Cortical activation during Braille reading is influenced by early visual experience in subjects with severe visual disability: a correlational fMRI study.

Functional magnetic resonance imaging was performed on blind adults resting and reading Braille. The strongest activation was found in primary somatic sensory/motor cortex on both cortical hemispheres. Additional foci of activation were situated in the parietal, temporal, and occipital lobes where visual information is processed in sighted persons. The regions were differentiated most in the correlation of their time courses of activation with resting and reading. Differences in magnitude and expanse of activation were substantially less significant. Among the traditionally visual areas, the strength of correlation was greatest in posterior parietal cortex and moderate in occipitotemporal, lateral occipital, and primary visual cortex. It was low in secondary visual cortex as well as in dorsal and ventral inferior temporal cortex and posterior middle temporal cortex. Visual experience increased the strength of correlation in all regions except dorsal inferior temporal and posterior parietal cortex. The greatest statistically significant increase, i.e., approximately 30%, was in ventral inferior temporal and posterior middle temporal cortex. In these regions, words are analyzed semantically, which may be facilitated by visual experience. In contrast, visual experience resulted in a slight, insignificant diminution of the strength of correlation in dorsal inferior temporal cortex where language is analyzed phonetically. These findings affirm that posterior temporal regions are engaged in the processing of written language. Moreover, they suggest that this function is modified by early visual experience. Furthermore, visual experience significantly strengthened the correlation of activation and Braille reading in occipital regions traditionally involved in the processing of visual features and object recognition suggesting a role for visual imagery.

Regional differences in mechanisms of cerebral circulatory response to neuronal activation.

Vibrissal stimulation raises cerebral blood flow (CBF) in the ipsilateral spinal and principal sensory trigeminal nuclei and contralateral ventroposteromedial (VPM) thalamic nucleus and barrel cortex. To investigate possible roles of adenosine and nitric oxide (NO) in these increases, local CBF was determined during unilateral vibrissal stimulation in unanesthetized rats after adenosine receptor blockade with caffeine or NO synthase inhibition with N(G)-nitro-L-arginine methyl ester (L-NAME) or 7-nitroindazole (7-NI). Caffeine lowered baseline CBF in all structures but reduced the percent increase during stimulation only in the two trigeminal nuclei. L-NAME and 7-NI lowered baseline CBF but reduced the percent increase during stimulation only in the higher stations of this sensory pathway, i.e., L-NAME in the VPM nucleus and 7-NI in both the VPM nucleus and barrel cortex. Combinations of caffeine with 7-NI or L-NAME did not have additive effects, and none alone or in combination completely eliminated functional activation of CBF. These results suggest that caffeine-sensitive and NO-dependent mechanisms are involved but with different regional distributions, and neither fully accounts for the functional activation of CBF.

Microglia, astrocytes, and macrophages react differentially to central and peripheral lesions in the developing and mature rat whisker-to-barrel pathway: a study using immunohistochemistry for lipocortin1, phosphotyrosine, s100 beta, and mannose receptors.

Adult and neonatal rats were subjected to transection of the left infraorbital nerve or ablation of the left parietal cortex. The ensuing glial reaction in the whisker-to-barrel pathway was studied with immunohistochemistry for Lipocortin1- (LC1+), phosphotyrosine- (PY+), S100 beta- (S100 beta+), and mannose receptor- (MR+) immunoreactive microglia, astrocytes, and macrophages. Four days after infraorbital nerve transection in adult rats, LC1+ and PY+ microglia were prominently increased in the trigeminal sensory brain-stem nuclei on the deafferented side compared with the intact side. Changes were negligible at the second synapse of the pathway, i.e., the thalamic ventroposterior medial nucleus. Cortical ablation in adults led to an increase in microglia in the ipsilateral ventroposterior medial nucleus that reciprocally connects with the ablated cortex. Moreover, microglial reactions occurred in the contralateral trigeminal sensory brain-stem nuclei in which corticofugal projections from the ablated cortex terminate. S100 beta+ astrocytes, in contrast, appeared unaltered after both types of lesion in adults. In neonates, LC1+, PY+, and S100 beta+ cells did not have the adult morphology of microglia or astrocytes. Four days after nerve transection, LC1+ and PY+ cells were sparse and remained unchanged. In contrast, S100 beta+ cells substantially increased in the deafferented trigeminal brain-stem nuclei. Four days after cortical ablation in neonates, LC1+, PY+, and S100 beta+ cells had accumulated in the deprived thalamus. In contrast to adults, many of these cells were MR+ macrophages. In the deprived brain-stem, only S100 beta+ cells increased and none were macrophages. Therefore, macrophages do not appear to stem from microglia, and neonatal LC1+, PY+, and S100 beta+ cells may possess functions different from those in adults.

