| 1. |
- Deshpande, J, et al.
(författare)
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Ultrastructural changes in the hippocampal CA1 region following transient cerebral ischemia: evidence against programmed cell death.
- 1992
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Ingår i: Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale. - 0014-4819. ; 88:1, s. 91-105
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Tidskriftsartikel (refereegranskat)abstract
- The ultrastructural changes in the pyramidal neurons of the CA1 region of the hippocampus were studied 6 h, 24 h, 48 h, and 72 h following a transient 10 min period of cerebral ischemia induced by common carotid occlusion combined with hypotension. The pyramidal neurons showed delayed neuronal death (DND), i.e. at 24 h and 48 h postischemia few structural alterations were noted in the light microscope, while at 72 h extensive neuronal degeneration was apparent. The most prominent early ultrastructural changes were polysome disaggregation, and the appearance of electron-dense fluffy dark material associated with tubular saccules. Mitochondria and nuclear elements appeared intact until frank neuronal degeneration. The dark material accumulated with extended periods of recirculation in soma and in the main trunks of proximal dendrites, often beneath the plasma membrane, less frequently in the distal dendrites and seldom in spines. Protein synthesis inhibitors (anisomycin, cycloheximide) and an RNA synthesis inhibitor (actinomycin D), administered by intrahippocampal injections or subcutaneously, did not mitigate neuronal damage. Therefore, DND is probably not apoptosis or a form of programmed cell death. We propose that the dark material accumulating in the postischemic period represents protein complexes, possibly aggregates of proteins or internalized plasma membrane fragments, which may disrupt vital cellular structure and functions, leading to cell death.
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| 2. |
- Lindeberg, Tony, 1964-, et al.
(författare)
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Foveal scale-space and the linear increase of receptive field size as a function of eccentricity
- 1994
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Rapport (övrigt vetenskapligt/konstnärligt)abstract
- This paper addresses the formulation of a foveal scale-space and its relation to the scaling property of receptive field sizes with eccentricity. It is shown how the notion of a fovea can be incorporated into conventional scale-space theory leading to a foveal log-polar scale-space. Natural assumptions about uniform treatment of structures over scales and finite processing capacity imply a linear increase of minimum receptive field size as a function of eccentricity. These assumptions are similar to the ones used for deriving linear scale-space theory and the Gaussian receptive field model for an idealized visual front-end.
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| 3. |
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| 4. |
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| 5. |
- Ekström, Per, et al.
(författare)
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A calmodulin inhibitor with high specificity, compound 48/80, inhibits axonal transport in frog nerves without disruption of axonal microtubules.
- 1991
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Ingår i: Acta physiologica Scandinavica. - 0001-6772. ; 142:2, s. 181-9
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Tidskriftsartikel (refereegranskat)abstract
- The calmodulin inhibitor compound 48/80 has previously been shown to arrest axonal transport in vitro in the regenerating frog sciatic nerve. The inhibition was limited to the outgrowth region of nerves, which had been allowed to regenerate in vivo for 6 days after a crush lesion, before they were incubated with or without drugs in vitro overnight. The effects of compound 48/80 on the regenerating nerve were further investigated. A concentration of compound 48/80 (50 micrograms ml-1), which effectively inhibits axonal transport, did not cause observable changes of the microtubules of regenerating axons in the outgrowth region as judged by electron microscopy. Furthermore, it was shown that also a lower concentration (25 micrograms ml-1) inhibited axonal transport. As a measure of possible metabolic effects, the level of ATP was assessed in the regenerating nerve after exposure to compound 48/80. Compound 48/80 at 25 micrograms ml-1 did not change the level of ATP in the nerve. The assembly of bovine brain microtubule proteins in a cell-free system was unaffected by 25 micrograms ml-1 of compound 48/80 and slightly inhibited by 50 micrograms ml-1. At higher concentrations (greater than 100 micrograms ml-1) assembly of microtubules appeared stimulated, and microtubule spirals as well as closely aligned microtubules could be seen. These effects appeared to be unrelated to the transport effects. The present results indicate that compound 48/80 arrests axonal transport via mechanisms other than destruction of axonal microtubules or interference with the energy metabolism. It is possible that these mechanisms involve inhibition of calmodulin-regulated events essential to the transport.
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| 6. |
- Johansson, Roland S, et al.
(författare)
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Somatosensory control of precision grip during unpredictable pulling loads. I. Changes in load force amplitude.
