Contributions of the reticulospinal system to the postural adjustments occurring during voluntary gait modifications. (65/976)

To test the hypothesis that reticulospinal neurons (RSNs) are involved in the formation of the dynamic postural adjustments that accompany visually triggered, voluntary modifications of limb trajectory during locomotion, we recorded the activity of 400 cells (183 RSNs; 217 unidentified reticular cells) in the pontomedullary reticular formation (PMRF) during a locomotor task in which intact cats were required to step over an obstacle attached to a moving treadmill belt. Approximately one half of the RSNs (97/183, 53%) showed significant changes in cell activity as the cat stepped over the obstacle; most of these cells exhibited either single (26/97, 26.8%) or multiple (63/97, 65.0%) increases of activity. There was a range of discharge patterns that varied in the number, timing, and sequencing of the bursts of modified activity, although individual bursts in different cells tended to occur at similar phases of the gait cycle. Most modified cells, regardless of the number of bursts of increased discharge, or of the discharge activity of the cell during unobstructed, control, locomotion, discharged during the passage of the lead forelimb over the obstacle. Thus, 86.9% of the modified cells increased their discharge when the forelimb ipsilateral to the recording site was the first to pass over the obstacle, and 72.2% when the contralateral limb was the first. Approximately one quarter of the RSNs increased their discharge during the passage of each of the four limbs over the obstacle in both the lead (27.1%) and trail (27.9%) conditions. In general, in any one cell, the number and relative sequencing of the subsequent bursts (with respect to the lead forelimb) was maintained during both lead and trail conditions. Patterns of activity observed in unidentified cells were very similar to the RSN activity despite the diverse population of cells this unidentified group may represent. We suggest that the increased discharge that we observed in these reticular neurons reflects the integration of afferent activity from several sources, including the motor cortex, and that this increased discharge signals the timing and the relative magnitude of the postural patterns that accompany the voluntary gait modification. However, based on the characteristics of the patterns of neuronal activity in these cells, we further suggest that while individual RSNs probably contribute to the selection of different patterns of postural activity, the ultimate expression of the postural response may be determined by the excitability of the locomotor circuits within the spinal cord.  (+info)

Pontine gustatory activity is altered by electrical stimulation in the central nucleus of the amygdala. (66/976)

Visceral signals and experience modulate the responses of brain stem neurons to gustatory stimuli. Both behavioral and anatomical evidence suggests that this modulation may involve descending input from the forebrain. The present study investigates the centrifugal control of gustatory neural activity in the parabrachial nucleus (PBN). Extracellular responses were recorded from 51 single PBN neurons during application of sucrose, NaCl, NaCl mixed with amiloride, citric acid, and QHCl with or without concurrent electrical stimulation in the ipsilateral central nucleus of the amygdala (CeA). Based on the sapid stimulus that evoked the greatest discharge, 3 neurons were classified as sucrose-best, 32 as NaCl-best, and 16 as citric acid-best. In most of the neurons sampled, response rates to an effective stimulus were either inhibited or unchanged during electrical stimulation of the CeA. Stimulation in the CeA was without effect in two sucrose-best neurons, nine NaCl-best neurons, and one citric acid-best neuron. Suppression was evident in 1 sucrose-best neuron, 18 NaCl-best neurons, and 15 citric acid-best neurons. In NaCl-best neurons inhibited by CeA stimulation, the magnitude of the effect was similar for spontaneous activity and responses to the five taste stimuli. Nonetheless, the inhibitory modulation of gustatory sensitivity increased the relative effectiveness of NaCl resulting in narrower chemical selectivity. For citric acid-best neurons, the magnitude of inhibition produced by CeA activation increased with an increase in stimulus effectiveness. The responses to citric acid were inhibited significantly more than the responses to all other stimuli with the exception of NaCl mixed with amiloride. The overall effect was to change these CA-best neurons to CA/NaCl-best neurons. In a smaller subset of NaCl-best neurons (n = 5), CeA stimulation augmented the responsiveness to NaCl but was without effect on the other stimuli or on baseline activity. It appears that electrical stimulation in the CeA modulates response intensity, as well as the type of gustatory information that is transmitted in a subset of NaCl-best neurons. These findings provide an additional link between the amygdala and the PBN in the control of NaCl intake, modulating the response and the chemical selectivity of an amiloride-sensitive Na+ detecting input pathway.  (+info)

Tumorigenesis in transgenic mice in which the SV40 T antigen is driven by the brain-specific FGF1 promoter. (67/976)

Gene expression can be manipulated by the introduction of a hybrid gene formed by linking a highly tissue-specific regulatory element to a gene whose expression might be expected to alter cellular function. Previously, we have shown that the human FGF1 gene contains four distinct tissue-specific promoters. In an effort to perturb the programming of proliferation and differentiation in a subset of neural cells, we have produced transgenic mice bearing the brain-specific promoter of the human FGF1 gene joined to the SV40 immediate early gene, which encodes the large T antigen. The resulting mice, and offspring from four individual lines, developed brain tumors that originated in the pontine gray, just rostral to the fourth ventricle. Tumors were moderately vascularized, as demonstrated by staining with both hematoxylin and eosin and antibodies to three different endothelial cell markers, but vessels were histologically normal. Scattered tumor foci were present as early as postnatal day 26; and affected animals died between 5 - 8 months of age. In mature animals, tumors lacked terminal differentiation markers for astrocytes (glial fibrillary acidic protein) or neurons (synaptophysin and neuron-specific enolase). However, they expressed high levels of proliferating cell nuclear antigen and vimentin, markers for proliferating cells. This immunophenotype is consistent with the tumor being at an early stage of differentiation. Therefore, these mice may provide a valuable tool for the study of tumorigenesis, replenishment and differentiation of neural stem cells.  (+info)

