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  • 1
    Electronic Resource
    Electronic Resource
    Alterations in cerebral glutamic acid decarboxylase and3H-flunitrazepam binding during continuous treatment of rats for up to 1 year with haloperidol, sulpiride or clozapine (1987)
    Springer
    Journal of neural transmission 68 (1987), S. 113-125 
    Details
    ISSN: 1435-1463
    Keywords: Neuroleptics ; striatum ; substantia nigra ; GAD ; 3H-flunitrazepam binding
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Rats were treated continuously for 12 months with therapeutically equivalent doses of haloperidol (1.4–1.6 mg/kg/day), sulpiride (102–109 mg/kg/day) or clozapine (24–27 mg/kg/day) and examined for alterations in brain glutamic acid decarboxylase (GAD) and3H-flunitrazepam binding. Administration of haloperidol, but not sulpiride or clozapine, for 6 or 12 months increased striatal GAD activity. None of the drug treatments altered nigral GAD activity when examined after 1, 3, 6, 9 or 12 months administration. The number of specific3H-flunitrazepam binding sites (Bmax) in striatal membrane preparations were not altered by 12 months administration of haloperidol, sulpiride or clozapine. Surprisingly, Bmax for3H-flunitrazepam binding to cerebellar membrane preparations was decreased-by 12 months administration of all drug treatments. The dissociation constant (Kd) for3H-flunitrazepam binding in striatal and cerebellar preparations was not altered. The ability of GABA (0.25–100 μM) alone, and in conjunction with sodium chloride (200 mM), to stimulate specific3H-flunitrazepam binding in striatal and cerebellar preparations was unaltered by haloperidol, sulpiride or clozapine administration for 12 months. The selective effect of haloperidol, but not sulpiride or clozapine, treatment on striatal GAD activity parallels the ability of haloperidol, but not sulpiride or clozapine, to induce striatal dopamine receptor supersensitivity in the same animals. The actions of haloperidol may reflect its greater ability to induce tardive dyskinesia compared to sulpiride or clozapine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01244643
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  • 2
    Electronic Resource
    Electronic Resource
    Effects of motor cortex stimulation on spinal interneurones in intact man (1984)
    Springer
    Experimental brain research 54 (1984), S. 382-384 
    Details
    ISSN: 1432-1106
    Keywords: Cortical stimulation ; Ia inhibition ; H-reflex ; Spinal cord ; Human
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of a descending corticospinal volley on a spinal inhibitory pathway, has been studied in five intact human subjects. Approximately 63% inhibition of the H-reflex evoked in wrist and finger flexor muscles, was produced by motor threshold stimulation of the radial nerve. When a submotor threshold cortical shock was given 2 to 4 ms before the H-reflex, this inhibition was reduced to approximately 38%. The timing of this effect is compatible with either a monosynaptic or disynaptic corticospinal tract projection onto the spinal inhibitory interneurone.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00236241
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  • 3
    Electronic Resource
    Electronic Resource
    Motor strategies involved in the performance of sequential movements (1986)
    Springer
    Experimental brain research 63 (1986), S. 585-595 
    Details
    ISSN: 1432-1106
    Keywords: Movement ; Sequence ; Human
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The present study analyses the strategies adopted by normal subjects when they are asked to make two separate movements as rapidly as possible one after the other. Five subjects performed the following sequential movements in their own time. 1) Squeeze an isometric force transducer between fingers and thumb to a force of 30 N and then flex the elbow of the same arm through 15°. 2) Squeeze the transducer with one hand and then flex the elbow of the other arm. 3) Perform an isotonic opposition of finger and thumb and then flex the elbow of the same arm. 4) First flex the elbow through 15, 30 or 45° and then squeeze the transducer. 5) Flex and then extend the elbow as rapidly as possible. In tasks 1–4 there was no correlation between the times taken to complete the two separate components of the sequence. Because of this we suggest that the two movements remained under the control of two separate motor programmes. In contrast, in task 5, the times taken for the two components were correlated and hence we suggest that in this case a single programme was used to perform the sequence. In tasks 1–3, in which the mean duration of the first movement was some 135–162 ms, there was a mean pause of about 85 ms before the start of the second movement. Subjects tended to chose a minimum inter-onset latency between the start of the first and the start of the second movement of a sequence of some 230 ms. The reason for this appeared to be that if subjects were encouraged to decrease their interonset latencies to less than 200 ms, the speed of the second movement decreased sharply. However, if the duration of the first movement was prolonged as in task 4, the second movement could be delayed, although there now was little or no pause between the two movements. We conclude that when a single motor programme is run, it is followed by a “relative refractory period”. If a second programme is run within this period, it cannot be executed without loss of speed. Switching from one motor programme to another is achieved with an optimal minimum delay of 200 ms. Sequential movements which are controlled by a single programme do not share this limitation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00237481
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  • 4
    Electronic Resource
    Electronic Resource
    Habituation and conditioning of the human long latency stretch reflex (1986)
    Springer
    Experimental brain research 63 (1986), S. 197-204 
    Details
    ISSN: 1432-1106
    Keywords: Stretch reflex ; Habituation ; Human
