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Three forms of the scratch reflex in the spinal turtle: movement analyses.

The scratch reflex is a motor task exhibited by the hindlimb of a turtle after complete transection of the spinal cord just posterior to the forelimb enlargement. The scratch is elicited by applying gentle tactile stimulation to a site innervated by spinal segments caudal to the level of the transection. During the scratch response, the ipsilateral hindlimb reaches toward and rubs against the stimulated site. Each scratch response consists of either a single rub or a rhythmic series of rubs. There are three types or "forms" of the scratch reflex in the spinal turtle: rostral scratch (previously termed the scratch reflex in Refs. 5, 43, 45), pocket scratch, and caudal scratch. We have characterized each scratch form according to which portion of the hindlimb is used to rub against the stimulated site. During a rostral scratch, the dorsum of the foot and/or toes is used to rub against the stimulated site. During a pocket scratch, the side of the thigh, knee, and/or calf is used to rub. During a caudal scratch, the heel or side of the foot is used to rub. Each scratch form has a distinct receptive field on the turtle shell and skin. A rhythmic scratch response to maintained tactile stimulation consists of as many as 10-25 cycles. We have divided each cycle of movement into a prerub, rub, and postrub phase. Extension of the knee joint occurs during the rub phase of each scratch cycle for all scratch forms. The timing of the extension phase of the knee joint movement within the protraction-retraction (flexion-extension) cycle of the hip joint is different for each form of the scratch. During a rostral scratch, extension of the knee joint occurs when the hip is protracted. During a pocket scratch, knee extension occurs when the hip is retracting. During a caudal scratch, knee extension occurs when the hip is retracted. The spinal turtle therefore shifts the timing of movements of a distal joint (knee) with respect to the timing of movements of a proximal joint (hip) to obtain appropriate scratching movements to different regions of the body. A narrow transition zone exists between the receptive field for one form of the scratch and the nearby receptive field for another form of the scratch. There is a rostral-pocket transition zone and caudal-pocket transition zone in the spinal turtle.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Electrical activation of the pocket scratch central pattern generator in the turtle.

1. A low-spinal, immobilized turtle displays a fictive scratch reflex in hindlimb motor neurons in response to tactile stimulation of the shell (17, 19). Turtles exhibit three forms of the scratch reflex: rostral, pocket, and caudal. Each form is elicited by tactile stimulation of a different receptive field on the body surface. The ventral-posterior pocket (VPP) cutaneous nerve innervates the ventral-posterior portion of the pocket scratch receptive field (Fig. 1). Natural stimulation within the VPP nerve's receptive field evoked a pocket scratch reflex (Fig. 2A). Electrical stimulation of this nerve elicited robust pocket scratch reflexes (Fig. 2, B and C). 2. A single electrical pulse to the VPP nerve delivered at a voltage (greater than 5 V, 0.1 ms) that activated all the axons in the nerve was termed a "maximal" pulse. A single maximal pulse did not evoke a scratch motor response. It raised the excitability of the pocket scratch central pattern generator for several seconds, however. We revealed such excitability changes by applying maximal pulses to the VPP nerve at multisecond intervals (Figs. 5 and 6). When we delivered maximal pulses with interpulse intervals of less than or equal to 5 s, the first pulse produced no motor response and the second pulse evoked one or more cycles of pocket scratch. 3. A stimulus pulse applied to the VPP nerve was used as a probe for studying changes in the excitability of the pocket scratch CPG following scratch motor patterns. In a rested preparation, the stimulus pulse did not activate motor output. In contrast, the stimulus pulse evoked one or two cycles of pocket scratch activity if delivered within 2.5 s after the cessation of rhythmic pocket scratch motor activity (Figs. 7-9). These results are consistent with the hypothesis that the pocket scratch CPG has elevated excitability for seconds following the cessation of pocket scratch motor output. A single pulse applied to the VPP nerve evoked no response if delivered after the cessation of rostral scratch motor activity, however (Fig. 9D). 4. We used a train of maximal pulses to the VPP nerve to probe the form-specificity of the changes in the excitability following a rostral scratch motor pattern (Fig. 10). We set the stimulus parameters so that the train evoked one or two cycles of a pocket scratch motor pattern in a preparation that had rested for over 1 min.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Sensory-evoked pocket scratch motor patterns in the in vitro turtle spinal cord: reduction of excitability by an N-methyl-D-aspartate antagonist.

