsal, lateral posterior, and ventral lateral geniculate. SP innervation of somatosensory-related nuclei is also evident in central lateral nucleus, posterior complex (PO), and in ventroposterolateral (VPL) nucleus of both cats and rats. In VPL of cats SP fibers and terminals are present along its ventral and lateral border, a paralaminar area in which spinothalamic fibers have been shown to terminate and where neurons responsive to noxious stimuli have been reported. Also in rats the SP innervation of VPL is similar to that of spinothalamic tract fibers. The SP innervation of somatosensory thalamic nuclei may be supplied, at least in part, by spinothalamic afferent as suggested by the depletion of SP after anterolateral chordotomy but not after ablation of the dorsal column nuclei. The presence of SP-positive spinothalamic neurons in the spinal cord is reported in the following paper.     

Subcortical connections of normotopic and heterotopic neurons in sensory and motor cortices of the tish mutant rat

Orthograde and retrograde tracers were used to examine subcortical connections of neurons in the neurological mutant tish rat. This animal exhibits bilateral heterotopia similar to those observed in epileptic humans with subcortical band heterotopia. Terminal varicosities were labeled in the striatum, thalamus, brainstem, and spinal cord following injections of the anterograde tracer biotinylated dextran amine (BDA) into the heterotopic cortex. The general topography of corticothalamic projections was evaluated by injecting the retrograde tracer Fluoro-Gold (FG) into ventral thalamic nuclei. Retrograde labeling of small-to-medium sized neurons was observed in layer VI of topographically restricted portions of the normotopic cortex. Similar appearing cells were labeled in the neighboring portions of the underlying heterotopia; however, these neurons did not display characteristic lamination or radial orientation. Thalamocortical terminals labeled by injecting BDA into the ventroposterolateral nucleus (VPL) were observed primarily in layer IV of the medial aspect of the normotopic somatosensory cortex. In contrast, a radial column of terminals was present in the underlying heterotopia. Typical barrel labeling was found in the lateral aspect of the normotopic somatosensory cortex after injecting the ventroposteromedial nucleus (VPM), whereas more diffuse patches of labeling were observed in the underlying heterotopia. Heterotopic neurons in the tish cortex, thus, exhibit characteristic features of subcortical connectivity. Both normotopic and heterotopic neurons in the tish brain project to appropriate subcortical sites and establish bidirectional topographic connections with the thalamus. These results suggest that primary sensory-motor information is represented in a parallel manner in the normotopic and heterotopic cortices of the tish rat. J. Comp. Neurol. 395:29–42, 1998. © 1998 Wiley-Liss, Inc.     

Electrophysiologic study of descending effects of field 5b of the association cortex of the brain of the cat on the neurons of the ventroposterolateral nucleus of the thalamus

Responses of 65 thalamic ventroposterolateral (VPL) nucleus neurons to stimulation of the associative cortex (area 5b) were studied in acute experiments on cats anesthetized with ketamine (25 mg/kg) and immobilized with myorelaxine (2 mg/kg). Neurons studied were identified on the basis of peculiarities of their responses evoked by primary somatosensory cortex and medial lemniscus stimulation. Three neurons responded to stimulation of the area 5b antidromically. Primary orthodromic excitation and inhibition were observed in 17 (26.2%) VPL neurons. The role of the area 5b descending influences on the somatosensory impulses transmission through VPL relay neurons is discussed.     

