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Biomedical subjects

H Asanuma

Publications and source records attributed to H Asanuma.

At least 109 records · Page 6Linked to original sources
PubMed1992

Synaptic proliferation in the motor cortex of adult cats after long-term thalamic stimulation.

1. One of the hypotheses for information storage in the CNS postulates the induction of structural changes in synaptic circuits. This postulate predicts that behavioral experiences produce changes in neural activity that subsequently induce synaptogenesis in the mature CNS. Available data indicate that the establishment of engrams for novel motor acts may involve alterations of synaptic interactions within the primary motor cortex. The present study examines the hypothesis that patterns of synaptic circuitry and of synaptic activation are rearranged after enhanced neural activity in pathways projecting to the motor cortex. 2. Electrodes implanted in the ventroposterolateral (VPL) nucleus of the thalamus were used for long-term stimulation (20 microA, 4 days) of afferents to the motor cortex in freely behaving, adult cats. This stimulation primarily affected corticocortical inputs from the somatosensory cortex (area 2) to area 4 gamma of the motor cortex. Electron microscopy and stereological procedures were used to compare the numerical density (Nv) of various types of synapses in layers II/III of the stimulated (experimental) motor cortex with the Nv of the corresponding synapses in the contralateral (control) hemisphere. 3. Long-term stimulation produced a significant increase (25.6%) in synaptic Nv in experimental motor cortex. This increase was due primarily to an increase in the Nv of asymmetrical synapses with dendritic spines. The numbers of symmetrical synapses, and of asymmetrical synapses with dendritic shafts, were not affected by long-term stimulation. 4. Synaptic active zones [calculated by measuring the lengths of postsynaptic densities (PSDs)] were significantly longer in experimental motor cortex. Lengthening of PSDs occurred selectively in asymmetrical synapses with dendritic shafts (28% increase). 5. The Nv of synapses having perforations in their PSDs (perforated synapses) was significantly higher in experimental hemispheres. Also increased was the incidence of synapse-associated polyribosomes, which are most commonly found at the base of dendritic spines. An increase in the number of perforated synapses and of polyribosomes are both morphological hallmarks of synaptogenesis. 6. The percentages of synapses having different curvatures (i.e., presynaptically concave, convex, or flat) were similar in experimental and in control motor cortex.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Neurons of the pretectal area convey spinal input to the motor thalamus of the cat.

The aim of this study was to corroborate lesioning work (Mackel and Noda 1989), suggesting the pretectal area of the rostral midbrain acts as a relay between the spinal cord and the ventrolateral (VL) nucleus of the thalamus. For this purpose, extracellular recordings were made from neurons in the pretectal area which were antidromically activated by stimulation in the rostral thalamus, particularly in VL. The neurons were tested for input from the dorsal columns of the spinal cord, the dorsal column nuclei, and the ventral quadrant of the spinal cord. Latencies of the antidromic responses ranged between 0.6 and 3.0 ms (median 1.0 ms): no differences in latencies were associated with either location of the neurons in the pretectal area or with the site of their thalamic projection. Orthodromic responses to stimulation of ascending pathways were seen in the majority of neurons throughout the pretectal area sampled. Latencies of orthodromic responses varied considerably, with ranges of 0.9-9 ms, 6-20 ms, and 2.5-20 ms upon stimulating the dorsal column nuclei, dorsal columns, and ventrolateral quadrant, respectively. The shortest-latency responses to stimulation of the dorsal column nuclei or of the ventral quadrant were likely to be monosynaptic. Temporal and spatial facilitation of the responses to ascending input were common. The data show that neurons of the pretectal area are capable of relaying somatosensory input ascending from the spinal cord to the rostral thalamus. It is suggested that the pretectofugal output to VL converges with cerebellar input in VL neurons and becomes incorporated in cerebello-cerebral interactions and, ultimately, the control of movement.

Animals↗
PubMed1991

Minimal stimulus parameters and the effects of hyperpolarization on the induction of long-term potentiation in the cat motor cortex.

