Response properties of neurons in the inferior colliculus of the monaurally deafened ferret to acoustic stimulation of the intact ear

Response properties of neurons in the central nucleus of the inferior colliculus (ICC) were investigated after unilateral cochlear removal at various ages during infancy. Nineteen ferrets had the right cochlea surgically ablated, either in adulthood or on postnatal day (P) 5, 25, or 40, 3-18 mo before recording. Adult ablations were made on the same day as ("acute," n = 3), or 2-3 mo before ("chronic," n = 3), recording. Two ferrets were left binaurally intact. Single-unit (n = 702) and multiunit (n = 1,819) recordings were made in the ICC of barbiturate-anesthetized ferrets ipsilateral (all ages) or contralateral (P5 and acute adult only) to the intact ear. In binaurally intact animals, tonal stimulation of the contralateral ear evoked excitatory activity at the majority (94%) of recording loci, whereas stimulation of the ipsilateral ear evoked activity at only 33% of recording loci. In acutely ablated animals, the majority of contralateral (90%) and ipsilateral (70%) loci were excited by tonal stimulation of the intact ear. In chronically ablated animals, 80-90% of loci were excited by ipsilateral stimulation. Single-unit thresholds were generally higher for low-best frequency (BF) than for high-BF units, and higher in the ipsilateral than in the contralateral ICC. Analysis of covariance showed highly significant differences between all of the ipsilateral and contralateral groups, but no effects of age at ablation or survival time following ablation, other than that the group ablated at P25 had higher mean ipsilateral thresholds than the groups ablated at P5 or, acutely, in adulthood. Cochlear ablation at P5, 25, or 40 resulted in a significant increase in dynamic ranges of ipsilateral ICC unit rate-intensity functions relative to acutely ablated animals. Dynamic ranges of units in the contralateral ICC of P5-ablated ferrets were also significantly increased compared with those of acutely ablated animals. Cochlear ablation at P5, 25, or 40 resulted in a significant increase in single-unit spontaneous discharge rates in the ICC ipsilateral but not contralateral (P5 only) to the intact ear. These data show that unilateral cochlear removal in adult ferrets leads to a rapid and dramatic increase in the proportion of neurons in the ICC ipsilateral to the intact ear that is excited by acoustic stimulation of that ear. In addition, the data confirm that, in ferrets, cochlear removal in infancy leads to a further increase in responsiveness of individual neurons in the ipsilateral ICC. Finally, the data show that responses in the ICC contralateral to the intact ear are largely but not completely unchanged by unilateral cochlear removal.     

Long-lasting enhanced expression in the rat hippocampus of NMDAR1 splice variants in a kainate model of epilepsy

Chronic epilepsy is associated with increased excitability which may result from abnormal glutamatergic synaptic transmission involving altered properties of N-methyl-D-aspartate (NMDA) receptors. To date two gene families encoding NMDA receptor subunits have been cloned, NR1 and NR2. Eight NR1 mRNAs are generated by alternative splicing of exons 5, 21 and 22; the NR1-1 to NR1-4 C-terminal variants exist in the a or b version depending on the presence or absence of the domain encoded by exon 5. Epilepsy was induced in rats by unilateral intra-amygdalar injection of kainate and animals were killed from 6 h to 4 months following the injection. Increased NR1 mRNA levels were observed during status epilepticus (6-24 h after the injection), both psilateral and contralateral, while a second wave of NMDAR1 mRNA increase occurred in chronic epileptic animals, between 21 days and 4 months following kainate injection. Our data show: (i) a permanent increase of the NR1-2a and NR1-2b mRNA species (containing exon 22) in all hippocampal fields, both ipsilateral and contralateral, and (ii) an increase of the NR1-3 (a and b) mRNAs (containing exon 21) in the ipsilateral CA1, and NR1-3a mRNA in the ipsilateral dentate gyrus. No long-term changes were observed for the NR1-1 and NR14 splice variants. In the ipsilateral CA3 area a globally decreased mRNA expression was associated with neuronal loss. A possible contribution to the maintenance of the epileptic state by an increased expression of NMDA receptors is discussed.     