1. In intact turtles, tactile stimulation of the body surface in the "shell pocket" region surrounding the hindlimb elicits a pocket scratch reflex, in which the hindlimb reaches toward and rhythmically rubs the stimulated site. In the present study, we utilized reduced in vitro preparations of the turtle spinal cord with attached peripheral nerves to investigate the time course and pharmacology of sensory-evoked excitability in the pocket scratch neural network. Fictive pocket scratch motor output was elicited by electrically stimulating either the ventral-posterior pocket (VPP) cutaneous nerve or the distal D8 (d.D8) nerve. Both nerves contain afferents innervating part of the pocket scratch receptive field. 2. Six-segment (D7-S2) preparations of the spinal cord, which included the entire hindlimb enlargement, produced fictive pocket scratch motor output in response to VPP nerve stimulation (n = 6). We recorded fictive motor output as electroneurograms from up to five peripheral nerves in D7-S2 preparations, including three knee extensor muscle nerves (IT-KE, which innervates triceps femoris pars iliotibialis; AM-KE, which innervates pars ambiens; and FT-KE, which innervates pars femorotibialis), a hip flexor (protractor) muscle nerve (VP-HP, which innervates puboischiofemoralis internus, pars anteroventralis), and a mixed cutaneous-muscle nerve that exhibits hip-extensor-correlated motor output during the scratch (d.D8). The timing characteristics of activity in these nerves during in vitro motor patterns were similar to what has been observed during the in vivo pocket scratch. 3. Even a single segment of spinal cord from the anterior hindlimb enlargement (D8) contained sufficient neural circuitry to generate rhythmic motor patterns in AM-KE, VP-HP, and d.D8 nerves during repeated stimulation of VPP (n = 5) or d.D8 (n = 1). Stimulus trains delivered at 3-5 Hz for > or = 6 s elicited one or more VP-HP bursts with clear burst terminations; in some cases, these were followed by distinct hip-extensor-correlated d.D8 bursts. AM-KE timing was characteristic of a pocket scratch synergy, beginning during the VP-HP burst and continuing after VP-HP offset. Thus even isolated D8 segments were capable of expressing rhythmic alternation between hip-flexor- and hip-extensor-correlated motor bursts as well as a pocket-scratch-specific knee-hip synergy. 4. A single electrical pulse delivered to the VPP or d.D8 nerve increased the excitability of the pocket scratch network in D7-S2 and D8 preparations for > or = 5-10 s. We estimated the time course of increased excitability by observing the temporal summation of scratch motor output in response to single pulses applied to cutaneous afferents at multisecond intervals. Stimulus parameters were adjusted so that a single pulse delivered to a "rested" preparation (rested = no stimulation for > 2 min) was at or just below threshold for evoking motor output. Single pulses delivered at 5- to 10-s intervals evoked strongly summating scratch motor output in D7-S2 and D8 preparations. These results show that neural mechanisms that store sensory-evoked excitation in the pocket scratch circuit exist within the spinal hindlimb enlargement and even within the isolated D8 segment. 5. With the use of in vitro preparations, we have begun to examine the pharmacology of sensorimotor processing in the pocket scratch network. Application of the N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-5-phosphonovaleric acid (APV) (50-100 microM) to the spinal cord greatly reduced pocket scratch excitability. APV lowered the motor burst frequency of pocket scratch responses in D7-S2 preparations elicited by 3-Hz stimulation; it also reduced the amplitude of summating motor output in D7-S2 and D8 preparations in response to single electrical stimuli delivered at 5-s intervals. These results indicate that NMDA receptors have a key role in synaptic processing and sustained excitation within the pocket scratch neura

2-Amino-5-phosphonovalerate↗

Reconstruction of flexor/extensor alternation during fictive rostral scratching by two-site stimulation in the spinal turtle with a transverse spinal hemisection.