- 1992
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Ingår i: Experimental Brain Research. - 0014-4819 .- 1432-1106. ; 89:1, s. 181-191
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Tidskriftsartikel (refereegranskat)abstract
- In manipulating 'passive' objects, for which the physical properties are stable and therefore predictable, information essential for the adaptation of the motor output to the properties of the current object is principally based on 'anticipatory parameter control' using sensorimotor memories, i.e., an internal representation of the object's properties based on previous manipulative experiences. Somatosensory afferent signals only intervene intermittently according to an 'event driven' control policy. The present study is the first in a series concerning the control of precision grip when manipulating 'active' objects that exert unpredictable forces which cannot be adequately represented in a sensorimotor memory. Consequently, the manipulation may be more reliant on a moment-to-moment sensory control. Subjects who were prevented from seeing the hand used the precision grip to restrain a manipulandum with two parallel grip surfaces attached to a force motor which produced distally directed (pulling) loads tangential to the finger tips. The trapezoidal load profiles consisted of a loading phase (4 N/s), plateau phase and an unloading phase (4 N/s) returning the load force to zero. Three force amplitudes were delivered in an unpredictable sequence; 1 N, 2 N and 4 N. In addition, trials with higher load rate (32 N/s) at a low amplitude (0.7 N), were superimposed on various background loads. The movement of the manipulandum, the load forces and grip forces (normal to the grip surfaces) were recorded at each finger. The grip force automatically changed with the load force during the loading and unloading phases. However, the grip responses were initiated after a brief delay. The response to the loading phase was characterized by an initial fast force increase termed the 'catch-up' response, which apparently compensated for the response delay--the grip force adequately matched the current load demands by the end of the catch-up response. In ramps with longer lasting loading phases (amplitude greater than or equal to 2 N) the catch-up response was followed by a 'tracking' response, during which the grip force increased in parallel with load force and maintained an approximately constant force ratio that prevented frictional slips. The grip force during the hold phase was linearly related to the load force, with an intercept close to the grip force used prior to the loading. Likewise, the grip force responses evoked by the fast loadings superimposed on existing loads followed the same linear relationship.(ABSTRACT TRUNCATED AT 400 WORDS)
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| 7. |
- Johansson, Roland S, et al.
(författare)
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Somatosensory control of precision grip during unpredictable pulling loads. II. Changes in load force rate.
- 1992
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Ingår i: Experimental Brain Research. - 0014-4819 .- 1432-1106. ; 89:1, s. 192-203
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Tidskriftsartikel (refereegranskat)abstract
- In the previous paper regarding the somatosensory control of the human precision grip, we concluded that the elicited automatic grip force adjustments are graded by the amplitude of the imposed loads when restraining an 'active' object subjected to unpredictable pulling forces (Johansson et al. 1992a). Using the same subjects and apparatus, the present study examines the capacity to respond to imposed load forces applied at various rates. Grip and load forces (forces normal and tangential to the grip surfaces) and the position of the object in the pulling direction (distal) were recorded. Trapezoidal load force profiles with plateau amplitudes of 2 N were delivered at the following rates of loading and unloading in an unpredictable sequence: 2 N/s, 4 N/s or 8 N/s. In addition, trials with higher load rate (32 N/s) at a low amplitude (0.7 N) were intermingled. The latencies between the start of the loading and the onset of the grip force response increased with decreasing load force rate. They were 80 +/- 9 ms, 108 +/- 13 ms, 138 +/- 27 ms and 174 +/- 39 ms for the 32, 8, 4 and 2 N/s rates, respectively. These data suggested that the grip response was elicited after a given minimum latency once a load amplitude threshold was exceeded. The amplitude of the initial rapid increase of grip force (i.e., the 'catch-up' response) was scaled by the rate of the load force, whereas its time course was similar for all load rates. This response was thus elicited as a unit, but its amplitude was graded by afferent information about the load rate arising very early during the loading. The scaling of the catch-up response was purposeful since it facilitated a rapid reconciliation of the ratio between the grip and load force to prevent slips. In that sense it apparently also compensated for the varying delays between the loading phase and the resultant grip force responses. However, modification of the catch-up response may occur during its course when the loading rate is altered prior to the grip force response or very early during the catch-up response itself. Hence, afferent information may be utilized continuously in updating the response although its motor expression may be confined to certain time contingencies. Moreover, this updating may take place after an extremely short latency (45-50 ms).
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| 8. |
- Hillarp, Andreas, et al.