The relationship between stature, growth, and short-term changes in height and weight in normal prepubertal children

Electrical stimulation of the superior laryngeal nerve (SLN) can elicit reflex responses in the cricothyroid (CT) and thyroarytenoid (TA) muscles. We made bilateral recordings of the responses evoked in these muscles in piglets by the stimulation of either the right or the left superior laryngeal nerve (SLN). The stimulus intensity was gradually increased to study the "persistence" of the responses. We observed a direct, ipsilateral response in the CT muscle, and reflex, ipsilateral and crossed responses in both CT and TA muscles. The ipsilateral or contralateral responses obtained in TA muscles, following stimulation of the left SLN, were significantly delayed in comparison with those evoked by stimulation of the right SLN. This delay cannot be explained by the difference in length between the right and the left recurrent laryngeal nerves, but rather by an asymmetry in the sensory afferent pathway. The functional significance of this observation remains to be determined.     

A genetic propensity to high factor VII is not associated with the risk of myocardial infarction in men

Interictal brain SPECT is useful for the localization of a seizure focus. Concomitant hypoperfusion of the ipsilateral thalamus on interictal SPECT has been noted for temporal lobe epilepsy. In this study, we aimed to evaluate the prevalence of thalamic hypoperfusion ipsilateral to temporal hypoperfusion (ipsilateral thalamic hypoperfusion) and to assess the usefulness of this finding for the lateralization of epileptic foci on interictal SPECT for temporal lobe epilepsy patients. METHODS: Forty-six patients with refractory temporal lobe epilepsy underwent interictal brain SPECT after intravenous injection of 555-740 MBq of 99mTc-ECD. Perfusion impairments in the brain, especially the temporal lobe and thalamus, were evaluated. The localization of seizure foci was determined in conjunction with scalp, ictal and cortical electroencephalography, MRI and clinical outcomes. Ictal SPECT was performed for 5 of the 12 patients. RESULTS: Concomitant decreased perfusion in both the temporal lobe and the ipsilateral thalamus was observed for 12 (26%) of 46 temporal lobe epilepsy patients on interictal brain SPECT. Seven patients showed hypoperfusion in the left temporal lobe and ipsilateral thalamus. Five patients showed hypoperfusion in the right temporal lobe and ipsilateral thalamus. In addition, hypoperfusion in the ipsilateral basal ganglia (ten patients) or contralateral cerebellum (four patients) was observed. CONCLUSION: Ipsilateral thalamic hypoperfusion is not uncommon in temporal lobe epilepsy. The exact mechanism causing ipsilateral thalamic hypoperfusion is uncertain; however, corticothalamic diaschisis may be an important factor. This finding may aid in the lateralization of seizure foci on interictal brain SPECT.     

Binaural inhibition is important in shaping the free-field frequency selectivity of single neurons in the inferior colliculus