Analyses of fictive scratching motor patterns in the spinal turtle with transverse hemisection provided support for the concept of bilateral shared spinal cord circuitry among neurons responsible for generating left- and right-side rostral, pocket, and caudal fictive scratching. Rhythmic bursts of hip flexor activity, the hip extensor deletion variation of fictive rostral scratching, were elicited by ipsilateral stimulation in the rostral scratch receptive field of a spinal turtle [transection at the segmental border between the second (D2) and third (D3) postcervical spinal segments] with a contralateral transverse hemisection one segment anterior to the hindlimb enlargement (at the D6-D7 segmental border). In addition, other sites were stimulated in this preparation: (1) contralateral sites in a rostral, pocket, or caudal scratch receptive field or (2) ipsilateral sites in a caudal scratch receptive field. A reconstructed fictive rostral scratch motor pattern of rhythmic alternation between hip flexor and hip extensor activation was produced by simultaneous stimulation of one site in the ipsilateral rostral scratch receptive field and another site in one of the other scratch receptive fields. This reconstructed rostral scratch motor pattern resembled the normal rostral scratch motor pattern produced by one-site rostral scratch stimulation of a spinal turtle (D2-D3 transection) with no additional transections. The observation of a reconstructed rostral scratch motor pattern produced by two-site stimulation in the spinal turtle with transverse hemisection supports the concept that hip extensor circuitry activated by stimulation of other scratch receptive fields is shared with circuitry activated by ipsilateral rostral scratch receptive field stimulation.

Animals↗

Afferent control of central pattern generators: experimental analysis of scratching in the decerebrate cat.

Systematic quantitative analysis of changes in the spinal scratching generator motor activity evoked by tonic and phasic peripheral afferent signals during "fictitious" scratching was carried out in the cat. Correlations between the kinematics of hindlimb scratching movement, sensory inflow, and primary afferent depolarization were investigated. Reliable correlations between the parameters of generator motor activity during fictitious scratching were revealed: they depended on tonic peripheral afferent inflow. The functional role of these dependencies consists of providing stability for aiming the hindlimb to the itch site. It was shown that scratching generator reaction to a phasic sensory signal depended significantly on afferent input, signal intensity, and its arrival phase in the cycle of motor activity. Phase correction of "scratching" rhythm was performed by inhibition of the current stage of "scratching" cycle, the inhibition magnitude depending on the intensity of a sensory signal run along high threshold afferent fibers. The moments in the scratching cycle, in which the afferent signal caused no rearrangement in scratching generator activity, were discovered for all investigated afferent inputs. These moments corresponded to the transitions from one scratching cycle phase to another. Integral afferent activity was distributed unevenly in the cycle during real scratching. The main part of it was observed just in that scratching cycle part which included the above mentioned no rearrangement phase points. The data obtained allowed us to conclude that the scratching generator should be considered as a working program for the motor optimal control system containing the intrinsic model of the controlled object dynamics (e.g. hindlimb scratching movement dynamics), which produces an inner analog of peripheral flow. This inner flow interacts with peripheral afferent inflow just as one of the latter components. Centrally originated modulation of primary afferent depolarization is a result of affecting the depolarization generating system by this inner "sensory" activity. It is the model, with the aid of which the generator can work after deafferentation. The functional organization of a central pattern generator is considered.

Afferent Pathways↗

Quantitative assessment of directed hind limb scratching behavior as a rodent itch model.