The aim of the research program of which the present work is a part is to understand the neural mechanisms involved in motor learning and memory. One of the mechanisms postulated to be involved in this process is the induction of long-term potentiation (LTP) in the motor cortex. LTP can be induced in motor cortical neurons by tetanic stimulation of their afferents from the somatosensory cortex. In the present study, the effects of different stimulating parameters on the induction of LTP were examined, using in-vivo, intracellular recordings from anesthetized cats. The expression of LTP was documented by measuring the amplitude and rise-time of excitatory postsynaptic potentials (EPSPs) before and after tetanic stimulation. The minimal tetanic stimulation capable of systematically inducing LTP was found to consist of a train of stimuli at 50 Hz, 5 s. Shorter trains of stimulation produced only a short-lasting, transient potentiation. In different cells, identical stimulation parameters resulted in different degrees of potentiation of synaptic responses. Following all the stimulation trains examined, EPSP amplitudes were transiently depressed before reaching potentiated levels. The duration of this depression was directly correlated with the duration and the frequency of the tetanic stimulation. In all the cells in which LTP was induced, the variability in the amplitudes of potentiated EPSP was significantly greater than that of control EPSP amplitudes. Hyperpolarization of the postsynaptic cell, during the delivery of the tetanic stimulation, inhibited the induction of LTP. These phenomena are discussed in relation to the postulated mechanisms of LTP induction in the cortex.

Afferent Pathways↗
PubMed1991

Miniature manipulator with microelectrode for chronic recording of single units from freely-moving animals.

We report a simple recording and stimulating system, a miniature manipulator with a microelectrode (MMM) that can be mounted on animal's skull. The system consists of a miniature manipulator and a microelectrode which are used in one body. Several MMMs can be implanted simultaneously into the brain as the part of the manipulator is small. With this device, recording of single units from several different cortices is possible from awake and unrestricted animals.

Animals↗
PubMed1991

Neuronal mechanisms of motor learning in mammals.

Neural mechanisms subserving the acquisition of new motor skills are discussed in this article. Motor learning is defined, in this context, as the acquisition of novel motor skills. It is proposed that complex motor skills are acquired through a process of segmental motor learning, in which movement segments are formed, and retrieved for the execution of the learned skill. Individual movement segments are created by modulating neural activity in loop circuits that link the motor cortex and the periphery. This neural modulation occurs through synaptic plasticity in the motor cortex. Increase of synaptic efficacy in existing neural circuits, in the form of long-term potentiation (LTP), is proposed to be involved in earlier stages of motor learning. It is suggested that the retention of motor skills involves formation of new synapses.

Animals↗
PubMed1991

Long-term potentiation of thalamic input to the motor cortex induced by coactivation of thalamocortical and corticocortical afferents.

1. Intracellular recordings were obtained from neurons in the motor cortex (MCx), in which excitatory postsynaptic potentials (EPSPs) were evoked by microstimulation of the somatosensory cortex (SCx) and the ventrolateral nucleus (VL) of the thalamus. The effects of combined tetanic stimulation of SCx and VL on the amplitudes of these EPSPs were studied. 2. Amplitudes of both corticocortical (CC) and thalamocortical (TC) EPSPs were potentiated after combined tetanic stimulation. This potentiation occurred exclusively in neurons that were located in the superficial layers (II/III) and that received direct input from both the SCx and VL, with both inputs synapsing in close proximity to each other. In all cases, the potentiation lasted until the electrode went out of the cell (21 +/- 25 min, mean +/- SD) the longest being 90 min. We therefore refer to this potentiation as long-term potentiation (LTP). 3. Tetanic stimulation of the thalamus only did not produce LTP in neurons receiving direct input from the VL. 4. LTP was not induced in either CC or TC EPSPs in neurons located in layer V and/or in neurons receiving long-latency CC EPSPs. 5. It is concluded that TC input from the VL to the MCx is potentiated only when coactivated with the CC input from the SCx.

Animals↗
PubMed1990

Identification of neurons producing long-term potentiation in the cat motor cortex: intracellular recordings and labeling.