(författare)
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Cloning of cDNA coding for the beta chain of human complement component C4b-binding protein : sequence homology with the alpha chain
- 1990
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424. ; 87:3, s. 1183-1187
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Tidskriftsartikel (refereegranskat)abstract
- The major form of complement component C4b-binding protein, a regulator of the complement system, is composed of seven identical 70-kDa alpha chains, each containing a binding site for the complement protein C4b. We recently showed that C4b-binding protein also contains a unique 45-kDa beta chain. It is disulfide-linked to the central core and contains a binding site for the vitamin K-dependent protein S. We have now isolated and characterized full-length cDNA clones for the beta chain. In addition, 57% of the structure was determined by protein sequencing of tryptic and chymotryptic peptides. Two clones, A8 and C1, isolated from different libraries were sequenced. Except for a deleted triplet encoding Ala-3 in clone A8, the two clones were identical and coded for a leader sequence of 17 amino acids and a mature protein of 235 amino acids (including Ala-3). By N-terminal amino acid sequencing, the Ala-3 heterogeneity was confirmed and a third beta-chain species starting at Glu-4 was identified. The beta chain contains five potential N-linked glycosylation sites, and endoglycosidase digestion suggested that the beta chain contained multiple complex carbohydrate side chains. Northern blot analysis of human liver mRNA, using the beta-chain cDNA as the probe, demonstrated a major mRNA species of approximately 1.0 kilobase. From the N terminus, the beta chain contains three tandem repeat units (60 amino acids long) that are homologous to those present in the alpha chain. The C-terminal region, which was unrelated to the tandem repeats, demonstrated sequence similarity with the corresponding region of the alpha chain. In both alpha and beta chains these regions contain two cysteine residues that probably form the interchain disulfide bridges.
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| 9. |
- Ekström, Peter, et al.
(författare)
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Localization of 2-[125I]lodomelatonin binding sites in the brain of the atlantic salmon, salmo salar L.
- 1992
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Ingår i: Neuroendocrinology. - : S. Karger AG. - 0028-3835 .- 1423-0194. ; 55:5, s. 529-537
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Tidskriftsartikel (refereegranskat)abstract
- The photosensory pineal organ of teleost fish shows a circadian rhythm in melatonin synthesis, and melatonin is known to influence a number of physiological functions. However, the target sites for melatonin are not known. We have investigated the distribution of melatonin binding sites in the brain of the salmon, Salmo salar. Brains were collected for receptor binding assay and autoradiography at each of three time points; just after lights on, just before lights off, and in the dark at midnight (photoperiod light-dark 12: 12, lights on at 08.00 h, lights off at 20.00 h). Specific binding of 2-[125I]iodomelatonin was observed in several brain areas. High densities were associated with (1) the optic tectum, (2) the preoptic area, (3) an area encompassing the magnocellu-lar superficial pretectal nucleus ('nucleus rotundus') and the glomerular complex, (4) the inferior lobes of the hypothalamus, (5) the lateral mesencephalic tegmentum including the torus semicircularis, and (6) the molecular layer of the cerebellum. No binding was observed in the pineal organ or in the pituitary. We observed no differences in labeling between brains collected at different time points, except in the preoptic area where binding was high at 20.00 and 24.00 h, but low at 08.00 h, and in the corpus cerebelli, where labeling in the molecular laver was higher at 24.00 and 08.00 h than at 20.00 h. Saturation experiments with crude brain membranes indicated the presence of a single binding site with no significant differences related to the time of day, with Kd values ranging from 30 to 54 pM, and Bmax values from 7.0 to 10.8 fmol/mg protein. Nonspecific binding, determined with 0.1 μM melatonin, was < 20%. The Kd and Bmax, values are in the same range as those reported for the so-called high-affinity binding site in mammalian neural tissue.
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| 10. |
- Grundemar, L, et al.
(författare)
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Long-lasting inhibition of the cardiovascular responses to glutamate and the baroreceptor reflex elicited by neuropeptide Y injected into the nucleus tractus solitarius of the rat
- 1991
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Ingår i: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 122:1, s. 135-139
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Tidskriftsartikel (refereegranskat)abstract
- Neuropeptide Y (NPY) microinjected unilaterally into the nucleus tractus solitarii (NTS) of anesthetized paralyzed rats elicits a gradual dose-dependent and reversible fall in arterial pressure (AP) and heart rate (HR) lasting 20 min. It also abolished the brief (less than 1 min) dose-dependent and reversible fall of AP and HR elicited by L-glutamate (L-Glu) injected into the nucleus. The blockade of L-Glu by NPY appeared gradually and was prolonged, lasting over 2 h, and recovering by 24 h. It was not replicated by desamido-NPY or galanin. Unlike 2% lidocaine it did not block the hypotension elicited by focal electrical stimulation at the injection site indicating the response was not that of a local anesthetic. Bilateral injection of NPY into the NTS resulted, after an initial fall, in an elevation of AP (+48 +/- 10.6 mmHg). At this time the reflex bradycardia evoked by elevating AP with phenylephrine was markedly reduced. We conclude that in the NTS, NPY antagonizes the actions of L-Glu and may attenuate baroreceptor reflexes. Since the NTS is richly innervated by NPY neurons and contains many NPY binding sites and since primary baroreceptor afferents appear to be glutamatergic the results suggested that NPY may serve in NTS as a long-term regulator of baroreceptor reflex activity.
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