Hind limb scratching is used increasingly as an itch model in rodents. Scratching is usually quantified as the number of scratching bouts over a 60 min period. Since the antipruritic effect of scratching should depend on the total time of skin contact, then the duration of scratching bouts and within-bout scratching frequency may also be important factors. Therefore, we measured these parameters during episodes of scratching directed toward the site (nape of neck) of intradermal injection of serotonin in Sprague-Dawley rats. Serotonin elicited significantly more scratching bouts than saline. There was a biphasic pattern of scratching over time, with peaks at 10-20 and 40-50 min. Although cumulative bout duration (2-min intervals) had a similar biphasic distribution, the mean individual bout duration (2.1 s) did not change significantly over time. Within-bout scratching frequency remained constant over time at 8 Hz. The number of scratching bouts was suppressed in a dose dependent manner by naltrexone (3 and 5 mg/kg), while the individual bout duration and the within-bout frequency were not significantly different compared with serotonin-evoked scratching without naltrexone. These results validate the total number of scratching bouts as an indicator of the magnitude of itch-related scratching.

Animals↗

Three forms of the scratch reflex in the spinal turtle: central generation of motor patterns.

A turtle with a complete transection of the spinal cord, termed a spinal turtle, exhibits three types or "forms" of the scratch reflex: the rostral scratch, pocket scratch, and caudal scratch (21). Each scratch form is elicited by tactile stimulation of a site on the body surface innervated by afferents entering the spinal cord caudal to the transection. We recorded electromyographic (EMG) potentials from the hindlimb during each of the three forms of the scratch in the spinal turtle (see Fig. 1). Common to all scratch forms is the rhythmic alternation of the activity of the hip protractor muscle (VP-HP) and hip retractor muscle (HR-KF). Each form of the scratch displays a characteristic timing of the activity of the knee extensor muscle (FT-KE) with respect to the cycle of activity of the hip muscles VP-HP and HR-KF. In a rostral scratch, activation of FT-KE occurs during the latter portion of VP-HP activation. In a pocket scratch, activation of FT-KE occurs during HR-KF activation. In a caudal scratch, activation of FT-KE occurs after the cessation of HR-KF activation. The timing characteristics of these muscle activity patterns correspond to the timing characteristics of changes in the angles of the knee joint and the hip joint obtained with movement analyses (21). We recorded electroneurographic (ENG) potentials from peripheral nerves of the hindlimb during each of the three forms of the "fictive" scratch in the spinal turtle immobilized with neuromuscular blockade (see Fig. 4). Common to all forms of the fictive scratch is the rhythmic alternation of the activity of hip protractor motor neurons (VP-HP) and hip retractor motor neurons (HR-KF). Each form displays a characteristic timing of the activity of knee extensor motor neurons (FT-KE) with respect to the cycle of VP-HP and HR-KF motor neuron activity. The timing characteristics of these motor neuron activity patterns are similar to the timing characteristics of the muscle activity patterns obtained in the preparation with movement (cf. Figs. 1 and 4). The motor pattern for each scratch form is generated centrally within the spinal cord. In the spinal immobilized preparation, neuromuscular blockade prevents both limb movement and phasic sensory input, and complete spinal transection isolates the cord from supraspinal input.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Characterization of scratching responses in rats following centrally administered morphine or bombesin.

The aim of this study was to characterize scratching behavior elicited by central administration of morphine or bombesin in rats, and to determine the role of opioid receptors in scratching induced by both pruritogenic agents. Central administration included intracisternal (i.c.), intrathecal (i.t.), and intracerebroventricular (i.c.v.) routes. Scratching events made with hind paws were counted by observers blinded to treatment conditions. Intracisternal morphine (0.01-0.1 microg) produced dose-dependent increases in scratching; the maximum response to i.c. morphine 0.1 microg was approximately 500 scratches within a 1-hour period. Neither i.t. nor i.c.v. morphine significantly increased scratching. Bombesin (0.01-0.32 microg) elicited robust scratching following i.c. administration. The maximum response to i.c. bombesin 0.32 microg was approximately 4000 scratches within a 1-hour period. Both i.t. and i.c.v. bombesin produced profound scratching at similar doses. Antagonist studies confirmed that mu-opioid receptors selectively mediate i.c. morphine-induced scratching. However, selective mu-, kappa-, and delta-opioid antagonists did not attenuate i.c. bombesin-induced scratching. These results demonstrate that morphine and bombesin elicit scratching through different receptor mechanisms, at different central sites, and to different degrees.