Intracellular, in vivo recordings were used to identify and subsequently to label neurons in the cat motor cortex in which long-term potentiation (LTP) was induced. Thirty-nine motor cortical neurons that produced excitatory postsynaptic potentials (EPSPs) in response to microstimulation in areas 1-2 (SI) or in area 5a (SIII) were studied. Amplitudes of EPSPs produced in response to test stimulation (1 Hz) were recorded before and after tetanic stimulation (200 Hz, 20 seconds). In 25/39 cells (64%), EPSP amplitudes were significantly increased following the tetanic stimulation (65 +/- 51% average increase), and remained at the potentiated level as long as stable recordings could be maintained (20 +/- 18 minutes, maximum = 90 minutes). LTP was induced exclusively in cells that produced monosynaptic EPSPs in response to area 1-2 or area 5a stimulation. Of the 39 analyzed cells, 13 were labeled by intracellular injections of 5% biocytin. Neurons in which LTP was induced included both pyramidal and nonpyramidal cells and were located exclusively in layers II or III of the motor cortex; cells in deeper cortical layers were not potentiated. These findings indicate that various corticocortical inputs can increase the efficacy of synaptic transmission in a subset of motor cortical neurons. We propose that this plasticity in synaptic transmission constitutes one of the bases of motor learning and memory.

Animals↗
PubMed1990

Formation of new synapses in the cat motor cortex following lesions of the deep cerebellar nuclei.

The effects of unilateral lesions of the deep cerebellar nuclei on the corticocortical (CC) projection from the somatosensory to the motor cortex were studied in adult cats, utilizing electrophysiological and electron microscopical methods. Axon terminals in the motor cortex belonging to CC afferents were labeled by degeneration induced by lesions of the somatosensory cortex; neurons in the motor cortex were labeled by the Golgi/EM method. In each cat, data from the motor cortex (MCx) contralateral (experimental) and ipsilateral (control) to the cerebellar lesion were compared. Cerebellar lesions produced marked motor deficits, which receded gradually and disappeared after 30 to 40 days. Subsequent lesions of the somatosensory cortex (area 2) contralateral to the cerebellar lesions resulted in the reappearance of the cerebellar symptoms. The number of CC synapses per unit area in experimental MCx was significantly higher than in control MCx. The increase in the number of CC synapses was apparent throughout layers II-V of the MCx, but was most prominent in layers II/III. The increase in the number of CC synapses in experimental MCx was due mainly to an increase of axon terminals synapsing with dendritic spines belonging to pyramidal neurons. In comparison, the numbers and spatial distribution of CC synapses with aspinous, nonpyramidal neurons from both experimental and control MCx were similar. Field potentials in the experimental MCx, evoked by stimulation of area 2, were altered following cerebellar lesions. In experimental MCx, the polarity of the early component of the field potentials reversed at cortical depths corresponding to layers II-III, whereas this reversal was not observed in control MCx. These findings suggest that lesions of the cerebellar nuclei induced sprouting of axon terminals in the MCx to establish a new function. The results provide the first anatomical evidence for the generation of new synapses in the adult CNS which is not induced by elimination of existing synapses.

Animals↗
PubMed1990

Morphological and physiological identification of neurons in the cat motor cortex which receive direct input from the somatic sensory cortex.

The population of neurons in the cat motor cortex which receives monosynaptic input from a specific functional region of the somatic sensory cortex was identified with the techniques of intracellular recording and staining with HRP. Both pyramidal and nonpyramidal cells located in the superficial layers of the pericruciate cortex responded to stimulation of the sensory cortex with short latency, excitatory postsynaptic potentials. More than half of the labeled cells were classified as pyramidal cells and the remainder as sparsely spinous or aspinous nonpyramidal cells. The characteristics of the EPSP's of the 2 groups of cells, ie. latency, time from beginning to peak and amplitude were found to vary only slightly. The results suggest that input from the sensory cortex impinges upon neurons which may in turn have an excitatory or inhibitory effect on cortico-fugal neurons in the motor cortex.

Animals↗
PubMed1990

Long-term potentiation in the cat somatosensory cortex.