Quantitative measurement of cerebral acetylcholinesterase using. (68/976)

[11C]physostigmine, an acetylcholinesterase inhibitor, has been shown to be a promising positron emission tomography ligand to quantify the cerebral concentration of the enzyme in animals and humans in vivo. Here, a quantitative and noninvasive method to measure the regional acetylcholinesterase concentration in the brain is presented. The method is based on the observation that the ratio between regions rich in acetylcholinesterase and white matter, a region almost entirely deprived of this enzyme, was found to become approximately constant after 20 to 30 minutes, suggesting that at late time points the uptake mainly contains information about the distribution volume. Taking the white matter as the reference region, a simplified reference tissue model, with effectively one reversible tissue compartment and three parameters, was found to give a good description of the data in baboons. One of these parameters, the ratio between the total distribution volumes in the target and reference regions, showed a satisfactory correlation with the acetylcholinesterase concentration measured postmortem in two baboon brains. Eight healthy male subjects were also analyzed and the regional enzyme concentrations obtained again showed a good correlation with the known acetylcholinesterase concentrations measured in postmortem studies of human brain.  (+info)

Distribution of reticulocerebellar neurons in chicken reticular formation. (69/976)

The distribution of reticulocerebellar (RC) neurons was examined by the retrograde transport of horseradish peroxidase (HRP) or wheat germ agglutinin bound to HRP (WGA-HRP) in 7 White Leghorn chickens. A large number of labeled cells were found in the nucleus reticularis pontis caudalis (RP) of the pontomedullary junction and in the nucleus reticularis gigantocellularis (Rgc), parvocellularis (Rpc), subtrigiminalis (Rst), paragigantocellularis (Rpg) and paramedianus (RpaM) in the medulla. Slightly ventral to the vestibulocochlear nerve were many large RC neurons arranged in a longitudinal manner along the lateral edge of the brainstem reticular formation (the Dorsolateral edge cells, DLe cells). RC neurons were most numerous in the Rgc and accounted for 31.9% of the total number of labeled cells, followed by RP (24.2%), Rpc (12.7%), Rpg (10.8%), RpaM (6.7%), DLe cells (6.3%) and Rst (4.9%). The great number of RC neurons was found around the levels of the vestibulocochlear nerve.  (+info)

Extracellular calcium fluctuations and intracellular potentials in the cortex during the slow sleep oscillation. (70/976)

During slow wave sleep the main activity of cortical neurons consists of synchronous and rhythmic alternations of the membrane potential between depolarized and hyperpolarized values. The latter are long-lasting (200-600 ms) periods of silence. The mechanisms responsible for this periodical interruption of cortical network activity are unknown. Here we report a decrease of approximately 20% in the extracellular calcium concentration ([Ca](out)) progressively taking place in the cortex between the onset and the offset of the depolarizing phase of the slow sleep oscillation. Since [Ca](out) exerts a high gain modulation of synaptic transmission, we estimated the associated transmitter release probability and found a corresponding 50% drop. Thus the periods of silence occurring in the cortical network during slow wave sleep are promoted by recurrent [Ca](out) depletions.  (+info)

Effects of Veratrum nigrum alkaloids on central catecholaminergic neurons of renal hypertensive rats. (71/976)

AIM: To study the central hypotensive mechanism of Veratrum nigrum L var ussurience Nakai alkaloids (VnA) in renal hypertensive rats(RHR). METHODS: The quantitative method of immunocytochemistry (ICC) was used to observe and detect the effect of VnA (30 micrograms.kg-1, i.v.) on activity of central catecholaminergic (CA) neurons of C1, C2, A1, and A5 areas in RHR. RESULTS: VnA increased the immunoreactivity (IR) of tyrosine 3-monooxygenase (TM)-immunopositive (IP) neurons of C1, C2, and A5 areas in RHR experimental group compared with RHR control group [positive units: (1.9 +/- 0.4), (1.18 +/- 0.23), (1.2 +/- 0.4) vs (0.15 +/- 0.22), (0.31 +/- 0.16), (0.69 +/- 0.20), respectively]; IR of TM-IP neurons of C1 and C2 areas in RHR control group was decreased compared with sham-operated group [positive units: (0.15 +/- 0.22), (0.31 +/- 0.16) vs (1.45 +/- 0.29), (1.36 +/- 0.25), respectively]. CONCLUSION: VnA increased the activity of central CA neurons in RHR to exert its hypotensive effect.  (+info)

Effects of anesthetics on ponto-geniculo-occipital waves from the oculomotor nucleus of the cat. (72/976)

Effects of anesthetics and doxapram on pontogeniculo-occipital (PGO) waves from the oculomotor nucleus were studied in acute experiments in cats paralyzed by gallamine triethiodide. The anesthetic agents studied in the present experiment (thiopental, ketamine, Innovar, nitrous oxide, and halothane) decreased, while doxapram increased, the total number of PGO waves. As the doses of anesthetics increased, PGO waves were abolished, but they returned to control levels or below control levels when the concentrations of anesthetics were decreased. The results indicate that the anesthetics studied inhibit the activity of the central mechanism associated with the oculomotor system. PGO waves may prove a useful index of the level of anesthesia.  (+info)