Metabolic activity in optic tectum during regeneration of retina in adult goldfish.

Retinal and visual function returns following retinal destruction by ouabain in adult goldfish (Carassius auratus). Although the precise cellular mechanisms are unclear, the ability to regenerate CNS neurons and connections that subsequently sustain visual behavior is remarkable, especially for an adult vertebrate. In this paper, we ask whether visual stimulation via new retinal cells can activate existing cells in the optic tectum, which normally receives the largest retinal projection in this species. The right eyes of adult goldfish were injected with ouabain. After 1-18 weeks the conscious, freely moving fish were exposed to spatially and temporally varying visual stimuli and the resulting tectal metabolic activity was determined with the autoradiographic deoxyglucose method. In normal controls without lesions, visual stimulation produced equally strong metabolic activity in both tectal hemispheres, peaking in the layer where most retinotectal projections terminate (N = 6). One week after ouabain injection, metabolic activity in the contralateral, deprived tectum was dramatically reduced (N = 5), closely resembling the effect of unilateral ocular enucleation (N = 5). However, 9-18 weeks after ouabain injection, metabolic activity in the deprived tectum recovered to a level that was statistically indistinguishable from normal controls (N = 6). These findings suggest that, after a comprehensive cytotoxic lesion of the retina, regenerated ganglion cells not only establish new connections with the preexisting optic tectum, but also effectively transmit visual information they receive from newly generated photoreceptors to the "old" tectum.

Differential contributions of magnocellular and parvocellular pathways to the contrast response of neurons in bush baby primary visual cortex (V1).

How neurons in the primary visual cortex (V1) of primates process parallel inputs from the magnocellular (M) and parvocellular (P) layers of the lateral geniculate nucleus (LGN) is not completely understood. To investigate whether signals from the two pathways are integrated in the cortex, we recorded contrast-response functions (CRFs) from 20 bush baby V1 neurons before, during, and after pharmacologically inactivating neural activity in either the contralateral LGN M or P layers. Inactivating the M layer reduced the responses of V1 neurons (n = 10) to all stimulus contrasts and significantly elevated (t = 8.15, P < 0.01) their average contrast threshold from 8.04 (+/- 4.1)% contrast to 22.46 (+/- 6.28)% contrast. M layer inactivation also significantly reduced (t = 4.06, P < 0.01) the average peak response amplitude. Inactivating the P layer did not elevate the average contrast threshold of V1 neurons (n = 10), but significantly reduced (t = 4.34, P < 0.01) their average peak response amplitude. These data demonstrate that input from the M pathway can account for the responses of V1 neurons to low stimulus contrasts and also contributes to responses to high stimulus contrasts. The P pathway appears to influence mainly the responses of V1 neurons to high stimulus contrasts. None of the cells in our sample, which included cells in all output layers of V1, appeared to receive input from only one pathway. These findings support the view that many V1 neurons integrate information about stimulus contrast carried by the LGN M and P pathways.

Plasticity of cerebral metabolic whisker maps in adult mice after whisker follicle removal--I. Modifications in barrel cortex coincide with reorganization of follicular innervation.