Intracellular, in-vivo recordings were used to identify neurons in the cat somatosensory cortex in which long-term potentiation (LTP) was induced. Amplitudes of EPSPs produced by microstimulation in the motor cortex (area 4 gamma) were recorded before and after tetanic stimulation (200 Hz, 20 s). In 8/13 cells (62%), EPSP amplitudes increased significantly following the tetanic stimulation. LTP was induced exclusively in cells which produced monosynaptic EPSPs. Six of these cells were labeled by intracellular injections of biocytin. All the cells in which LTP was induced were pyramidal neurons, and were located exclusively in layers II or III of the somatosensory cortex; cells in deeper cortical layers were not potentiated. These data substantiate our previous findings demonstrating LTP in corticocortical pathways and suggest that these pathways play an important role in cortical synaptic plasticity.

Animals↗
PubMed1990

Long-lasting facilitation of pyramidal tract input to spinal interneurons.

The purpose of this study was to determine whether long-term changes in synaptic efficacy can be induced in the pyramidal tract (PT). Tetanic stimulation of the PT induced long-term facilitation of PT input to spinal cord neurons. In contrast, tetanic stimulation of the pyramidal tract did not alter the efficacy of synaptic inputs of PT cells' intracortical axon collaterals to other cortical neurons. These findings suggest that the PT participates in motor learning by modulating the excitability of spinal cord neurons. The results also indicate that induction of LTP in the PT is dependent on postsynaptic mechanisms.

Animals↗
PubMed1989

Physiological properties and patterns of projection in the cortico-cortical connections from the second somatosensory cortex to the motor cortex, area 4 gamma, in the cat.

The physiological properties of neurons in the second somatosensory cortex (SII), and the pattern of projection of these neurons to area 4 gamma of the motor cortex in cat were studied by using single unit recording and collision techniques. Antidromically activated neurons were recorded along the anterior and posterior regions of the lateral bank of the anterior suprasylvian sulcus (ASSS) and from the middle part of the anterior ectosylvian gyrus (AESG) following weak intracortical microstimulation (ICMS) to area 4 gamma. Stimulation of the region around the activated neurons failed to produce muscle contraction or movement with currents of 30 microA or less. The majority of antidromically identified neurons received somatotopically organized afferent inputs from the skin on the contralateral side of the body. A small number of SII neurons received bilateral input. In 91% of the cases receptive field information was available for both the antidromically activated SII neuron and for neurons around the stimulating electrode in area 4 gamma. In 71% of these cases, both cortical sites were activated by sensory input from the same or adjacent peripheral area of the body. Neurons in the rostrocaudal region of the lateral bank of ASSS and the upper part of AESG (forelimb area) projected to the lateral cruciate gyrus of the motor cortex (forelimb area), while neurons in the ventrocaudal region of the medial part of AESG (hindlimb area) projected to the medial part of the postcruciate subregion of the motor cortex (hindlimb area). Antidromically activated SII neurons were typically found in layer III. These results suggest a topographically organized pattern of projection to the motor cortex from SII.

Animals↗
PubMed1989

Functional role of the sensory cortex in learning motor skills in cats.

The functional role of corticocortical input projecting to the motor cortex in learning motor skills was investigated by training 3 cats with and without the projection area. After unilateral removal of areas 1, 2, 2 praeinsularis and a part of 5, the cat was placed in a box and trained to pick up a small piece of food from a beaker in front of the box. Since the beaker and the edge of the box had a space in between, the cat had to develop a new motor skill to being the food back to the box across the space. This skill consisted of combined supination and flexion of the paw to hold the food over the gap. In all 3 cats, the training period necessary for acquisition of the motor skill for the forelimb contralateral to the lesioned brain was significantly longer than the period necessary for the forelimb ipsilateral to the lesioned cortex. Ablation of the remaining projection area after completion of the training did not impair the learned motor skill. The results suggest that the input from the lesioned area to the motor cortex participates in learning motor skills.

Animals↗
PubMed1989

Long-term potentiation in the motor cortex.

Long-term potentiation (LTP) is a model for learning and memory processes. Tetanic stimulation of the sensory cortex produces LTP in motor cortical neurons, whereas tetanization of the ventrolateral nucleus of the thalamus, which also projects to the motor cortex, does not. However, after simultaneous high-frequency stimulation of both the sensory cortex and the ventrolateral nucleus of the thalamus, LTP of thalamic input to motor cortical neurons is induced. This associative LTP occurs only in neurons in the superficial layers of the motor cortex that receive monosynaptic input from both the sensory cortex and the ventrolateral nucleus of the thalamus. Associative LTP in the motor cortex may constitute a basis for the retention of motor skills.