Early and specific expression of monocyte chemoattractant protein-1 in the thalamus induced by cortical injury

For many years it has been known that retrograde degeneration of thalamic neurons occurs following damage to the cerebral cortex, however, the molecular mechanisms which control this process are unknown. Recent studies have demonstrated microglial activation in thalamic nuclei well before the onset of retrograde neuronal cell death. Activated monocytes and microglia synthesize factors detrimental to neuronal survival as well as phagocytose damaged and dying neurons. Our previous studies demonstrated that monocyte chemoattractant protein-1 (MCP-1), a β chemokine which attracts cells of monocytic origin to sites of injury, is rapidly expressed in the brain following visual cortical lesions. The present study examined the expression of MCP-1 messenger RNA and protein in the thalamus following a visual cortical lesion. Aspiration lesions of visual cortex were made in adult mice. At specific times after lesion, brains were harvested and dissected into specific regions. MCP-1 message as detected using northern analysis was absent in uninjured brain, but was elevated in the ipsilateral thalamus as rapidly as 1 h following the lesion. In situ hybridization localized MCP-1 message to subpial glial cells of the lateral geniculate nucleus (LGN) of the ipsilateral thalamus after injury. ELISA showed that MCP-1 protein levels were significantly elevated in the ipsilateral thalamus at 6 h, peaked at 12 h, and remained above baseline levels for at least 1 week post lesion. In addition, anti-GFAP staining demonstrated activated astrocytes localized to the ipsilateral LGN at 24 and 72 h after injury. The early expression and regional localization of MCP-1 mRNA and protein strongly suggest that MCP-1 is a critical molecule in the regulation of thalamic retrograde neuronal degeneration.     

Spinothalamocortical projections to the secondary somatosensory cortex (SII) in squirrel monkey

Anterograde labeling of the cervical spinothalamic tract was combined with retrograde labeling of thalamocortical cells projecting to the hand region of the second somatosensory cortex (hSII) to identify likely sites in the thalamus for processing and transmitting nociceptive information to hSII. Anterograde labeling of terminals was done with 2% WGA-HRP injections in the cervical enlargement; thalamocortical cells were retrogradely labeled with fluorescent tracers. In one experiment, the contralateral primary somatosensory cortex hand region (hSI) was injected to provide a direct comparison with hSII thalamic label. Both labeled cells and terminal-like structures were visualized in single thalamic sections and their numbers and positions quantitatively analyzed. The number of labeled cells within 100 microns from the STT terminals were counted as overlapping cells. Four thalamic nuclei, ventroposterior inferior (VPI), ventroposterior lateral (VPL), posterior nucleus (PO) and centrolateral nucleus (CL) combined to contain 86.5% of all hSII-projecting overlapping cells. Of all hSII-projecting thalamic overlapping cells, VPI contained the largest number (36.4% of the total) followed by the anterior portion of the posterior nuclear complex (POa; 20.4%), VPL (18.3%) and CL (11.4%). Results of the hSI injection show a different pattern of overlap in agreement with our earlier study. The relative distribution of overlapping cells was dependent on the antero-posterior position of the SII injections. The most anterior injections resulted in small numbers of labeled cells, with the majority of overlapping cells located in PO and CL. The more posterior injections resulted in overlapping cells mainly in VPI and VPL. The results indicate that, in the squirrel monkey, VPI, VPL, POa and CL relay nociceptive information from the spinal cord to the second somatosensory cortex.     

Thalamocortical dysfunction and thalamic injury after asphyxial cardiac arrest in developing rats

Global hypoxia-ischemia interrupts oxygen delivery and blood flow to the entire brain. Previous studies of global brain hypoxia-ischemia have primarily focused on injury to the cerebral cortex and to the hippocampus. Susceptible neuronal populations also include inhibitory neurons in the thalamic reticular nucleus. We therefore investigated the impact of global brain hypoxia-ischemia on the thalamic circuit function in the somatosensory system of young rats. We used single neuron recordings and controlled whisker deflections to examine responses of thalamocortical neurons to sensory stimulation in rat survivors of 9 min of asphyxial cardiac arrest incurred on postnatal day 17. We found that 48-72 h after cardiac arrest, thalamocortical neurons demonstrate significantly elevated firing rates both during spontaneous activity and in response to whisker deflections. The elevated evoked firing rates persist for at least 6-8 weeks after injury. Despite the overall increase in firing, by 6 weeks, thalamocortical neurons display degraded receptive fields, with decreased responses to adjacent whiskers. Nine minutes of asphyxial cardiac arrest was associated with extensive degeneration of neurites in the somatosensory nucleus as well as activation of microglia in the reticular nucleus. Global brain hypoxia-ischemia during cardiac arrest has a long-term impact on processing and transfer of sensory information by thalamic circuitry. Thalamic circuitry and normalization of its function may represent a distinct therapeutic target after cardiac arrest.     