Analgesics, Opioid↗

Spinal cord coordination of hindlimb movements in the turtle: intralimb temporal relationships during scratching and swimming.

Spinal cord neuronal circuits generate motor neuron activity patterns responsible for rhythmic hindlimb behaviors such as scratching and swimming. Kinematic analyses of limb movements generated by this motor neuron output reveal important characteristics of these behaviors. Intralimb kinematics of the turtle hindlimb were characterized during five distinct rhythmic forms of behavior: three forms of scratching and two forms of swimming. In each movement cycle for each form, the angles of the hip and knee joints were measured as well as the timing of a behavioral event, e.g., rub onset in scratching or powerstroke onset in swimming. There were distinct differences between the kinematics of different forms of the same behavior, e.g., rostral scratch versus pocket scratch. In contrast, there were striking similarities between forms of different behaviors, e.g., rostral scratch versus forward swimming. For each form of behavior there was a characteristic angular position of the hip at the onset of each behavioral event (rub or powerstroke). The phase of the onset of knee extension within the hip position cycle occurred while the hip was flexing in the rostral scratch and forward swim and while the hip was extending in the pocket scratch, caudal scratch, and back-paddling form of swimming. The phase of the onset of the behavioral event was not statistically different between rostral scratch and forward swim; nor was it different between pocket scratch and caudal scratch. These observations of similarities at the movement level support the suggestion that further similarities, such as shared spinal circuitry, may be present at the neural circuitry level as well.

Animals↗

Scratch hardness of stone models--measuring conditions.

This study investigated the effects of scratch load, scratch speed, and storage period of specimen on the scratch hardness of stone models. Types 4 and 5 stone specimens were made from vinyl silicone rubber and alginate impressions respectively. After specimens were stored in a desiccator with silica gel at room temperature for 24 hours or 1 week, scratches were created on the surface with three different scratch loads (1N, 2N, and 3N) and two different scratch speeds (50 and 100 mm/min). Then, the depths of scratches were measured. Scratch depth of stone specimens increased with increasing scratch load. Scratch depths of Type 4 stone specimens after 1-week storage were smaller than those after 24-hour storage at a speed of 100 mm/min. However, the effect of scratch speed on scratch depth did not follow a specific trend.

Alginates↗

Spinal cord segments containing key elements of the central pattern generators for three forms of scratch reflex in the turtle.

The immobilized, low-spinal turtle produces 3 forms of the fictive scratch reflex in response to tactile stimulation of specific sites on its body surface (Robertson et al., 1985). We used complete transections of the spinal cord at different rostrocaudal levels to reveal the minimum length of spinal cord sufficient to produce each scratch form. Additional transections revealed the progressive loss of elements of the motor pattern and the eventual loss of rhythmogenesis. We have identified, therefore, spinal cord segments containing key elements of each scratch form's central pattern generator (CPG). The turtle spinal cord consists of 8 cervical segments (C1-C8), 10 dorsal segments (D1-D10), 2 sacral segments (S1, S2) and about 16 caudal segments (Ca1-Ca16; Kusuma et al., 1979). The cell bodies of motor neurons innervating the hindlimb muscles are located in the hindlimb enlargement, segments D8-S2 (Ruigrok and Crowe, 1984). The receptive field for the rostral scratch is innervated by segments D3-D6; the pocket scratch receptive field is innervated by segments D6-D8; the caudal scratch receptive field is innervated by segments S2, Ca1, and more caudal segments (Mortin and Stein, 1985). A rostral scratch motor pattern could be produced with as few as 5 or 6 segments, i.e., segments D5-D9 or D3-D8. The anterior 3 segments of the hindlimb enlargement, D8-D10, could produce a pocket scratch motor pattern. A single segment, either D7 or D8, is capable of rhythmogenesis in response to stimulation of sites in its part of the pocket receptive field. A caudal scratch motor pattern could be produced by D8-End (the hindlimb enlargement and more caudal segments). The posterior 40-80% of the hindlimb enlargement is not necessary for the production of a rostral or pocket motor pattern. The anterior segment of the enlargement is necessary for the production of a normal caudal scratch motor pattern. Key elements of the CPG for each of the 3 scratch forms reside in segments D7-D10. The pattern-generating capacity of the anterior half of the hindlimb enlargement is greater than the posterior half; such an asymmetric distribution of pattern-generating elements in the enlargement of the spinal cord has been described for cat scratching (Deliagina et al., 1983). These results are consistent with the hypothesis that the CPGs producing different motor patterns for the hindlimb share neuronal elements (Grillner, 1981; Robertson et al., 1985; Currie and Stein, 1988, 1989).