Animals↗
PubMed1988

Functional role of corticoperipheral loop circuits during voluntary movements in the monkey: a preferential bias theory.

The functional role of the sensory input to the motor cortex in the execution of voluntary movements is still controversial. We have proposed that the input functions by changing the excitability of cortical efferent columns before and during movements (Asanuma and Arissian, 1984). Experiments were performed to support this hypothesis. Monkeys were trained to sit still in a chair and to pick up a food pellet from a food board rotating at a high speed, so that the subjects had to concentrate their efforts to pick up the pellet. Microelectrode recordings were made from pre- and post-central cortical neurons related to hand movement during the pickup task. It was found that neurons in the motor (10%) and in the sensory (5%) cortices started discharging far ahead of actual movement of the hand. EMGs in the target muscles, which were identified by microstimulation at the recording sites, revealed that some muscles changed their tone during these premovement discharges, although there were no visible movements of the hand. Section of the dorsal columns abolished the premovement discharges and also produced retardation of motor skills. The results supported the hypothesis that circulation of impulses between the cortical efferent columns and the periphery before the movement plays an important role in the execution of skilled movements.

Animals↗
PubMed1987

Importance of the projection from the sensory to the motor cortex for recovery of motor function following partial thalamic lesion in the monkey.

Motor deficits produced by thalamic lesions were studied using adult cynomolgus monkeys. Lesioned areas included n. ventralis anterior (VA), ventralis lateralis (VL), n. ventralis posterolateralis pars oralis (VPLo), pars caudalis (VPLc) n. subthalamus (STN) and n. centrum medianum (CM). When the lesion included VA, VL and VPLo, there was a cerebellar syndrome, i.e., ataxia and dysmetria. When the lesion included VPLo and VPLc, the animal was paralyzed. When the lesion included VPLo and rostral part of VPLc, there was loss of orientation in hand movement and clumsiness of finger manipulation. These motor deficits gradually disappeared within 1-2 weeks and the function recovered near to normal except for when VPLo and VPLc were totally destroyed. After recovery of motor function, the somatic sensory cortex (areas 1, 2, 3b) ipsilateral to the thalamic lesion was removed. Removal of the sensory cortex resulted in abolition of the recovered function, but when the border area between VPLo and VPLc was intact, the function recovered again. On the other hand, when the thalamic lesion included this border area, succeeding cortical lesion permanently abolished the recovered function or the reappeared function was substantially worse than that before the cortical lesion. Neuronal mechanisms subserving these differences are discussed and it is concluded that when direct sensory input to the motor cortex was interrupted by lesion of the border area between VPLo and VPLc, the lost function was compensated by reorganization of the projection from the sensory cortex to the motor cortex.

Animals↗
PubMed1987

Reorganization of the projection from the sensory cortex to the motor cortex following elimination of the thalamic projection to the motor cortex in cats; Golgi, electron microscope and degeneration study.

Changes of terminal connections of projection fibers from area 2 of the sensory cortex to the motor cortex following chronic lesion in the thalamus were examined using the electron microscope. The lesioned areas included nucleus ventralis anterior, n. ventralis lateralis and rostral part of n. ventralis posterolateralis. The synaptic sites were identified using the Golgi impregnation method to identify postsynaptic neurons in the motor cortex and the axonal degeneration method to identify presynaptic terminals of fibers originating from area 2. The following results were obtained. (1) The number of degenerating terminals per unit area in the motor cortex was increased to nearly twice that in normal animals. (2) The number of degenerating terminals synapsing with stellate cells was not increased but stayed more or less the same as in normal animals. (3) The number of degenerating terminals contacting pyramidal cells increased substantially, to more than twice that in normal animals. (4) These newly formed synapses were found on proximal dendritic shafts of the pyramidal cells in both layers III and V, suggesting that these synapses occupied the spaces where the thalamocortical terminals were located. (5) The functional significance of these newly formed synapses was discussed in relation to the recovery of motor function following thalamic lesion.

Animals↗