Anatomic evidence of nociceptive inputs to primary somatosensory cortex: relationship between spinothalamic terminals and thalamocortical cells in squirrel monkeys

This study examined anatomic pathways that are likely to transmit noxious and thermal cutaneous information to the primary somatosensory cortex. Anterograde and retrograde labeling techniques were combined to investigate the relationship between spinothalamic (STT) projections and thalamocortical neurons in the squirrel monkey (Saimiri sciureus). Large injections of diamidino yellow (DY) were placed in the physiologically defined hand region of primary somatosensory cortex (hSI), and wheat germ agglutinin-horseradish peroxidase (WGA-HRP) was injected in the contralateral cervical enlargement (C5-T1). Both DY-labeled neuronal cell bodies and HRP-labeled STT terminal-like structures were visualized within single thalamic sections in each animal. Quantitative analysis of the positions and numbers of retrogradely labeled neurons and anterogradely labeled terminal fields reveal that: 1) ventral posterior lateral (VPL), ventral posterior inferior (VPI), and central lateral (CL), combined, receive 87% of spinothalamic inputs originating from the cervical enlargement; 2) these three nuclei contain over 91% of all thalamocortical neurons projecting to hSI that are likely to receive STT input; and 3) these putatively contacted neurons account for less than 24% of all thalamic projections to hSI. These results suggest that three distinct spinothalamocortical pathways are capable of relaying nociceptive information to the hand somatosensory cortex. Moreover, only a small portion of thalamocortical neurons are capable of relaying STT-derived nociceptive and thermal information to the primary somatosensory cortex.     

Interhemispheric reciprocal interaction between ventroposterolateral thalamic nuclei involving cortical relay neurons

Extracellular and intracellular recordings were performed in the somatosensory cortex of cats anesthetized with sodium pentobarbital. Commissural neurons identified antidromically from the corpus callosum (CC) were activated synaptically at latencies compatible with a monosynaptic delay following stimulation of the thalamic ventroposterolateral (VPL) nucleus. Corticothalamic cells identified antidromically from the VPL nucleus were synaptically driven at latencies compatible with either a mono- or disynaptic delay following CC stimulation. We propose that an interhemispheric reciprocal interaction exists between VPL nuclei via cortical relay cells involving commissural and corticothalamic neurons.     

Thalamic connections of two functional subdivisions of the somatosensory forepaw cerebral cortex of the raccoon