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of stretch repetition rate, prior warning stimuli and self administered stretch were examined on the size of the short and long latency components of the stretch reflex electromyographic EMG response in flexor pollicis longus and the flexor muscles of the wrist and fingers. Stretches of constant velocity and extent were given every 10 s, 5 s, 2 s, or 1 s to either the wrist or thumb during a small background contraction of the flexor muscles. The size of the long latency component of the stretch reflex (measured as the area under the averaged rectified EMG responses) declined dramatically at faster repetition rates, especially in the wrist and finger flexors. The size of the short latency component was relatively unaffected. The size of the electrically elicited H-reflex in forearm muscles also failed to habituate under the same conditions. If each individual trial of a series was examined, the long latency component of the stretch reflex EMG could be seen to decrease in size over the first three to six stretches if stretches were given every 1 s, but not if stretches were given every 10 s. When stretches were given every 5 s to either wrist or thumb, an electrical stimulus applied to the digital nerves of the opposite hand 1 s before stretch reduced the size of the long latency component of the reflex EMG response. The short latency component was unaffected. Self triggering of wrist or thumb stretch by the subject pressing the stimulator button himself with his opposite hand, also decreased the size of the long latency component of the reflex EMG response without affecting the short latency component. It is concluded that factors other than stretch size or velocity can have marked effects on the size of the long latency component of the stretch reflex. These factors must be taken into account when comparing values of reflex size obtained with different stretching techniques and in different disease states in man.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00235664
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  • 5
    Electronic Resource
    Electronic Resource
    Postural electromyographic responses in the arm and leg following galvanic vestibular stimulation in man (1993)
    Springer
    Experimental brain research 94 (1993), S. 143-151 
    Details
    ISSN: 1432-1106
    Keywords: Vestibular system ; Galvanic stimulation ; Posture ; Electromyogram ; Human
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Application of a small (around 1 mA), constant electric current between the mastoid processes (galvanic stimulation) of a standing subject produces enhanced body sway in the approximate direction of the ear behind which the anode is placed. We examined the electromyographic (EMG) responses evoked by such stimulation in the soleus and in the triceps brachii muscles. For soleus, subjects stood erect, with their eyes closed, leaning slightly forward. The head was turned approximately 90° to the right or left relative to the feet. In averaged records (n=40), current pulses of 25 ms or longer modulated the EMG in a biphasic manner: a small early component (latency 62±2.4 ms, mean ± SEM) was followed by a larger late component (latency 115±5.2ms) of opposite sign, which was appropriate to produce the observed body sway. The early component produced no measurable body movement. Lengthening the duration of the stimulus pulse from 25 to 400 ms prolonged the late component of the response but had little effect on the early component. Short- and long-latency EMG responses were also evoked in the triceps brachii muscle if subjects stood on a transversely pivoted platform and had to use the muscle to maintain their balance in the anteroposterior plane by holding a fixed handle placed by the side of their hip. The latency of the early component was 41±2.6 ms; the latency of the late component was 138±4.3 ms and was again of appropriate sign for producing the observed body sway. Galvanic stimulation evoked no comparable responses in either triceps brachii or soleus muscles if these muscles were not being used posturally. The responses were most prominent if vestibular input provided the dominant source of information about postural stability, and were much smaller if subjects lightly touched a fixed support or opened their eyes. The difference in latency between the onset of the early component of the response in arm and leg muscles suggests that this part of the response uses a descending pathway which conducts impulses down the spinal cord with a velocity comparable with that of the fast conducting component of the corticospinal tract. The late component of the EMG response occurs earlier in the leg than the arm. We suggest that it forms part of a patterned, functional response which is computed independently of the early component.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00230477
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  • 6
    Electronic Resource
    Electronic Resource
    Frequency peaks of tremor, muscle vibration and electromyographic activity at 10 Hz, 20 Hz and 40 Hz during human finger muscle contraction may reflect rhythmicities of central neural firing (1997)
    Springer
    Experimental brain research 114 (1997), S. 525-541 
    Details
    ISSN: 1432-1106
    Keywords: Key words Tremor ; Electromyogram ; Muscle vibration ; Frequency analysis ; Human