We investigated alterations of the metabolic whisker map of barrel cortex after the removal of the follicles of left whiskers C1, C2 and C3 in adult albino mice. The quantitative autoradiographic [14C]deoxyglucose method was used to measure local cerebral metabolic rates for glucose in barrel cortex of mice two, four, eight, 64, 160 and 250 days after the lesion. Metabolic rates were measured in three groups of animals: (i) mice with lesions that had all whiskers clipped; (ii) mice with lesions that had left whiskers B1-3 and D1-3 stimulated; and (iii) unoperated mice that had left whiskers B1-3 and D1-3 stimulated. Compared with the metabolic rates in barrels C1-3 of stimulated unoperated mice, barrels C1-3 of stimulated mice with lesions showed the first discernible increase in metabolic rate four days after the lesion. The increase became distinct at 64 days, but attained statistical significance only approximately 160 days after the lesion. The lesion per se, i.e. without whisker stimulation, caused only a small increase in metabolic rate in barrels C1-3 accounting for not more than one fourth of the increase in metabolic rate measured after whisker deflection. The removal of whisker follicles C1-3 led, therefore, to an enlargement of the metabolic representations of the adjacent whiskers into the barrels deprived by the lesion. The gradual consolidation of the alterations of the metabolic whisker map coincided with the regeneration of follicular nerves in the whiskerpad. We detected anomalous deep nerves innervating follicles surrounding the lesion at approximately 64 days, and the number of myelinated nerve fibres in the deep nerves of these follicles was increasing with increasing time after the lesion. The coincidence of peripheral and central change suggests that the reorganization of the innervation of the sensory periphery plays an important role in the persistent alterations of the cortical somatotopy in adults following a lesion in the sensory periphery.

Plasticity of cerebral metabolic whisker maps in adult mice after whisker follicle removal--II. Modifications in the subcortical somatosensory system.

The follicles of whiskers C1-3 were removed from the left side of the snout of adult mice. Adjacent whiskers B1-3 and D1-3 were stimulated while local rates of glucose utilization were measured with the [14C]2-deoxyglucose method two, four, eight, 64, 160 and approximately 250 days after follicle removal. Local metabolic activity in the trigeminal sensory brainstem and somatosensory thalamus was compared with that of unoperated mice with the same stimulation and of mice with the same lesion that had all whiskers clipped. Actual rates of glucose utilization were measured in brainstem subnuclei caudalis and interpolaris whereas metabolic activation was only assessable by colour-coded imaging in brainstem nucleus principalis and in the thalamic ventrobasal complex. Whisker stimulation activated the somatotopically appropriate loci in brainstem and thalamus. In addition, the territory deprived by follicle removal was metabolically activated in subnuclei caudalis and interpolaris at all time intervals examined. The activation was statistically significant in subnucleus interpolaris at two days, indicating that the metabolic representations of whiskers neighbouring the lesion rapidly expanded into the deprived territory. Nucleus principalis showed a broad metabolic activation at two and four days that was absent at the longer time intervals examined. Instead, at approximately 250 days the metabolic representations of the whiskers adjacent to the lesion were enlarged into the deprived territory as in the subnuclei. Since metabolic whisker representation in the ventrobasal complex appeared to have changed in the same fashion, follicle removal apparently resulted in congruent modifications of the whisker map in the three nuclei of termination as well as in the thalamic relay at the longest time interval examined. Since metabolic responsiveness of the deprived barrels in barrel cortex of the same animals increased statistically significantly only several months after follicle removal, the novel neural responses in the brainstem were not effectively transmitted to barrel cortex immediately and the slowly evolving cortical modifications are more likely to be associated with regrowth of the connectivity of primary neurons. By contrast, unmasking of hitherto suppressed inputs may underlie the early expansion of metabolic whisker representation in the brainstem.

Infraorbital nerve transection and whisker follicle removal in adult rats affect microglia and astrocytes in the trigeminal brainstem. A study with lipocortin1- and S100beta-immunohistochemistry.

