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At least 343 records · Page 19Linked to original sources

PubMed2000

Contralateral movement and extensor force generation alter flexion phase muscle coordination in pedaling.

The importance of bilateral sensorimotor signals in coordination of locomotion has been demonstrated in animals but is difficult to ascertain in humans due to confounding effects of mechanical transmission of forces between the legs (i.e., mechanical interleg coupling). In a previous pedaling study, by eliminating mechanical interleg coupling, we showed that muscle coordination of a unipedal task can be shaped by interlimb sensorimotor pathways. Interlimb neural pathways were shown to alter pedaling coordination as subjects pedaling unilaterally exhibited increased flexion-phase muscle activity compared with bilateral pedaling even though the task mechanics performed by the pedaling leg(s) in the unilateral and bilateral pedaling tasks were identical. To further examine the relationship between contralateral sensorimotor state and ipsilateral flexion-phase muscle coordination during pedaling, subjects in this study pedaled with one leg while the contralateral leg either generated an extensor force or relaxed as a servomotor either held that leg stationary or moved it in antiphase with the pedaling leg. In the presence of contralateral extensor force generation, muscle activity in the pedaling leg during limb flexion was reduced. Integrated electromyographic activity of the pedaling-leg hamstring muscles (biceps femoris and semimembranosus) during flexion decreased by 25-30%, regardless of either the amplitude of force generated by the nonpedaling leg or whether the leg was stationary or moving. In contrast, rectus femoris and tibialis anterior activity during flexion decreased only when the contralateral leg generated high rhythmic force concomitant with leg movement. The results are consistent with a contralateral feedforward mechanism triggering flexion-phase hamstrings activity and a contralateral feedback mechanism modulating rectus femoris and tibialis anterior activity during flexion. Because only muscles that contribute to flexion as a secondary function were observed, it is impossible to know whether the modulatory effect also acts on primary, unifunctional, limb flexors or is specific to multifunctional muscles contributing to flexion. The influence of contralateral extensor-phase sensorimotor signals on ipsilateral flexion may reflect bilateral coupling of gain control mechanisms. More generally, these interlimb neural mechanisms may coordinate activity between muscles that perform antagonistic functions on opposite sides of the body. Because pedaling and walking share biomechanical and neuronal control features, these mechanisms may be operational in walking as well as pedaling.

Adult↗

PubMed1993

Rationale for the rational development of new cardiac imaging agents.

There are several prerequisites for the development of new diagnostic cardiovascular radiopharmaceuticals. Agents which are proposed for clinical use must offer significant advantages in one or more of the following categories: I) Radiopharmacy [dosimetry, dose preparation, dose availability]; II) Imaging characteristics [spatial and temporal resolution, radiotracer biokinetics, patient throughput and acquisition protocols]; and III) Measurement of a previously unmeasurable physiologic or pharmacologic event [metabolic pathways, receptors, neural pathways, preclinical disease]. Technetium-99m-based radiopharmaceuticals are particularly attractive, in view of their excellent characteristics for imaging with the Anger gamma camera. In addition, the increasing use of tomographic imaging and reconstruction techniques has magnified the importance of developing radiotracers with minimal soft tissue attenuation effects. Technetium-99m and positron emitting radioisotopes offer this advantage. A wide choice of biologically and pharmacologically relevant ligands are available for complexing with these radiotracers. The clinical studies are underway in order to validate these new agents, and to determine their value in the modern practice of nuclear medicine. Technetium-99m sestamibi is just one example of a novel radiotracer with improved imaging characteristics that has undergone careful pre-clinical and clinical testing, and which has emerged as a useful diagnostic imaging agent. Future studies should be directed towards the development of tracers with well-defined biokinetic characteristics, which are advantageous for tomographic imaging. The future applications of tracer imaging techniques for the pre-clinical diagnosis of cardiovascular, oncologic and other medical conditions are significant and are expanding.(ABSTRACT TRUNCATED AT 250 WORDS)

Heart↗

PubMed1994

The neural mechanism of apomorphine-induced erection: an experimental study by comparison with electrostimulation-induced erection in the rat model.