The purpose of this study was to compare the thalamic interconnectivities of 2 functionally distinct subdivisions of the somatosensory (Sml) forepaw cortex of the raccoon--the somatotopic subdivision representing the glabrous skin of the digits and the more heterogeneous subdivision representing the hairy skin and claws. Injections of HRP were made into one or the other functional subdivision of a specific digit subgyrus of Sml cortex in 10 adult raccoons. The distribution of HRP-labeled neurons and axon terminals in the thalamus revealed that the 2 sectors have different patterns of thalamic projections. The glabrous skin region of each cortical digit zone was interconnected with a specific crescent-shaped lamella of neurons that extended rostrocaudally through the ventral posterior lateral (VPL) nucleus and typically was separated from adjacent lamellae by small bundles of myelinated fibers. The VPL lamellae constituted relatively distinct digit subnuclei that were connected somatotopically with the glabrous subdivisions of the corresponding cortical digit areas. The projections were dense, topographic, and reciprocal; labeled neurons and axon terminals within a particular lamella overlapped considerably and tended to be arranged in clusters. In contrast, the heterogeneous region of each cortical digit zone was reciprocally connected with the somatotopically appropriate VPL digit subnucleus and with adjoining subnuclei as well. The projections were comparatively sparse, less topographic, and more widely distributed than those of the glabrous skin sectors; groups of HRP-positive neurons and terminals in VPL tended to straddle the borders of the appropriate lamella and extended into adjacent lamellae. Furthermore, small clusters of labeling were found in the dorsal, presumed kinesthetic region of VPL and in portions of the ventral posterior inferior nucleus and the posterior nucleus. These results indicate that the glabrous cortical subdivisions have precise, somatotopically organized connections with specific VPL subnuclei, whereas the heterogeneous cortical subdivisions have more diffuse and scattered connections with several subregions of VPL and other thalamic nuclei as well. These 2 thalamocortical projection patterns may account for many of the differing functional properties of neurons residing within the 2 cortical sectors. Finally, the convergent thalamic projections to the heterogeneous cortical regions could contribute, at least indirectly, to the functional reactivation that occurs within Sml cortex of the raccoon following peripheral nerve transection (Kelahan and Doetsch, 1984).     

Calbindin and parvalbumin cells in monkey VPL thalamic nucleus: distribution, laminar cortical projections, and relations to spinothalamic terminations.

The ventral posterior lateral nucleus (VPL) of the monkey thalamus was investigated by histochemical staining for cytochrome oxidase (CO) activity and by immunocytochemical staining for the calcium-binding proteins parvalbumin and 28 kDa calbindin. Anterograde and retrograde tracing experiments were used to correlate patterns of differential distribution of CO activity and of parvalbumin and calbindin cells with the terminations of spinothalamic tract fibers and with the types of cells projecting differentially to superficial and deeper layers of primary somatosensory cortex (SI). VPL is composed of CO-rich and CO-weak compartments. Cells are generally smaller in the CO-weak compartment. Parvalbumin-immunoreactive cells and parvalbumin-immunoreactive medial lemniscal fiber terminations are confined to the CO-rich compartment. Calbindin-immunoreactive cells are found in both the CO-rich and CO-weak compartments. The CO-weak compartment, containing only calbindin cells, forms isolated zones throughout VPL and expands as a cap covering the posterior surface of the ventral posterior medial nucleus (VPM). Spinothalamic tract terminations tend to be concentrated in the CO-weak compartment, especially in the posterior cap. Other CO-weak, parvalbumin-negative, calbindin-positive nuclei, including the posterior, ventral posterior inferior, and anterior pulvinar and the small-celled matrix of VPM are also associated with concentrations of spinothalamic and caudal trigeminothalamic terminations. Parvalbumin cells are consistently larger than calbindin cells and are retrogradely labeled only after injections of tracers in middle and deep layers of SI. The smaller calbindin cells are the only cells retrogradely labeled after placement of retrograde tracers that primarily involve layer I of SI. The compartmental organization of VPL is similar to but less rigid than that previously reported in VPM. VPL and VPM relay cells projecting to different layers of SI cortex can be distinguished by differential immunoreactivity for the two calcium-binding proteins. The small-celled, CO-weak, calbindin-positive zones of VPL and VPM appear to form part of a wider system of smaller thalamic neurons unconstrained by traditional nuclear boundaries that are preferentially the targets of spinothalamic and caudal trigeminal inputs, and that may have preferential access to layer I of SI.     

Functional changes in thalamic relay neurons after focal cerebral infarct: a study of unit recordings from VPL neurons after MCA occlusion in rats.