Transections of the infraorbital nerve in adult rats resulted in progressive alterations of microglia identified by Lipocortinl immunoreactivity at the sites where the primary afferents terminate, i.e. in the trigeminal brainstem sensory nuclei. Microglia proliferated three- to four-fold. Their cell bodies enlarged and their processes thickened. Microglial responses were similar to the removal of whisker follicles. However, they were restricted to discrete nuclear subregions that matched with the known whisker somatotopy. Astrocytes identified by S100beta immunoreactivity showed minor increases in size and in population density. No microglial or astrocytic reactions were found in the second and third synaptic relays of the somatosensory pathway. Because both types of lesion reportedly lead to the reorganization of primary afferents, our results establish the two experimental designs as valuable tools to elucidate the role of microglia and Lipocortin1 in adult brain plasticity.

Stimulus-dependent expression of immediate-early genes in rat somatosensory cortex.

Using in situ hybridization histochemistry, we investigated the effects of whisker stimulation in freely moving rats on the expression of the immediate-early genes zif 268 and c-fos in the barrel cortex. Whiskers equipped with metal filaments were stimulated for 5-15 minutes with a pulsating magnetic field. Such whisker stimulation resulted in increased zif 268 and c-fos expression that was largely restricted to radial columns across the barrels representing the stimulated whiskers. In these columns, gene expression was elevated, to a variable degree, across the entire cortical thickness, with a distinct maximum in layer IV. The magnitude of gene expression in a barrel was proportional to the intensity of stimulation. Cellular analysis confirmed that whisker stimulation induced c-fos expression mostly in stellate cells of layer IV and in some pyramidal cells in other layers. However, even after the strongest stimulation, only subsets of neurons were labeled in all layers, suggesting that subpopulations of neurons with a differential genomic response to sensory input exist. These results indicate that the expression of these immediate-early genes is regulated by normal neuronal activity under physiological conditions, and suggest that such gene regulation is an integral part of neuronal function.

Plasticity of metabolic whisker maps in somatosensory brainstem and thalamus of mice with neonatal lesions of whisker follicles.

We employed the autoradiographic deoxyglucose method to study metabolic whisker maps of the adult mouse somatosensory brainstem and thalamus after the neonatal removal of left whisker follicles C1, C2 and C3. Left whiskers B1-3 and D1-3 were deflected to metabolically activate the somatosensory pathway. Unoperated mice that were stimulated in the same fashion served as controls. Whisker stimulation resulted in an ipsilateral increase in metabolic activity in the three trigeminal brainstem structures in which the whiskers are represented topologically by segments of high cytochrome oxidase activity, i.e. subnucleus caudalis, subnucleus interpolaris and nucleus principalis. In the two subnuclei of mice with lesions and of controls, there was an increase in metabolic activity of the representations of the deflected whiskers, whereas the metabolic activity of representations A1-3 and E1-3 was low. Apart from these similarities, the metabolic activation of the representations originally representing whiskers C1-3 was remarkably greater in mice with lesions than in controls. This increase reached statistical significance in subnucleus caudalis and approached statistical significance in subnucleus interpolaris. In nucleus principalis the deprived territory was only partially activated and the degree of metabolic activation was less than in the subnuclei. In the thalamic ventrobasal complex of mice with lesions metabolic activity was unpatterned whereas two areas of metabolic activation were distinct in controls. Hence, the removal of whisker follicles in newborn mice resulted in the suppression of localized metabolic responses to whisker stimulation in the thalamus, whereas in the brainstem stimulus-related activity was prominent and the deprived territory became responsive to the stimulation of whisker follicles adjacent to the lesion. Apparently, the modification of the whisker representation at the first synapse of the pathway induces a diminution of localized responsivity in the thalamus.

Whisker follicle removal affects somatotopy and innervation of other follicles in adult mice.

The present study shows that in the whisker-to-barrel pathway of adult mice surgical removal of three whisker follicles leads to the expansion of the functional cortical representation of the whiskers adjacent to the lesion into the deprived barrels within 8 months. Concomitant with this enlargement, there is an increase in follicular innervation of the corresponding whiskers. This reorganization of the peripheral innervation may be important for the observed reshaping of cortical somatotopy.