The rat model of an apomorphine (APO)-induced erection is accepted as a rapid, reproducible way of observing whether erectile capability is present. However there are still questions that can be asked about whether an APO erection shares the same neural pathway as a physiologic erection. We compared APO-induced erections of sham-operated rats with those in rats that had the hypogastric, pelvic and cavernous nerves ablated bilaterally. The results suggest that an APO-induced erection is a vascular event primarily mediated via the sacral parasympathetic nerve system and that, in case of injury to the parasympathetic nerve system, it may also be mediated by the thoracolumbar sympathetic pathway. Similarity in the neural pathways between APO-induced erection and a psychogenic erection makes this animal model useful for study of psychogenic erectile reflexes.

Animals↗

PubMed1999

The role of opioid-dopamine interactions in the induction and maintenance of ethanol consumption.

1. Alcohol is one of the most widely used recreational drugs, but also one of the most widely abused, causing vast economic, social and personal damage. 2. Several animal models are available to study the reinforcing mechanisms that are the basis of the abuse liability of ethanol. Innate differences in opioid or dopamine neurotransmission may enhance the abuse liability of ethanol, as indicated by animal and human studies. 3. Opioid antagonists have been shown to be effective, both experimentally and clinically, in decreasing ethanol consumption, presumably since ethanol induces the release of endogenous opioid peptides in vivo. However, ethanol may also stimulate the formation of opiate-like compounds, which could interact with opioid (or dopamine) receptors. Ethanol may cause changes in neurotransmission mediated via opioid receptors that determines whether alcohol abuse is more or less likely. 4. Ethanol appears to facilitate dopamine release by increasing opioidergic activity, disinhibiting dopaminergic neurons (by inhibition of GABAergic neurotransmission) via mu-opioid receptors in the ventral tegmental area (VTA) and delta-opioid receptors in the nucleus accumbens (NAcc). The effects of ethanol would be antagonised by presynaptic kappa-opioid receptors present on dopaminergic terminals in the NAcc. 5. Mesolimbic dopamine release induced by ethanol consumption seems to indicate ethanol-related stimuli are important, focussing attention on and enabling learning of the stimuli. However, studies indicate that there are redundant pathways, and neural pathways 'downstream' of the mesolimbic dopamine system, which also enable the reinforcing properties of ethanol to be mediated.

Alcohol Drinking↗

PubMed2004

Orexins (hypocretins) directly interact with neuropeptide Y, POMC and glucose-responsive neurons to regulate Ca 2+ signaling in a reciprocal manner to leptin: orexigenic neuronal pathways in the mediobasal hypothalamus.

Orexin-A and -B (hypocretin-1 and -2) have been implicated in the stimulation of feeding. Here we show the effector neurons and signaling mechanisms for the orexigenic action of orexins in rats. Immunohistochemical methods showed that orexin axon terminals contact with neuropeptide Y (NPY)- and proopiomelanocortin (POMC)-positive neurons in the arcuate nucleus (ARC) of the rats. Microinjection of orexins into the ARC markedly increased food intake. Orexins increased cytosolic Ca(2+) concentration ([Ca(2+)](i)) in the isolated neurons from the ARC, which were subsequently shown to be immunoreactive for NPY. The increases in [Ca(2+)](i) were inhibited by blockers of phospholipase C (PLC), protein kinase C (PKC) and Ca(2+) uptake into endoplasmic reticulum. The stimulation of food intake and increases in [Ca(2+)](i) in NPY neurons were greater with orexin-A than with orexin-B, indicative of involvement of the orexin-1 receptor (OX(1)R). In contrast, orexin-A and -B equipotently attenuated [Ca(2+)](i) oscillations and decreased [Ca(2+)](i) levels in POMC-containing neurons. These effects were counteracted by pertussis toxin, suggesting involvement of the orexin-2 receptor and Gi/Go subtypes of GTP-binding proteins. Orexins also decreased [Ca(2+)](i) levels in glucose-responsive neurons in the ventromedial hypothalamus (VMH), a satiety center. Leptin exerted opposite effects on these three classes of neurons. These results demonstrate that orexins directly regulate NPY, POMC and glucose-responsive neurons in the ARC and VMH, in a manner reciprocal to leptin. Orexin-A evokes Ca(2+) signaling in NPY neurons via OX(1)R-PLC-PKC and IP(3) pathways. These neural pathways and intracellular signaling mechanisms may play key roles in the orexigenic action of orexins.