We evaluated neuronal and histological changes of thalamic neurons 1, 4, 7, and 14 days after middle cerebral artery (MCA) occlusion in rats. After the somatosensory evoked potentials (SEPs) were measured from the cerebral cortex, the thalamic relay neuronal activities were recorded with a glass microelectrode following repetitive electrical stimulation of the contralateral forepaw at frequencies ranging from 1 to 50 Hz. In approximately 95% of the occluded rats, the ipsilateral somatosensory cortex and/or the subcortical somatosensory pathway developed infarct, resulting in SEP loss. We evaluated unit data from rats with abolished SEPs. The average firing rate of the nucleus ventralis posterolateralis (VPL) neurons in response to 25 stimulations at 30 Hz was significantly reduced to 0.1 spike/stimulus 1 day after MCA occlusion. In sham-operated rats, the same stimulation produced 0.7 spike/stimulus. The firing rate recovered to 0.4 spike/stimulus at 30-Hz stimulation 4 and 7 days after occlusion. This was followed by resuppression (0.1 spike/stimulus) 14 days after occlusion. Histological study revealed some abnormal neurons in the ipsilateral thalamus 7 days after occlusion. We were unable to find normal-shaped neurons in the VPL 14 days after occlusion. The present study demonstrates that cortical infarct produces functional and morphologic changes that gradually and progressively affect the ipsilateral thalamus, although incomplete transient recovery of somatosensory transmission may occur.     

The effect of cortical ablation on afferent activity in the cat somatosensory system

The modulatory influence of primary S1 cortex upon afferent activity in the somatosensory system was examined in acute cats. Modulatory influences due both to prior afferent activity and efferent activity on peripherally evoked neural responses in thalamic n. ventralis posterolateralis (VPL) and the dorsal column nuclei (DCN) were analyzed. The right superficial radial nerve was stimulated with suprathreshold pulses applied randomly in time. Evoked activity was recorded from ipsilateral DCN, contralateral VPL, and contralateral S1 cortex before and after ablation of S1 cortex. The data were analyzed using a modified functional power series. The responses were characterized by first- and second-order kernels computed by cross-correlation. S1 ablation reduced or eliminated the second positive peak in the VPL response. Incomplete S1 ablation produced a graded effect on this peak. In addition, S1 ablation eliminated the negative notch on the leading edge of the response observed in the nucleus cuneatus. The results from VPL suggest that the second VPL positive peak is produced by a tonic S1 influence on another region of the central nervous system that is coupled to VPL, rather than by a direct VPL-cortical-VPL reflex loop. The results from the DCN confirm earlier studies suggesting a cuneate-cortical-cuneate reflex loop.     

Thalamic projection to motor area and area 3a of the cat cerebral cortex

The distributions of thalamic neurons projecting to the motor cortex and cortical area 3a were studied in cat by means of the retrograde double-labeling technique using Nuclear Yellow (NY) and Fast Blue (FB) as tracers. Following injection of NY and FB into the motor cortex and area 3a respectively, the NY-labeled neurons were found to be mainly located in ventrolateral (VL) nucleus and FB-labeled neurons in ventro-posterolateral nucleus (VPL). However, these two kinds of neurons were intermingled with each other in the border area between VL and VPL. A small number of neurons were double-labeled by both NY and FB. They were also distributed in the border area. Some of them could often be found in centromedian and parafascicular nuclei.     

Early Morphological Changes in the Thalamocortical Projection Onto the Parietal Cortex Following Ablation of the Motor Cortex in the Cat

Following a previous report that the cerebellar-induced cerebral response in the parietal cortex changes acutely after ablation of the frontal motor cortex, the present experiments tested whether morphological changes of the thalamo-parietal projection occur after ablation of the motor cortex. Anterograde and retrograde tracing with wheat germ agglutinin conjugated with horseradish peroxidase was used in intact and lesioned cats. The thalamocortical projection was labeled anterogradely by tracer injection into the thalamic ventral anterior and ventral lateral (VA-VL) nuclear complex that mainly relays the cerebello-cerebral projection, and thalamic neurons were labeled retrogradely by injection of the tracer into the parietal cortex. The labeled terminals in the parietal cortex of the intact animals were distributed densely in layer I and sparsely in layers III–IV, whereas those of the lesioned animals were distributed densely in layers I and III–IV. The distribution of the retrogradely labeled neurons after multiple tracer injections in layers III–IV of the parietal cortex was different in the intact and lesioned cats. In the intact animals, the labeled neurons were distributed sparsely in the central lateral nucleus and in the lateral posterior and pulvinar nuclear complex. In contrast, after ablation of the frontal cortex, the labeled neurons were also observed in the VA-VL nuclear complex. These differences between the intact and lesioned animals were detectable within 48 h after the lesion.     