1. We have shown previously that under free-field stimulation in the frontal field, frequency selectivity of the majority of inferior colliculus (IC) neurons became sharper when the loudspeaker was shifted to ipsilateral azimuths. These results indicated that binaural inhibition may be responsible for the direction-dependent sharpening of frequency selectivity. To test the above hypothesis directly, we investigated the frequency selectivity of IC neurons under several conditions: monaural stimulation using a semiclosed acoustical stimulation system, binaural stimulation dichotically also using a semiclosed system, free-field stimulation from different azimuths, and free-field stimulation when the ipsilateral ear was occluded monaurally (coated with a thick layer of petroleum jelly, which effectively attenuated acoustic input to this ear). 2. The binaural interaction pattern of 98 IC neurons of northern leopard frogs (Rana pipiens pipiens) were evaluated; of these neurons, there were 34 EE and 64 EO neurons. The majority of IC neurons (92 of 98) showed some degree of binaural inhibition (i.e., showing diminished response when the ipsilateral and contralateral ears were stimulated simultaneously) whether they were designated as EE or EO; these IC neurons thus were classified as EE-I or EO-I. Neurons were classified as exhibiting strong inhibition if the ILD function showed a pronounced response decrement, i.e., a decrease of > or = 50% of the response to monaural stimulation of the contralateral ear. Those neurons that showed smaller response decrements (decrease was > or = 25% but < 50%) were designated as showing weak inhibition. Most of these EE-I and EO-I neurons (n = 68) showed strong binaural inhibition. 3. In agreement with results from our earlier studies, frequency threshold curves (FTCs) of IC neurons were altered by sound azimuth. Independent of binaural interaction pattern, most IC neurons (59 of 98) showed a narrowing of the FTC as sound direction was changed from contralateral 90 deg (c90 degrees) to ipsilateral 90 deg (i90 degrees). IC neurons that exhibited the largest direction-dependent changes in frequency selectivity were typically those that displayed stronger binaural inhibition. Occlusion of the ipsilateral ear, which reduced the strength of binaural inhibition by this ear, abolished direction-dependent frequency selectivity. 4. FTCs of IC neurons that exhibited little to moderate direction-dependent effects on frequency selectivity were associated typically with neurons that displayed weak binaural inhibition. Associated with this weak binaural inhibition, central neural responses under monaural occlusion also displayed only small effects; the FTCs were only slightly broader than those derived in the intact condition, and as before, the experimental manipulation resulted in abolishment of direction-dependent frequency selectivity. 5. In contrast to most IC neurons, which showed direction-dependent narrowing of the FTC, about one-third (34 of 98) of IC neurons studied showed a broadening of the FTC when sound direction was shifted to ipsilateral azimuths. Interestingly, for 90% of these 34 neurons, monaural occlusion resulted in narrowing of the bandwidth at each azimuth instead of broadening of the FTC bandwidth. We have evidence to suggest that this direction-dependent broadening is actually a consequence of a truncation or loss of the tip of the FTC derived at c90 degrees, which results from strong binaural inhibition. 6. To compare the frequency threshold tuning in response to monaural stimulation of each ear with free-field FTCs, we measured FTCs for each of the 34 EE neurons to independent contralateral and ipsilateral stimulation. FTCs derived from ipsilateral monaural stimulation were significantly narrower than those resulting from contralateral monaural stimulation, independent of a neuron's direction-dependent changes in frequency selectivity.     

Tactile extinction following unilateral lesions in the rat anteromedial cortex: Effects of a contralateral cue.

Following unilateral lesions of the anteromedial cortex (AMC) or the caudal forelimb representation (CFL), rats prefer to remove an adhesive patch placed on the forelimb ipsilateral to the lesion before removing a simultaneously applied contralateral patch (i.e., ipsilateral asymmetry). The present experiment was designed to investigate the possibility that attention has some role in these asymmetries. Specifically, the researchers investigated whether a contralateral tactile cue presented before the simultaneous presentation of bilateral tactile stimuli would neutralize the ipsilateral asymmetry. In 14 male rats with AMC lesions, the contralateral cue neutralized the ipsilateral bias, whereas the cue had no effect on 6 male rats with CFL lesions. These data suggest that the ipsilateral bias observed in AMC-damaged rats may reflect an impairment in attention. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Expression of mRNAs encoding dopamine receptors in striatal regions is differentially regulated by midbrain and hippocampal neurons

The glutamate analogue kainic acid was injected into the hippocampus of intact or 6-hydroxydopamine deafferented rats to investigate the influence of hippocampal neurons on the expression of dopamine D1 and D2 receptor mRNAs in subregions of the striatal complex and possible modulation by dopaminergic neurons. Quantitative in situ hybridization using 35S-labeled oligonucleotide probes specific for dopamine D1 and D2 receptor mRNAs, respectively, were used. It was found that an injection of kainic acid into the hippocampal formation had alone no significant effect on dopamine D1 or D2 receptor mRNA levels in any of the analyzed striatal subregions in animals analyzed 4 h after the injections. Kainic acid stimulation in the hippocampus ipsilateral to the dopamine lesion produced an increase in D1 receptor mRNA levels in the ipsilateral medial caudate-putamen, and a bilateral increase in core and shell of nucleus accumbens (ventral striatal limbic regions). A unilateral 6-hydroxydopamine lesion alone caused an increase in D2 receptor mRNA in the lateral caudate-putamen (dorsal striatal motor region) ipsilateral to the lesion and an increase in D1 receptor mRNA in the accumbens core ipsilateral to the lesion. However, in dopamine-lesioned animals, dopamine D1 receptor mRNA levels were increased bilaterally in nucleus accumbens core and shell and in the ipsilateral medial caudate-putamen following kainic acid stimulation in the hippocampus ipsilateral to the dopamine lesion. These results indicate a differential regulation of the expression of dopamine D1 and D2 receptor mRNAs by midbrain and hippocampal neurons.(ABSTRACT TRUNCATED AT 250 WORDS)     