Animals↗

PubMedDate not supplied

Response to maintenance of tourniquet inflation in a primate model.

Several theories have been proposed, but the etiology and pathway of neural transmission for the sensation of tourniquet pain remain unknown. This study was designed to observe the circulatory response and to measure the stress response markers associated with maintenance of tourniquet inflation in an anesthetized primate model. Eight African Green monkeys (Cercopithecus aethiops) were anesthetized, and heart rate (HR) and systolic and diastolic blood pressure (SBP and DBP) were measured every five minutes. In each animal, a control trial without tourniquet inflation was compared to an experimental trial with tourniquet inflation on the left lower extremity to 300 mmHg for a period of 90 minutes. After maintenance of tourniquet inflation for a period of 30-45 minutes, each animal demonstrated a gradual, progressive increase in HR, SBP and DBP as compared to preinflation baseline values (p less than 0.05). An increase in serum cortisol and plasma norepinephrine was demonstrated to correlate with the circulatory response in this model. The results of this study suggest that the circulatory response to maintenance of tourniquet inflation in this animal model may be mediated by a neurohumoral response to tourniquet pain and that an animal model may be appropriate for further studies into the etiology and neural pathways associated with the sensation of tourniquet pain.

Anesthesia, General↗

PubMed1995

Anterograde tracing of trigeminal afferent pathways from the murine tooth pulp to cortex using herpes simplex virus type 1.

Due to its predominantly nociceptive innervation, viral tracing from the tooth pulp provides a potential means for tracing central pain pathways. The neural pathways from the tooth pulp to cortex were determined using in situ hybridization to detect the anterograde transneuronal spread of herpes simplex virus type 1 strain H129 following inoculation into the murine mandibular incisor pulp. Virus first appeared in the brain at day 3 in the dorsomedial region of all three subnuclei of the spinal trigeminal nucleus and the principal sensory nucleus. By days 5-6 virus had spread to the contralateral medial nucleus of the medial geniculate complex, posterior thalamus, and ventroposteromedial thalamus. At days 7-8 virus was detected in laminae IV and Va of the primary somatosensory cortex and lamina IV of the secondary somatosensory cortex in regions previously shown to receive input from the lower jaw. Several mice also showed infection of laminae II/III of the ipsilateral dysgranular insular cortex, along with labeling for virus in the ipsilateral external lateral parabrachial nucleus, posterior thalamus, and posterior basolateral amygdala. Our results are highly consistent with previous tracing and electrophysiological studies utilizing the tooth pulp and with studies implicating the infected structures in nociception. Viral spread appeared to define two separate afferent systems with infection of structures which have been implicated in the sensory-discriminative aspects of pain, such as the ventroposteromedial thalamus and somatosensory cortex, as well as in the dysgranular insular cortex and related subcortical nuclei which may have a role in the affective-motivational aspects of pain.

Afferent Pathways↗

PubMed1997

Regulation of interneuron function in the C. elegans thermoregulatory pathway by the ttx-3 LIM homeobox gene.

Neural pathways, which couple temperature-sensing neurons to motor and autonomic outputs, allow animals to navigate away from and adjust metabolism rates in response to the temperature extremes often encountered. ttx-3 is required for the specification of the AIY interneuron in the C. elegans neural pathway that mediates thermoregulation. ttx-3 null mutant animals exhibit the same thermotactic behavioral defect as that seen with laser ablation of AIY in wild type, suggesting that AIY does not signal in this mutant. ttx-3 encodes a LIM homeodomain protein. A ttx-3-GFP fusion gene is expressed specifically in the adult AIY interneuron pair, which connects to thermosensory neurons. In ttx-3 mutant animals, the AIY interneuron is generated but exhibits patterns of abnormal axonal outgrowth. Thus, the TTX-3 LIM homeodomain protein is likely to regulate the expression of target genes required late in AIY differentiation for the function of this interneuron in the thermoregulatory pathway. The ttx-3-dependent thermosensory pathway also couples to the temperature-modulated dauer neuroendocrine signaling pathway, showing that ttx-3 specifies AIY thermosensory information processing of both motor and autonomic outputs.

Amino Acid Sequence↗

PubMed1984

Latex beads as probes of a neural crest pathway: effects of laminin, collagen, and surface charge on bead translocation.