Stimulus induced and seizure related changes in extracellular potassium concentration in cat thalamus (VPL).

Extracellular potassium activity (ak) and field potentials (fp) were measured in the nucleus ventro-postero-lateralis (VPL) thalami in order to assess the extent of thalamic participation in cortical seizure activity. Small increases (up to 0.7 mmole/l) or decreases (up to 0.2 mmole/l) in ak were induced by electrical stimulation of the contralateral forepaw. These changes in ak were spatially more limited than the simultaneously recorded fp. Similar observations were made during weak electrical stimulation of the somatosensory cortex and during interictal spikes in a cortical penicillin focus. Large and widespread increases in ak to levels of 11.6 mmoles/l and slow negative fps of 8 mV accompanied seizure generation either in a cortical penicillin focus or during intense repetitive electrical stimulation of the cortical surface. Subsequent to such increases ak fell to subnormal levels. The amplitudes and durations of such undershoots were correlated with the amplitudes of the preceding increases in ak. Sometimes thalamic seizures ceases before cortical epileptic episodes. This resulted in a decrease of cortical EEG amplitudes. After ablation of the sensorimotor cortex seizures in forepaw-VPL could be induced by stimulation of the somatosensory cortex. These results further support the conclusion that specific thalamic nuclei participate in seizure generation and may serve as a subcortical route of seizure spread.     

Expression of BCL-2 via adeno-associated virus vectors rescues thalamic neurons after visual cortex lesion in the adult rat

Lesions of the mammalian visual cortex cause the retrograde degeneration of the thalamic neurons projecting to the damaged cortex. The proto-oncogene bcl-2 is known to inhibit neuronal apoptosis induced by a variety of noxious stimuli and preserve the functional integrity of the injured cells. Here we have tested whether the overexpression of bcl-2 via adeno-associated virus (AAV) vectors is able to protect the neurons in the lateral geniculate nucleus after visual cortex ablation in adult rats. Recombinant AAV vectors encoding Bcl-2 (AAV-Bcl-2) or green fluorescent protein (AAV-GFP) as a control were stereotaxically injected into the geniculate. Three weeks after vector injection, the ipsilateral visual cortex was removed by aspiration, and cell survival was assessed 2 weeks later. We found that 20% of the geniculate neurons were transduced by the Bcl-2 vector. These cells were completely protected from death following cortical ablation. Delivery of AAV-GFP transduced an identical number of geniculate neurons but had no effect on cell survival after lesion. The total number of surviving geniculate neurons was found to be significantly higher in animals injected with AAV-Bcl-2 than in rats injected with AAV-GFP or in control lesioned rats. These data indicate that Bcl-2 gene therapy with AAV vectors represents an effective treatment to promote neuronal survival after central nervous system insults.     