Increases in local cerebral blood flow associated with somatosensory activation are not mediated by NO.

Effects of inhibition of nitric oxide (NO) synthase by NG-nitro-L-arginine methyl ester (L-NAME) on the increases in local cerebral blood flow (LCBF) produced in the whisker-to-barrel sensory pathway by vibrissal stimulation were studied in conscious rats with the autoradiographic iodo[14C]antipyrine method. Unilateral whisker stroking increased LCBF in the ipsilateral trigeminal spinal and principal sensory nuclei, contralateral ventral posteromedial thalamic nucleus, and contralateral somatosensory barrel cortex. Intravenous L-NAME (30 mg/kg) lowered baseline LCBF without altering the percent increases due to stimulation. Intracisternal infusions of L-NAME in doses about 10 times the molar content of free arginine in brain inhibited brain NO synthesis activity by 88%, but the percent augmentations of LCBF by stimulation remained unchanged. Chronic treatment with L-NAME (50 mg/kg ip twice daily for 4 days) inhibited NO synthase activity in brain by 84% but also failed to reduce the percent increases in LCBF due to stimulation. These results indicate that NO does not mediate the increases in LCBF associated with functional activation.

Maturation of the neuronal metabolic response to vibrissa stimulation in the developing whisker-to-barrel pathway of the mouse.

We examined functional maturation in the mouse whisker-to-barrel pathway from P2 (P0 is the day of birth) to adulthood using the autoradiographic deoxyglucose (DG) method. After intraperitoneal DG injection, left whiskers C1-3 and E1 were stimulated. Sections were cut transversely through the brainstem, and coronally or tangentially through the parietal cortex. After autoradiography, the sections were stained for Nissl or for cytochrome oxidase (CO) activity. In subnuclei caudalis and interpolaris of the spinal trigeminal nucleus ipsilateral to stimulation, DG uptake evoked by the deflection of whiskers C1-3 was present at P2; in subnucleus oralis, nucleus principalis and the contralateral nucleus ventrobasalis of the thalamus, at P4; and in the contralateral barrel cortex, at P7. The first stimulus-dependent DG uptake appeared a few days after the appearance of whisker-related patterns seen in the CO- or Nissl-stained sections. In subnuclei caudalis and interpolaris, areas of stimulus-dependent DG uptake were initially larger than the CO segments representing the stimulated whiskers. Later, areas of stimulus-dependent DG uptake and CO segments matched well. DG uptake evoked by the stimulation of whisker E1 appeared 2-3 days later than that evoked by stimulation of whiskers C1-3. In nucleus principalis, one large area of stimulus-dependent DG uptake covered the representations of the caudal whiskers of all five rows--an observation made at all ages studied. In thalamus, stimulus-dependent DG uptake was found laterally in nucleus ventrobasalis. In barrel cortex, at P7, stimulus-dependent DG uptake was restricted to layers III and IV, but covered more barrels than whiskers stimulated. At P9, a second spot of high DG uptake was seen in deep layer V in register with that in layers III and IV. From P10 onwards, stimulus-dependent DG uptake stretched from layer II to layer VI, and in layer IV, in which it was highest, it was restricted to the barrels C1-3 and E1. In all stations, stimulus-dependent DG uptake decreased in magnitude after P10. While the onset of stimulus-dependent DG uptake is the result of the establishment of functional projections up to that station, the subsequent changes in size of the responding areas may well be due to the partial elimination of terminals, the maturation of local inhibitory circuits, and/or the development of cortical projections to the nuclei of termination and to the thalamic relay.

Mouse barrel cortex functionally compensates for deprivation produced by neonatal lesion of whisker follicles.