Time course of changes in lactate and free fatty acids after experimental brain injury and relationship to morphologic damage

Regional levels of lactate and free fatty acids (FFA) were measured after lateral fluid percussion (FP) brain injury in rats. At 5 min after injury, tissue concentrations of lactate were elevated in the cortices and hippocampi of both ipsilateral and contralateral hemispheres. Whereas lactate levels had returned to normal by about 20 min after injury in the penumbra and contralateral cortices, their elevation persisted in the ipsilateral injured cortex and hippocampus for 24 h after injury. Increases in the levels of FFA (particularly stearic and arachidonic acids) were observed in the cortices and hippocampi of both ipsilateral and contralateral hemispheres at 5 min after injury; these levels returned to normal in only the penumbra and contralateral cortices by 20 min after injury. Increased amounts of palmitic and oleic acids were also found only in the injured left cortex and ipsilateral hippocampus at 20 min or later after injury. In general, these elevations persisted for as long as 6 to 24 h in the injured cortex and for 2.5 to 24 h after injury in the ipsilateral hippocampus. Histologic studies revealed a similar extent of damage in the cortex between 5 min and 24 h after injury, whereas damage in the CA3 region of the ipsilateral hippocampus increased during that period. These findings suggest a role for lactic acid and FFA, two secondary injury factors, in neuronal cell loss after brain injury.     

Islet amyloid polypeptide and calcitonin gene-related peptide expression are down-regulated in dorsal root ganglia upon sciatic nerve transection

Islet amyloid polypeptide (IAPP) is structurally related to calcitonin gene-related peptide (CGRP) and has been implicated in glucose homeostasis and diabetes pathogenesis because it is expressed in insulin cells and forms amyloid in pancreatic islets from type II diabetic patients. IAPP is also constitutively co-expressed with CGRP in rat sensory neurons. Whether expression of IAPP is altered by nerve injury with or without regeneration was investigated in adult rats subjected to unilateral sciatic axotomy; IAPP and CGRP expression were determined by quantitative in situ hybridization and immunocytochemistry at days 3, 10 and 30 after axotomy. In ipsilateral L4-L5 dorsal root ganglia (DRG), the percentages of nerve cell profiles labelled for IAPP and CGRP mRNA were reduced at all time points studied. IAPP and CGRP mRNA expression were lower in nerve cell profiles in ipsilateral DRGs compared to the contralateral side after axotomy alone whereas epineurial nerve suture maintained or restored IAPP and CGRP expression. The numbers of IAPP- and CGRP-immunoreactive DRG nerve cell profiles and dorsal horn fibers were reduced on the ipsilateral side at all time points. Thus, IAPP and CGRP expression are down-regulated upon axotomy. Nerve repair maintains or restores IAPP and CGRP expression in individual neurons but does not prevent the loss of CGRP/IAPP phenotype of some of these neurons in response to axotomy.     

Reconstruction of flexor/extensor alternation during fictive rostral scratching by two-site stimulation in the spinal turtle with a transverse spinal hemisection

Analyses of fictive scratching motor patterns in the spinal turtle with transverse hemisection provided support for the concept of bilateral shared spinal cord circuitry among neurons responsible for generating left- and right-side rostral, pocket, and caudal fictive scratching. Rhythmic bursts of hip flexor activity, the hip extensor deletion variation of fictive rostral scratching, were elicited by ipsilateral stimulation in the rostral scratch receptive field of a spinal turtle [transection at the segmental border between the second (D2) and third (D3) postcervical spinal segments] with a contralateral transverse hemisection one segment anterior to the hindlimb enlargement (at the D6-D7 segmental border). In addition, other sites were stimulated in this preparation: (1) contralateral sites in a rostral, pocket, or caudal scratch receptive field or (2) ipsilateral sites in a caudal scratch receptive field. A reconstructed fictive rostral scratch motor pattern of rhythmic alternation between hip flexor and hip extensor activation was produced by simultaneous stimulation of one site in the ipsilateral rostral scratch receptive field and another site in one of the other scratch receptive fields. This reconstructed rostral scratch motor pattern resembled the normal rostral scratch motor pattern produced by one-site rostral scratch stimulation of a spinal turtle (D2-D3 transection) with no additional transections. The observation of a reconstructed rostral scratch motor pattern produced by two-site stimulation in the spinal turtle with transverse hemisection supports the concept that hip extensor circuitry activated by stimulation of other scratch receptive fields is shared with circuitry activated by ipsilateral rostral scratch receptive field stimulation.     