Basic fibroblast growth factor prevents thalamic degeneration after cortical infarction

In the focal infarction model of the rat middle cerebral artery (MCA), the thalamus of the occluded side becomes gradually atrophic, mainly because of retrograde degeneration. We determined whether basic fibroblast growth factor (bFGF) administered intracisternally could prevent this thalamic atrophy. We occluded the left MCA through a small cranial opening, and animals were then divided into two groups. One group received intracisternal injections of recombinant bFGF (1 microgram dissolved in 0.1 ml of saline with 2% rat serum) starting 1 day after occlusion and repeated once a week to a total dose of 4 micrograms by four injections. The other group received vehicle solution by the same schedule. The animals were perfused and fixed at 28 days after occlusion, and histological examination was made at the level of the caudoputamen and thalamus. In the bFGF-treated rats, the area of the posterior ventral thalamus of the occluded side was 93% of that of the contralateral side, i.e., significantly larger than in the normal saline-treated rats (75%, p less than 0.01). The infarction size was not statistically different in the two groups. Microscopic observation indicated that normal-saline-treated animals showed shrinkage and disappearance of thalamic neurons, whereas bFGF-treated groups showed preservation of thalamic neurons. Computerized analysis of the cell size substantiated this observation. To assess the effect of bFGF on astrocytes, bFGF or vehicle solution was injected into normal rats, and their histology was evaluated at 1, 2, and 4 weeks after injection. The bFGF-injected group showed a significant increase in glial fibrillary acidic protein-positive astrocytes in the brain tissue facing the ventriculocisternal system.(ABSTRACT TRUNCATED AT 250 WORDS)     

Thalamic Input to Representations of the Teeth,Tongue, and Face in Somatosensory Area 3b of Macaque Monkeys

Representations of the parts of the oral cavity and face in somatosensory area 3b of macaque monkeys were identified with microelectrode recordings and injected with different neuroanatomical tracers to reveal patterns of thalamic projections to tongue, teeth, and other representations in primary somatosensory cortex. The locations of injection sites and resulting labeled neurons were further determined by relating sections processed to reveal tracers to those processed for myeloarchitecture in the cortex and multiple architectural stains in the thalamus. The ventroposterior medial subnucleus (VPM) for touch was identified as separate from the ventroposterior medial parvicellular nucleus (VPMpc) for taste by differential expression of several types of proteins. Our results revealed somatotopically matched projections from VPM to the part of 3b representing intra‐oral structures and the face. Retrogradely labeled cells resulting from injections in area 3b were also found in other thalamic nuclei including: anterior pulvinar (Pa), ventroposterior inferior (VPI), ventroposterior superior (VPS), ventroposterior lateral (VPL), ventral lateral (VL), center median (CM), central lateral (CL), and medial dorsal (MD). None of our injections, including those into the representation of the tongue, labeled neurons in VPMpc, the thalamic taste nucleus. Thus, area 3b does not appear to be involved in processing taste information from the thalamus. This result stands in contrast to those reported for New World monkeys. J. Comp. Neurol. 521:3954–3971, 2013. © 2013 Wiley Periodicals, Inc.     

Reversible and irreversible knockout of the ventroposterolateral thalamic nucleus measured by intracerebral SEP recordings in the rat brain--an aid to neuronavigation in small nuclei

Centrally active drugs are often hard to administer because of the blood brain barrier, and frequently high systemic doses are required to reach sufficient brain parenchyma concentrations, since these drugs are, additionally, diluted in the total blood volume. Moreover, topical administration via the systemic route is not possible. We here propose a technique for the local, quantitative deposition of active substances at defined intracerebral targets, e.g. the thalamic nuclei. We used a long micropipette and stereotactically advanced it to the desired coordinates under electrophysiological control. The pipette acted as both an electrode for intracerebral recordings and as a transportation means for the drug. The amplitude of intracerebral evoked potentials relayed by the thalamic nucleus to the sensorimotor cortex indicated the distance between the pipette tip and the neurons of the targeted nucleus. Data were obtained from anesthetized rats, where the micropipette was advanced towards the nucleus ventralis posterolateralis (VPL) during contralateral electrical forepaw stimulation and intracerebral recording of somatosensory evoked potentials. Within the VPL we either injected lidocaine or kainic acid, both resulting in an attenuation of the intracerebral as well as the cortical evoked potentials. This proposed tool may be useful for functional investigations of deep brain structures.