Animals↗

Messages conveyed by spinocerebellar pathways during scratching in the cat. II. Activity of neurons of the ventral spinocerebellar tract.

(1) The activity of neurons of the ventral spinocerebellar tract (VSCT) during scratching was studied in thalamic and decapitate cats. The neurons were identified antidromically either by stimulation of the hindlimb area in the anterior lobe of the cerebellum (in thalamic cats) or by stimulation of the contralateral ventrolateral funiculus of the spinal cord (in decapitate cats). The scratch reflex was elicited by stimulation of either the pinna (in thalamic cats) or the cervical spinal cord (in decapitate cats). In most experiments, animals were immobilized and the activity of VSCT neurons was recorded during fictitious scratching. (2) During both actual and fictitious scratching, the discharge of VSCT neurons was rhythmically modulated in relation with the scratch cycle: neurons fired in bursts separated with periods of silence. Phases of activity of different neurons were unevenly distributed over the scratch cycle: most neurons fired within the limits of the flexor phase of the cycle. (3) The firing pattern of VSCT neurons during fictitious scratching was similar to that during actual scratching. Therefore, rhythmical burst firing of VSCT neurons is determined mainly by central mechanisms and not by a rhythmical sensory input. (4) The firing pattern of VSCT neurons in decapitate cats was similar to that in thalamic cats. Therefore, rhythmical burst firing of VSCT neurons is determined mainly by the central spinal mechanism and not by supraspinal motor centers. (5) The VSCT neurons which fired in long bursts during the greater part of the flexor phase were usually activated during the latent period of scratching, while those firing later in the cycle were usually either inhibited or not affected during this period. (6) The antidromic response in most VSCT neurons could be evoked from a large number of points in the hindlimb area of the cerebellar anterior lobe, both in the vermis and in the pars intermedia. Due to such extensive branching of axons, each point of the cortex receives signals from neurons firing in different phases of the cycle. But axons of VSCT neurons firing in long bursts during the greater part of the flexor phase terminate more extensively in the pars intermedia, while axons of neurons firing later in the cycle terminate more extensively in the vermis. (7) The functioning of the VSCT is essentially similar to that of the spino-reticulocerebellar pathway (SRCP). Both pathways convey messages about activity of the central spinal mechanism generating the motor output pattern of scratching, but the VSCT is active mainly in the flexor phase of the scratch cycle and the SRCP in the extensor one. A hypothesis is advanced that these pathways monitor activity of different groups of spinal interneurons.

Animals↗

A peripheral 5-HT1D-like receptor involved in serotonergic induced hindlimb scratching in rats.