In the trunk region of avian embryos, neural crest cells migrate along two pathways: dorsally just under the ectoderm, and ventrally between the neural tube and the somites. Previous work from this laboratory has shown that uncoated latex beads are able to translocate along the ventral neural crest pathway after injection into young embryos; however, beads coated with fibronectin are restricted from the ventral route ( Bronner -Fraser, M.E., 1982, Dev. Biol., 91: 50-63). Here, we extend these observations to determine the effects of other macromolecules on bead distribution. The data show that laminin-coated beads, like fibronectin-coated beads, are restricted from the ventral pathway. In contrast, beads coated with type I collagen translocate ventrally after injection. Because macromolecules have characteristic charge properties, changes in surface charge caused by coating the beads may confound interpretation of the results. Electrostatic effects on bead movement were examined by coating the latex beads with polyamino acids in order to predictably alter the initial surface charge. The surface charge before injection was measured for beads coated with amino acid polymers or with various biologically important macromolecules; the subsequent translocation ability of these beads was then monitored in the embryo. Polylysine-coated beads (positively charged) were restricted from the ventral pathway as were fibronectin and laminin-coated beads, even though fibronectin and laminin beads were both negatively charged. In contrast, polytyrosine -coated beads ( neutrally charged) translocated ventrally as did negatively charged collagen-coated or uncoated beads. The results demonstrate that no correlation exists between the charge properties on the latex bead surface and their subsequent ability to translocate along the ventral pathway. Therefore, an adhesion mechanism independent of surface charge effects must explain the restriction or translocation of latex beads on a neural crest pathway.

Animals↗

PubMed2002

Interneuronal signalling is involved in induction of collateral sprouting of nociceptive axons.

Collateral sprouting of cutaneous nociceptive axons into the adjacent denervated skin critically depends on the nerve growth factor, presumably originating from the degenerated neural pathways and denervated skin. We hypothesised that the degenerated neural pathways are necessary, but not sufficient, to induce collateral sprouting of nociceptive axons, and, in addition, that the interaction between the injured and non-injured neurones within a dorsal root ganglion can trigger sprouting of nociceptive axons also in the absence of the denervated skin. End-to-side nerve anastomosis, made in female Wistar rats by suturing the end of an excised peroneal nerve segment to the side of the intact sural nerve, was used as a model for sprouting which allowed us to study the putative induction mechanisms separately. If the nerves adjacent to the sural nerve were transected concomitantly with the coaptation of the end-to-side anastomosis, robust nociceptive axon sprouting into the anastomosed nerve segment was observed by the nerve pinch test and counting of myelinated axons. Collateral sprouting did not occur, however, either if the cells in the anastomosed nerve segment were killed by freezing and thawing, or if the adjacent nerves had not been injured. However, if the ipsilateral dorsal cutaneous nerves, having their neurones in the same dorsal root ganglia as the sural nerve, were transected, but no other nerves were injured, then the sural nerve axons sprouted in abundance through the anastomosis even in the absence of denervated skin around the sural nerve terminals. From these results we suggest that cells (probably proliferating Schwann cells) in the degenerated neural pathways are necessary but not sufficient to induce collateral sprouting of nociceptive axons, and that interactions between the injured and non-injured neurones within the dorsal root ganglion (i.e. direct or indirect interneuronal signalling) are important in this regard.

Animals↗

PubMed1979

Interlimb coordination during stepping in the cat: an electromyographic analysis.

1. Simultaneous electromyographic (EMG) records were obtained from a single-joint extensor muscle of each of the four limbs of intact cats during repeated overground stepping trials. 2. In each limb, the temporal spacing of step cycles was determined by measurements of the intervals between consecutive terminations of EMG activity, since this occurs in a consistent relationship to the removal of the limb from the ground. By measuring the latencies between step cycles so determined, the temporal spacing of step cycles between limbs was determined. Each latency was expressed as a function of step duration or as a phase interval. 3. Analysis of the cooordination of step cycles of both homologous limb pairs (the forelimbs and hindlimbs), both homolateral limb pairs (the fore- and hindlimb on the right and left sides), and both sets of diagonal limbs suggest that the step cycles of the four limbs are coordinated according to a few frequently occurring patterns. However, the representation of a large number of phase intervals between these preferred patterns indicates a substantial amount of variability in interlimb coupling. 4. Analysis of the interaction of different interlimb-coupling patterns indicates that during alternate coordination of hindlimbs, coupling of the other limbs is fairly predictable. The step cycles of the forelimbs and hindlimbs are spaced according to a trotting form of coupling. During in-phase coordination of hindlimbs, the patterns of coordination of the other limbs are more diffuse. Forelimbs step cycles are coupled via a number of different modes, as are those of the forelimbs and hindlimbs. 5. It is concluded that the step cycles of different limbs are coordinated, but the association of observed patterns of coordination with any known neural pathways or the interaction of neural pathways should be approached with caution. The variability about the frequently occurring patterns is interpreted as an expression of the faculatative capabilities of the neural mechanisms controlling locomotion. Thus, these data favor a model of interlimb control during stepping, which recognizes preferred patterns of coordination and the variability about these patterns.