In the murine somatosensory pathway, the metabolic whisker map in barrel cortex derived with the autoradiographic deoxyglucose method is spatially in register with the morphological whisker map represented by the barrels. The barrel cortex of adult mice, in which we had removed three whisker follicles from the middle row of whiskers shortly after birth, contained a disorganized zone surrounded by enlarged barrels with partially disrupted borders. With the fully quantitative autoradiographic deoxyglucose method, we investigated in barrel cortex of such mice the magnitude and the pattern of metabolic responses evoked by the deflection of whiskers. Most remarkably, the simultaneous deflection of six whiskers neighbouring the lesion activated not only the territory of the corresponding barrels, but also the unspecifiable area intercalated between the clearly identified barrels. This metabolic whisker map, unpredictable from the morphological 'barrel' map, may reflect a functional compensation for the deficit in input.

Comparison of rates of local cerebral glucose utilization determined with deoxy[1-14C]glucose and deoxy[6-14C]glucose.

The activity of the pentose phosphate shunt pathway in brain is thought to be linked to neurotransmitter metabolism, glutathione reduction, and synthetic pathways requiring NADPH. There is currently no method available to assess flux of glucose through the pentose phosphate pathway in localized regions of the brain of conscious animals in vivo. Because metabolites of deoxy[1-14C]glucose are lost from brain when the experimental period of the deoxy[14C]glucose method exceeds 45 min, the possibility was considered that the loss reflected activity of this shunt pathway and that this hexose might be used to assay regional pentose phosphate shunt pathway activity in brain. Decarboxylation of deoxy[1-14C]glucose by brain extracts was detected in vitro, and small quantities of 14C were recovered in the 6-phosphodeoxygluconate fraction when deoxy[14C]glucose metabolites were isolated from freeze-blown brains and separated by HPLC. Local rates of glucose utilization determined with deoxy[1-14C]glucose and deoxy[6-14C]glucose were, however, similar in 20 brain structures at 45, 60, 90, and 120 min after the pulse, indicating that the rate of loss of 14CO2 from deoxy[1-14C]glucose-6-phosphate in normal adult rat brain is too low to permit assay pentose phosphate shunt activity in vivo. Further metabolism of deoxy[1-14]glucose-6-phosphate via this pathway does not interfere during routine use of the deoxyglucose method or explain the progressive decrease in calculated metabolic rate when the experimental period exceeds 45 min.

Plasticity in the barrel cortex of the adult mouse: effects of chronic stimulation upon deoxyglucose uptake in the behaving animal.

We investigated experience-dependent regulation of neuronal activity in the whisker-to-barrel pathway of the adult mouse using the autoradiographic deoxyglucose (DG) method. Animals were placed in the Lausanne whisker stimulator, and three of their whisker follicles were passively stimulated for a period of 1, 2, or 4 d. After this period, mice received a dose of DG and were placed in a cage containing a pile of wooden sticks. Mice that underwent the same procedure except the passive stimulation served as controls. Patterns of stimulus-dependent DG uptake were studied in the somatosensory cortex and in the trigeminal sensory brainstem complex. DG uptake in the barrels corresponding to the passively stimulated whiskers was lower than in controls. This decrease was present throughout the radial extent of a barrel column and was observed in all passively stimulated animals. Quantitative analysis confirmed these observations and, furthermore, showed a statistically significant decrease in DG uptake in barrels neighboring the passively stimulated ones. In half of the animals, the brainstem nuclei showed a decreased DG uptake in the representation of the passively stimulated whiskers, whereas in the other animals the pattern of DG uptake was as in controls. We propose that the signs of cortical plasticity are due to a mechanism that operates in layer IV and functions as a gate for peripheral sensory activity to enter cortical circuitry.

[Gabexate mesilate in the treatment of acute pancreatitis. Results of a Hannover multicenter double-blind study with 50 patients]. / Gabexat mesilat in der Behandlung der akuten Pankreatitis. Ergebnisse der hannoverschen multizentrischen Doppelblindstudie mit 50 Patienten.