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The output from the central nervous system to muscles may be rhythmic in nature. Previous recordings investigating peripheral manifestations of such rhythmic activity are conflicting. This study attempts to resolve these conflicts by employing a novel arrangement to measure and correlate rhythms in tremor, electromyographic (EMG) activity and muscle vibration sounds during steady index finger abduction. An elastic attachment of the index finger to a strain gauge allowed a strong but relatively unfixed abducting contraction of the first dorsal interosseous (1DI). An accelerometer attached to the end of the finger recorded tremor, surface electrodes over 1DI recorded EMG signals and a heart-sounds monitor placed over 1DI recorded vibration. This arrangement enabled maintenance of a constant overall muscle contraction strength while still allowing measurement of the occurrence of tremulous movements of the finger. Ten normal subjects were studied with the index finger first extended at rest and then contracting 1DI to abduct the index finger against three different steady forces up to 50% of maximal voluntary contraction (MVC). Power spectral analysis of tremor, EMG activity and muscle vibration signals each revealed three frequency peaks occurring together at around 10 Hz, 20 Hz and 40 Hz. Coherence analysis showed that the same three peaks were present in the three signals. Phase analysis indicated a fixed time lag of tremor behind EMG of around 6.5 ms. This is compared with previous measurements of electromechanical delay. Other experiments indicated that the three peaks were of central nervous origin. Introducing mechanical perturbations or extra loading to the finger and making recordings under partial anaesthesia of the hand and forearm demonstrated preservation of all the peaks, suggesting that they did not originate from mechanical resonances or peripheral feedback loop resonances. It is concluded that, at least for a small hand muscle, there exist not one but a number of separate peak frequencies of oscillation during active contraction, and that these oscillations reflect synchronization of motor units at frequencies determined within the central nervous system. It is proposed that the multiple oscillations may be a means of frequency coding of motor commands.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00005662
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  • 7
    Electronic Resource
    Electronic Resource
    Alterations in the distribution of glutathione in the substantia nigra in Parkinson's disease (1997)
    Springer
    Journal of neural transmission 104 (1997), S. 661-677 
    Details
    ISSN: 1435-1463
    Keywords: Parkinson's disease ; substantia nigra ; glutathione ; oxidative stress
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Depletion of reduced glutathione occurs in the substantia nigra in Parkinson's disease and in incidental Lewy body disease (presymptomatic Parkinson's disease) which may implicate oxidative stress in the neurode-generative process. In this study mercury orange fluorescent staining and immunostaining with an antibody to reduced glutathione have been used to determine the distribution of reduced glutathione in the substantia nigra in Parkinson's disease compared with normal individuals. Mercury orange staining showed moderate background levels of fluorescence in the neuropil in both control and Parkinson's disease substantia nigra and localised reduced glutathione to the somata of melanized nigral neurons and glial elements of the neuropil. Neuronal nuclei revealed a relative lack of fluorescence after mercury orange staining. There was a significant depletion of reduced glutathione in surviving neurons in Parkinson's disease compared to nerve cell populations in control tissue. Mercury orange fluorescence indicated a high concentration of reduced glutathione in a subpopulation of non-neuronal cells, most likely astrocytes or microglia. Immunohistochemical examination of nigral tissue from the same Parkinson's disease and control patients with an antibody to glutathione showed staining in neuronal perikarya and axonodendritic processes of melanized nigral neurons which was generally most intense in control neurons. Moderately intense staining of the background neuropil, most prominent in control nigras, and staining of capillary walls was also detected. Intense staining was seen in cells with the morphological features of glial cells in both control and PD nigra. These data show a significant presence of reduced glutathione in the cell bodies and axons of nigral neurons. They are in agreement with biochemical studies showing depletion of reduced glutathione in substantia nigra in Parkinson's disease, and indicate a significant loss of neuronal reduced glutathione in surviving nigral neurons in Parkinson's disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01291884
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  • 8
    Electronic Resource
    Electronic Resource
    Thioctic acid does not restore glutathione levels or protect against the potentiation of 6-hydroxydopamine toxicity induced by glutathione depletion in rat brain (1996)
    Springer
    Journal of neural transmission 103 (1996), S. 315-329 
    Details
    ISSN: 1435-1463
    Keywords: Thioctic acid ; 6-OHDA toxicity ; buthionine sulphoximine ; glutathione depletion ; substantia nigra
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Decreased reduced glutathione (GSH) levels are an early marker of nigral cell death in Parkinson's disease. Depletion of rat brain GSH by intracerebroventricular administration of buthionine sulphoximine (BSO) potentiates the toxicity of 6-hydroxydopamine (6-OHDA) to the nigrostriatal pathway. We have investigated whether thioctic acid can replenish brain GSH levels following BSO-induced depletion and/or prevent 6-OHDA induced toxicity. Administration of BSO (2 × 1.6 mg ICV) to rats depleted striatal GSH levels by upto 75%. BSO treatment potentiated 6-OHDA (75 μg ICV) toxicity as judged by striatal dopamine content and the number of tyrosine hydroxylase immunoreactive cells in substantia nigra. Repeated treatment with thioctic acid (50 or 100mg/kg i.p.) over 48h had no effect on the 6-OHDA induced loss of dopamine in striatum or nigral tyrosine hydroxylase positive cells in substantia nigra. Also thioctic acid treatment did not reverse the BSO induced depletion of GSH or prevent the potentiation of 6-OHDA neurotoxicity produced by BSO. Thioctic acid (50mg or 100mg/kg i.p.) alone or in combination with BSO did not alter striatal dopamine levels but increased dopamine turnover. Striatal 5-HT content was not altered by thioctic acid but 5-HIAA levels were increased. Under conditions of inhibition of GSH synthesis, thioctic acid does not replenish brain GSH levels or protect against 6-OHDA toxicity. At least in this model of Parkinson's disease, thioctic acid does not appear to have a neuroprotective effect.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01271243
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