Animals↗

PubMedDate not supplied

Neuroanatomical specificity of the circuits controlling sympathetic outflow to different targets.

1. Despite the emerging framework that central neural pathways controlling the activity of the sympathetic nervous system are capable of producing highly selective responses, the specific neural pathways governing different sympathetic outflows are poorly understood. 2. Anatomical studies suggest that five brain areas, namely the rostral ventrolateral medulla, the rostral ventromedial medulla, the caudal raphe nuclei, the region containing the A5 noradrenergic neurons and the paraventricular hypothalamic nucleus, provide dominant supraspinal innervation of sympathetic preganglionic neurons. 3. The anatomical parcellation of different functions within and among these cell groups is uncertain. However, recent studies using transynaptic retrograde labelling of neural pathways connected to various sympathetic targets suggest that the circuits controlling these different targets may be partially distinct. Similarly, anatomical studies relying on stimulus-evoked expression of immediate early genes, such as c-fos, suggest that different sympathetic responses may be controlled by distinct, neural circuits. 4. Thus, although many similarities exist in the anatomical circuits innervating different sympathetic targets, possibly supporting the orchestration of global sympathetic responses, differences are also discernible.

Adipose Tissue, Brown↗

PubMed1988

Effect of bladder outlet obstruction on micturition reflex pathways in the rat.

The effect of outlet obstruction on neural pathways to the bladder was examined six weeks after urethral ligation in rats. Ligated rats exhibited a seven-fold increase in bladder weight, a six-fold increase in volume, and significant increases (p less than 0.001) in micturition pressure, residual volume and compliance measured under urethane anesthesia. Unanesthetized ligated rats in comparison to control rats voided smaller volumes of urine more frequently (0.7 vs 1.1 voids/hr., p less than 0.001). Electrophysiological examination of vesical afferent and efferent peripheral neural pathways in the pelvic and hypogastric nerves and sympathetic chain did not reveal any differences in thresholds, axonal conduction velocities or ganglionic transmission. A significant difference (p less than 0.05) was noted in the percentage of obstructed rats (100%) exhibiting a short latency spinal reflex as compared to controls (35%). The long latency supraspinal micturition reflex was similar in both groups. These data suggest that obstruction in rats is accompanied by some degree of neural plasticity resulting in a more prominent spinal reflex that could contribute to the development of the unstable bladder following obstruction in humans and unanesthetized animals.

Animals↗

PubMed2001

PACAP mediates the neural proliferative pathway of Mastomys enterochromaffin-like cell transformation.

BACKGROUND AND AIM: Pituitary adenylate-cyclase activating peptide (PACAP) is a more potent proliferative agent than gastrin for rat enterochromaffin-like (ECL) cell proliferation in vitro. The role of this neurotransmitter during gastrin-mediated ECL cell tumor formation and gastrin-autonomous ECL cell neoplasia is unknown. METHODS AND RESULTS: ECL cell transformation was induced in the Mastomys using 16 wk H2 receptor blockade of acid inhibition. Examination of the epithelial fundic mucosa demonstrated that PACAP-immunoreactivity significantly increased in the tumor mucosa compared to the naïve stomach, and was associated with ECL cells. Naïve and tumor ECL cells were then purified (approximately 95%) from Mastomys and the presence of all three PACAP/VPAC receptor subtypes was demonstrated by polymerase chain-reaction amplification. Thereafter, cells were maintained in short-term (48 h) primary cultures. PACAP significantly (p<0.05) increased 24 h bromo-deoxyuridine uptake (approximately 4-fold) in both cell types with estimated EC(50) values of approximately 4x10(-16) M and approximately 2x10(-16) M, respectively. Specific receptor antagonists (PAC1/VPAC1) of PACAP competitively inhibited these proliferative effects in naïve cells. Oligonucleotide antisense directed against PAC1 significantly inhibited PACAP-stimulated DNA synthesis by approximately 85% (p<0.05) in tumor cells. CONCLUSION: PACAP is a potent and effective modulator of ECL cell proliferation. The expression of this neuropeptide and its receptors, particularly PAC1, suggest the existence of a neural regulatory pathway of ECL cell proliferation and transformation.