Contrasting immunopathogenic properties of highly homologous peptides from rat and human thyroglobulin

Morphological changes in the vestibular nerves and superior vestibulocular neurons (SVON) after unilateral labyrinthectomy in cats revealed a progressive loss of axons in the ipsilateral vestibular nerve (35%) and synaptic profiles (SP) on ipsilateral SVON (60%) up to a 1-year survival period. Although the ipsilateral vestibular nerve showed further degeneration (45%) at 2 years post ablation, the number of SP on ipsilateral SVON increased to 60% of normal (40% loss). These SP likely represent sprouting from crossing commissural or cerebellar pathways. Contralateral vestibular nerves at 1 and 2 years post ablation revealed normal numbers and size spectrum, but the number of SP contacting the contralateral SVON at 8 weeks, 1 and 2 years paralleled the levels of SP found on ipsilateral SVON. The symmetry in adjustment of SP on the SVON of both sides of the brainstem after ablation may be explained by the neurotrophin hypothesis.     

Changes in brain-derived neurotrophic factor immunoreactivity in rat dorsal root ganglia, spinal cord, and gracile nuclei following cut or crush injuries

In the present study, we evaluated changes in brain-derived neurotrophic factor (BDNF) immunoreactivity in the rat lumbar (L) 5 dorsal root ganglion (DRG) and areas where afferents from the DRG terminate, the L5 spinal cord and gracile nuclei, following unilateral sciatic nerve transection or crush. From 3 days to 4 weeks following cut or crush injury, the percentage of medium and large BDNF-immunoreactive neurons in the ipsilateral DRG increased significantly compared with those on the contralateral side. Following cut injury, there was no significant change in the percentage of small BDNF-immunoreactive neurons in the ipsilateral DRG; however, the intensity of immunoreactivity of these cells decreased. Following crush injury, however, both the percentage and intensity of small BDNF-immunoreactive neurons in the ipsilateral DRG significantly increased. Following cut injury, the expression of BDNF-immunoreactive axonal fibers decreased markedly in the ipsilateral superficial laminae of the L5 spinal cord and increased significantly in the ipsilateral deeper laminae of the spinal cord and gracile nuclei. Crush injury induced a marked increase in the expression of BDNF-immunoreactive axonal fibers in the superficial laminae of the spinal cord and gracile nuclei. These differences in BDNF response in the DRG and spinal cord after cut or crush injuries may reflect differences in trophic support to the injured DRG neurons and altered neuronal activity in the spinal cord and gracile nuclei following different types of peripheral nerve injury.     

Ipsilateral motor activation in patients with cerebral gliomas

OBJECTIVE: The aim of this study is to provide neurophysiologic evidence of ipsilateral hemispheric activation in patients affected by intracerebral gliomas via the use of transcranial magnetic stimulation. BACKGROUND: The mechanisms involved in such ipsilateral activation have yet to be established, but they may involve preexisting routes that either are suppressed or undetected in the normal brain. Ipsilateral pathways may act in reserve, activated by the impairment of contralateral control. This hypothesis is suggested by the fact that the considerable size of the tumors in our patients is not matched by a proportionate loss of motor performance in the limbs contralateral to the affected hemisphere. However, it remains possible that ipsilateral motor-evoked potentials (iMEPs) may reflect reorganizational changes without significant functional effects. METHODS: The effects of such activation were investigated using both focal and nonfocal coils stimulating cortical motor areas, with MEPs recorded from both left and right thenar muscles. Fifteen healthy control subjects and seven patients were examined. RESULTS: iMEPs were generally absent in normal subjects, but in contrast they were obtained in the patients by stimulating the healthy hemisphere using both round and figure-of-eight coils. Distinct from contralateral MEPs, iMEPs are obtained with higher thresholds (range, 60 to 80% of stimulator output) and display longer latencies (20.9 msec versus 19.4 msec). CONCLUSIONS: Taken in conjunction with recent research using functional imaging brain exploration and a variety of clinical, anatomic, and neurophysiologic studies, our results reflect a growing awareness of ipsilateral motor control and its potential compensatory role when contralateral routes are damaged.     