The pharmacological characteristics of hindlimb scratching induced by serotonergic compounds were studied. We conclude that hindlimb scratching induced by serotonergic compounds is mediated by a serotonin1D (5-HT1D) or 5-HT1D-like receptor outside the blood-brain barrier because hindlimb scratching could be induced by s.c. injection of 5-methoxytryptamine (5-MeOT), 5-carboxamidotryptamine (5-CT), bufotenine, 5-hydroxytryptamine (5-HT) and tryptamine. These compounds have high affinity for 5-HT1A and 5-HT1D receptors. The 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), the 5-HT1C receptor agonist MK 212, and the mixed 5-HT1C/5-HT2 receptor agonists (dl)-1-(2,5 dimethoxy-4-iodophenyl)-2-aminopropane (DOI) and quipazine did not induce hindlimb scratching. Rather, the latter compounds attenuated 5-MeOT-induced hindlimb scratching. The 5-HT releasing compounds fenfluramine and p-chloroamphetamine (PCA) inhibited whereas the 5-HT re-uptake inhibitors fluvoxamine and indalpine potentiated 5-MeOT-induced hindlimb scratching. 5-MeOT-induced hindlimb scratching could be inhibited dose dependently by the alpha 2-adrenoceptor blockers yohimbine and rauwolsince, which also have high affinity for 5-HT1D receptors, whereas the alpha 2-adrenoceptor blocker piperoxan only weakly counteracted hindlimb scratching. Haloperidol, apomorphine, morphine, clonidine and methiothepin strongly attenuated hindlimb scratching, atropine, naloxone and ICS 205930 attenuated it weakly whereas domperidone, methylatropine and mepyramine were inactive in doses up to 10 mg/kg. Hindlimb scratching induced by 5-MeOT was potentiated by the 5-HT receptor antagonists metergoline, methysergide, mesulergine, mianserin, ritanserin and xylamidine. Hindlimb scratching was not induced by i.c.v. injection of 5-MeOT.(ABSTRACT TRUNCATED AT 250 WORDS)

5-Methoxytryptamine↗

Mechanisms of supraspinal correction of scratching generator.

The influences of signals in descending systems on the parameters of scratching generator activity were studied on decerebrate immobilized cats. It was shown that phasic electric stimulation of descending systems evoked certain phase-dependent reorganization of the parameters of scratching generator efferent activity. Maximum increase in scratching cycle duration during electric stimulation of Deiters' nucleus, red nucleus and pyramidal tract is observed during stimulation in the first half of aiming phase. Stimulation in the second half of aiming phase and at the beginning of scratching jerk phase virtually does not change the scratching cycle duration. Maximum increase in scratching cycle duration during electric stimulation of the nucleus reticularis gigantocellularis is observed in the second half of aiming phase. Electric activation of descending pathways during aiming phase increases its intensity and decreases the intensity of scratching jerk phase. Activation of descending pathways during scratching jerk phase increases its intensity and virtually does not change the aiming phase intensity. Influences of electric activation of descending systems on scratching generator work reveal dependence on limb position. They are increased when the limb is deflected to the rear and are decreased during over-aimed position. Decerebellation leads to a decrease of scratching generator activity parameters rearrangement under influence of electric stimulation of the red nucleus and nucleus reticularis gigantocellularis, and to its increase during Deiters' nucleus stimulation. On the basis of these results the principles of supraspinal correction of scratching generator work are discussed.

Animals↗

Involvement of unique mechanisms in the induction of scratching behavior in BALB/c mice by compound 48/80.

Compound 48/80 induced scratching behavior in BALB/c mice, and the role of mast cell mediators in this behavior was examined. Mouse scratching behavior was detected and evaluated using a new apparatus, MicroAct. Compound 48/80 increased the incidence of scratching behavior and scratching time in a dose-dependent manner, accompanied by a potent activation of mast cells and a potent increase in vascular permeability. Dibucaine and mu-opioid receptor antagonists inhibited the scratching behavior. Although histamine H(1) receptor antagonists potently inhibited the vascular permeability increase, they did not affect the scratching behavior. Methysergide inhibited the scratching behavior slightly without affecting the vascular permeability increase, whereas cyproheptadine inhibited both. A cyclooxygenase inhibitor, a 5-lipoxygenase-activating protein inhibitor and a PAF receptor antagonist did not affect the scratching behavior. High doses of serotonin induced scratching behavior less frequently than did compound 48/80. Furthermore, mast cell-deficient WBB6F1-W/W(v) mice exhibited frequent scratching behavior after injection of compound 48/80. These results clearly indicate that compound 48/80 can induce scratching behavior in mice independent of mast cell mediators.

Animals↗