Animals↗

PubMed2004

Probabilistic pathway representation of cognitive information.

We present for mental processes the program of mathematical mapping which has been successfully realized for physical processes. We emphasize that our project is not about mathematical simulation of the brain's functioning as a complex physical system, i.e., mapping of physical and chemical processes in the brain on mathematical spaces. The project is about mapping of purely mental processes on mathematical spaces. We present various arguments--philosophic, mathematical, information, and neurophysiological--in favor of the p-adic model of mental space. p-adic spaces have structures of hierarchic trees and in our model such a tree hierarchy is considered as an image of neuronal hierarchy. Hierarchic neural pathways are considered as fundamental units of information processing. As neural pathways can go through the whole body, the mental space is produced by the whole neural system. Finally, we develop the probabilistic neural pathway model in that mental states are represented by probability distributions on mental space.

Cognition↗

PubMed2006

Activity-dependent regulation of synaptic strength and neuronal excitability in central auditory pathways.

Neural activity plays an important role in regulating synaptic strength and neuronal membrane properties. Attempts to establish guiding rules for activity-dependent neuronal changes have led to such concepts as homeostasis of cellular activity and Hebbian reinforcement of synaptic strength. However, it is clear that there are diverse effects resulting from activity changes, and that these changes depend on the experimental preparation, and the developmental stage of the neural circuits under study. In addition, most experimental evidence on activity-dependent regulation comes from reduced preparations such as neuronal cultures. This review highlights recent results from studies of the intact mammalian auditory system, where changes in activity have been shown to produce alterations in synaptic and membrane properties at the level of individual neurons, and changes in network properties, including the formation of tonotopic maps.

Animals↗

PubMed1988

Synaptic reorganization in the hippocampus induced by abnormal functional activity.

Abnormal functional activity induces long-lasting physiological alterations in neural pathways that may play a role in the development of epilepsy. The cellular mechanisms of these alterations are not well understood. One hypothesis is that abnormal activity causes structural reorganization of neural pathways and promotes epileptogenesis. This report provides morphological evidence that synchronous perforant path activation and kindling of limbic pathways induce axonal growth and synaptic reorganization in the hippocampus, in the absence of overt morphological damage. The results show a previously unrecognized anatomic plasticity associated with synchronous activity and development of epileptic seizures in neural pathways.

Animals↗

PubMed1990

Habenula as a relay in the descending pathway from nucleus accumbens to periaqueductal grey subserving antinociception.

This study explored the possibility of a relay at habenula for the descending neural pathway of antinociception. The latency of the escape response elicited by radiant heat on the snout of the rabbit was taken as index of nociception. (1) Microinjection of 20 micrograms of morphine into nucleus accumbens resulted in a one-fold increase in nociceptive threshold 20-40 min after the injection. This effect of morphine was markedly attenuated by naloxone or met-enkephalin antiserum administered to the nucleus habenula, suggesting that the release of met-enkephalin in habenula is essential for the antinociception induced by morphine injected into nucleus accumbens. (2) Injection of 10 micrograms of morphine into habenula produced a significant increase in escape response latency 20-40 min after the injection. This antinociceptive effect of morphine was attenuated by naloxone or muscimol, and enhanced by bicuculline methochloride administered to periaqueductal grey, suggesting that morphine may act on habenula to activate a descending neural pathway extending to periaqueductal grey to induce an antinociceptive effect, which seems to utilize endogenous opioid peptides and gamma-aminobutyric acid as its mediators. Taking together, the results suggest that habenula is an important relay in the descending neural pathway from nucleus accumbens to periaqueductal grey subserving antinociception.

Animals↗