We investigated the effect of a new synthetic protease- and phospholipase A2-inhibitor gabexate mesilate (FOY) in a multicenter (6 hospitals in Hannover and vicinity) double-blind study on the clinical course of acute pancreatitis. 50 patients were randomized into two subgroups. One group was treated with 3 X 300 mgs of gabexate mesilate per day for 9 days as a continuous intravenous infusion, the control group received placebo. There was no difference in these two groups regarding age and sex, but there was a discrepancy concerning the severity (stage I-IV) of the acute pancreatitis at the onset of treatment. More of the patients in the gabexate mesilate-group had severe disease on admission to hospital. Of the 7 patients (14%) who died, 5 were in the gabexate mesilate-group whereas only 2 were in the placebo group. This difference in the mortality rate is not significant. There was, however, a significant difference at the 5% level between the verum-group and the control group concerning the decline in alpha-amylase activity in serum and the number of complications. The difference was greatest in alcohol induced acute pancreatitis. A non-parametric test showed a significant reduction in hospitalisation time in the gabexate mesilate-group. Due to the small number of patients and the inhomogeneous clinical course of the acute pancreatitis a definite conclusion concerning the effect of gabexate mesilate on the clinical course of acute pancreatitis is not possible. Further studies with a much greater number of patients and more homogeneous groups with respect to the severity of the acute pancreatitis at the onset of the therapy with gabexate mesilate or placebo are necessary.

A deoxyglucose study on auditory responses in the bat Rhinolophus rouxi.

Responses in the auditory system of the echolocating bat Rhinolophus rouxi were mapped with [3H]deoxyglucose (DG) autoradiography. After unilateral stimulation with the constant frequency component of the individual bat's echolocation call, stimulus-related DG uptake occurred contralaterally in the dorsolateral and the ventromedial parts of the inferior colliculus, in the ventral medial geniculate body and in the contralateral neocortex. Unilateral 50 kHz-stimulation gave rise to a weakly activated lamina in the dorsolateral contralateral inferior colliculus. The distribution of frequency-evoked DG uptake within the inferior colliculus agrees with electrophysiological findings on an acoustic fovea in the auditory pathway of echolocating bats.

A magnetic device to stimulate selected whiskers of freely moving or restrained small rodents: its application in a deoxyglucose study.

After receiving an intraperitoneal injection of [14C]2-deoxy-D-glucose (2-DG), a total of 28 mice which had pieces of metal wire glued to certain whiskers (all others were clipped) were exposed to magnetic field bursts. The stimulated whiskers were B1 (freely moving mice, set I) or whiskers C1-3 and E1 (restrained mice, set II) on the left side. In set I, stimulated mice were compared with animals of various control groups. Autoradiography demonstrated an activation of columnar shape overlying the presumed corresponding barrel contralateral to stimulation; in a part of the ipsilateral barrelfield, 2-DG uptake was depressed significantly. In the subnuclei caudalis and interpolaris of the trigeminal brainstem complex a spot of activation was observed ipsilaterally but there was no depression contralaterally. Whereas several animals of the control groups showed some aspects of these responses, they were consistent only in stimulated mice. In set II, animals received stimulation with different intensities. 2-DG uptake was higher in barrels C1-3 than in E1. It increased with increasing intensity. The same observations were made in two nuclei of termination. The device we describe here can be used to study stimulus-specific responses at various levels of the somatosensory pathway.

The central auditory pathway of the gerbil Psammomys obesus: a deoxyglucose study.

The tonotopic organization of the central auditory pathway of the gerbil Psammomys obesus was mapped with deoxyglucose autoradiography under anesthesia. Animals, injected with tritiated deoxyglucose, were stimulated with 0.8, 2.5 and 17.0 kHz tone bursts monaurally in the free field and compared with non-stimulated controls. Apart from the medial geniculate body, all auditory structures showed sound-specific uptake of tracer. Frequency selective tracer accumulation could not be discriminated in the auditory cortex, the nuclei of the lateral lemniscus or the superior olivary complex. Isofrequency laminae could be determined most precisely in the dorsal cochlear nucleus and the central nucleus of the inferior colliculus. About half the mass of each of these nuclei is devoted to the processing of sound below 2.5 kHz. This disproportionately large representation of low frequencies matches the very high sensitivity of the peripheral auditory system in that range.