Hemorheological changes in blood transfusion-treated beta thalassemia major patients

Parkinson's disease is associated with progressive loss of nigrostriatal dopamine (DA). Models of the disorder, produced with neurotoxins (N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine or 6-hydroxydopamine) that selectively lesion DA neurons, are characterized by acute removal and gradual recovery of DA. We report slowly progressive loss of DA in ipsilateral nucleus accumbens following profound (>90%) acute unilateral depletion of DA in the caudate-putamen of neonatal rats, from 50% at age 27 days to 94% by 100 days. Metabolic turnover of DA markedly increased in ipsilateral accumbens, and may yield tissue-damaging neurotoxic by-products. This paradigm may help in elucidating mechanisms responsible for gradual degeneration of DA neurons and for screening potential neuroprotective agents.     

Self-stimulation of the habenular complex in the rat.

65 male hooded Long-Evans rats learned to barpress for rewarding electrical stimulation of the medial or lateral habenular nucleus or the fasciculus retroflexus, but not the surrounding thalamic nuclei. Response rates were moderate and steady and were not influenced by food or water deprivation. Habenular self-stimulation was significantly facilitated by placing lesions in the ipsilateral anterior part of the medial forebrain bundle (MFB). Similarly, MFB self-stimulation was enhanced by ipsilateral habenular lesions. Lesions centered in the region of median raphe nucleus suppressed habenular self-stimulation for more than 4 wks. Self-stimulation of median raphe was not affected by habenular lesions. Results show that habenular stimulation can produce a rewarding effect by exciting neurons in the region of the raphe nuclei but apparently without requiring the participation of the well-known MFB reward system. (44 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Expression of Fos in the rat forebrain following experimental tooth movement

Orthodontic tooth movement is known to cause pain and discomfort to patients. Mechanically induced inflammatory responses in the periodontium are assumed to be related to the mechanism of pain sensation. An immediate-early gene, c-fos, that is expressed within some neurons following synaptic activation, is widely used as a marker for neuronal activity following noxious or innocuous stimulation. We have recently demonstrated that experimental tooth movement produced Fos induction in the ipsilateral trigeminal subnucleus caudalis and in the bilateral lateral parabrachial nucleus, which is known to be involved in the transmission of nociceptive information. As a further step, we investigated the distribution of Fos-like immunoreactive neurons in the upper brain regions. Twenty-four hours after the commencement of the experimental tooth movement, the Fos-like immunoreactive neurons appeared in the central nucleus of the amygdala (Ce), paraventricular nucleus of the hypothalamus (PVH), and paraventricular nucleus of the thalamus (PV) of the experimental rats. The numbers of the labeled neurons were significantly increased by 639% (P < 0.001) and 644% (P < 0.001) in the ipsilateral and contralateral sides of the Ce, respectively, by 292% (P < 0.001) and 307% (P < 0.001) in the ipsilateral and contralateral sides of the PVH, and by 264% (P < 0.0001) in the PV with respect to sham control rats. These results suggest that nociceptive information caused by experimental tooth movement might be transmitted and modulated in several regions of the forebrain.     

Sonographic incidence of deep venous thrombosis contralateral to hip or knee replacement surgery

PURPOSE: This study assesses the sonographic incidence of deep venous thrombosis (DVT) contralateral to and the venographic incidence ipsilateral to hip or knee replacement surgery and the role of sonography in routine surveillance. METHODS: We prospectively evaluated 178 consecutive patients with sonography of the femoropopliteal venous systems of the contralateral lower extremity and venography of the ipsilateral lower extremity on days 3 and 4, respectively, after total hip or knee replacement surgery. RESULTS: No cases of acute DVT and only 1 case of chronic DVT isolated to the popliteal system were identified by sonography in the contralateral extremity. In the ipsilateral extremity, venography identified 26 patients with acute DVT (3 femoropopliteal, 21 calf, and 2 concurrent femoropopliteal and calf). CONCLUSIONS: Routine sonographic evaluation of the lower extremity contralateral to hip or knee replacement surgery is not cost-effective because of the extremely low incidence of detectable acute thrombus.     

Single unit activity in the inferior colliculus of the rat elicited by electrical stimulation of the cochlea

The activity of single neurons (n = 182) of the central nucleus of the inferior colliculus (CIC) of the rat was recorded in response to unilateral electrical stimulation of the left cochlea and/or acoustical stimulation of the right ear. The probability of response to both modes of stimulation was comparable (90 per cent for contralateral and 60 per cent for ipsilateral presentation). Response patterns consisted predominantly of onset excitations. Response latencies to electrical stimuli ranged from 3 to 21 ms, with an average value of 9.7 ms (SD = 3.5 ms) in the ipsilateral CIC and 6.6 ms (SD = 3.4 ms) in the contralateral CIC. With respect to binaural inputs, the majority of units were excited by stimulation of either ear (EE; about 60 per cent) while about one third were influenced by one ear only (EO). Units excited by one ear and inhibited by the other (EI) were rare. The main difference between the present implanted rats and normal animals was the virtual absence here of inhibitory effects for both types of stimuli when they were delivered to the ipsilateral ear (very few EI units).     

Proton magnetic resonance spectroscopy in children with Sturge-Weber syndrome

Quantitative proton magnetic resonance spectroscopy was performed on six children with Sturge-Weber syndrome following gadolinium enhanced magnetic resonance imaging (MRI). MRI revealed only unilateral involvement in all cases. The mean concentration (mmol/kg wet weight) of the neuronal marker N-acetyl-aspartate was significantly reduced by 37% in the ipsilateral gadolinium enhanced volume of interest compared to a similarly placed contralateral volume of interest (5.39 +/- 1.70 [SD] vs 8.50 +/- 1.14, P < .005, two-tailed paired Student's t-test). Decreased N-acetyl-aspartate in the ipsilateral volume of interest was observed in all patients studied. No significant differences were found in the concentrations of creatine/phosphocreatine or choline compounds between the ipsilateral and contralateral volumes of interest. These findings give possible new insight into the pathophysiology of this disease and suggest that quantitative proton magnetic resonance spectroscopy may be useful for the early characterization and monitoring of neuronal dysfunction or loss in infants and children with Sturge-Weber syndrome.     

A lateralized deficit in morphine antinociception after unilateral inactivation of the central amygdala

The amygdala is a forebrain region that is receiving increasing attention as a modulator of pain sensation. The amygdala contributes to antinociception elicited by both psychological factors (e.g., fear) and exogenous opioid agonists. Unlike the midbrain periaqueductal gray matter (PAG) or rostral ventromedial medulla, the amygdala is a pain-modulating region that has clear bilateral representation in the brain, making it possible to determine whether pain-modulating effects of this region are lateralized with respect to the peripheral origin of noxious stimulation. Unilateral inactivation of the central nucleus of the amygdala (Ce) plus adjacent portions of the basolateral amygdaloid complex (with either the excitotoxin NMDA or the GABAA agonist muscimol) reduced the ability of morphine to suppress prolonged, formalin-induced pain derived from the hindpaw ipsilateral, but not contralateral, to the inactivated region. This effect was evident regardless of the nociceptive scoring method used (weighted scores or flinch-frequency method) and was not accompanied by a concurrent reduction in morphine-induced hyperlocomotion. Unilateral lesions restricted to the basolateral amygdaloid complex (i.e., not including the Ce) did not reduce the ability of morphine to suppress formalin-induced pain derived from either hindpaw. The results constitute the first report of a lateralized deficit in opioid antinociception after unilateral inactivation of a specific brain area and show the first clear neuroanatomical dissociation between antinociceptive and motor effects of systemically administered morphine in the rat. The amygdala appears to modulate nociceptive signals entering the ipsilateral spinal dorsal horn, probably through monosynaptic connections with ipsilateral portions of the PAG.