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Olfactory responses in the gustatory area of the parabrachial pons.

Electrophysiological responses to olfactory and gustatory stimuli were recorded in the same neural elements in the parabrachial nuclei (PbN) of rats under Flaxedil. Responses to olfactory stimuli varied in temporal pattern and magnitude from responses to gustatory stimuli. Intravenous infusion of Nembutal while recording from one unit appeared to alter the pattern of responsiveness across stimuli. Most importantly the response to one olfactory stimulus (vanilla) was eliminated by this procedure. Olfactory-gustatory elements were located in the lateral portion of the taste-responsive area of the PbN, just below the brachium conjunctivum. These results suggest that the PbN receives input from both olfactory and gustatory pathways and that these pathways may converge on the same neural elements within the PbN. This convergence may be part of a neurophysiological substrate for the perception of flavor.

Administration, Oral↗

Effect of activity on the selective stabilization of the motor innervation of fast muscle posterior latissimus dorsi from chick embryo.

The role of neuromuscular activity in the maturation of the motor innervation was investigated in the fast focally innervated posterior latissimus dorsi (PLD) muscle of the chick embryo. The axonal supply in the PLD motor nerve, and the focal multiple innervation of the endplates were described on days 15 and 16 of embryonic life in normal and experimental embryos. In the first series of experiments, chick embryos were paralyzed by repeated injections between days 4 and 10 in ovo of the curare-like agent, flaxedil. Twice more axons in the PLD motor nerve and about twice more nerve terminal profiles at the endplates in the PLD muscles were found in paralyzed than in control embryos. In a second series of experiments, electrodes were implanted around the spinal cord of 7-day-old embryos and electric pulses delivered at 0.5 Hz frequency from day 10 to days 15-16 of incubation. At day 15.5, no change was observed in the axonal supply in the PLD motor nerve of stimulated embryos, while a two-fold decrease was observed in the number of motor nerve terminal profiles per endplate in the corresponding PLD muscle. The statistical distribution of the number of motor nerve terminal profiles per endplate was described from complete semi-serial sections in the PLD muscle from normal, paralyzed and stimulated chick embryos. In these three cases, the distribution of supernumerary nerve terminal profiles followed a Poisson law after one nerve ending had been subtracted from the number of nerve endings counted per endplate.

Animals↗

[The induction of seizures in "Papio papio" following allylglycine alone or in combination with intermittent photic stimulation (author's transl)].

Allylglycine, an inhibitor of GABA synthesis, produces increased sensitivity to photic stimulation and in convulsant doses spontaneous seizures arising occipitally in the baboon (Horton and Meldrum, 1973). In this study, convulsant doses of allylglycine induced either sharp wave and polyspike frontorolandic discharges (FR) or critical posterior discharges which then reinforce the fronto-rolandic spikes. A seizure may then arise from the fronto-rolandic region and secondarily spread to the rest of the cerebral cortex. Intermittent photic stimulation produces a reinforcement of the fronto-rolandic sharp waves and can also induce self-maintaining mechanisms similar to those just described. In this situation, however, and with the animals paralysed with Flaxedil no seizures arising occipitally have been observed. The role of the occipital cortex as the sensory visual and somatic afferent in photosensitive epilepsy in the baboon is discussed in the light of these results.

Allyl Compounds↗

Rapid laser flash photoaffinity labeling of binding sites for a noncompetitive inhibitor of the acetylcholine receptor.

Photoaffinity labeling of the nicotinic acetylcholine receptor from Torpedo marmorata electric tissue was performed in the presence of cholinergic effectors in the millisecond to second time range by a combination of a stopped-flow apparatus and a high-energy pulse laser. The label applied was [3H]triphenylmethylphosphonium, a lipophilic cation previously shown to be a specific blocker of the acetylcholine receptor ion channel. With the receptor in the resting state most of the label was incorporated into the alpha polypeptide chains. In the presence of agonists and antagonists increasing incorporation into the delta- and (less pronounced) the beta-chain was observed. The time course of this increase had a half-life of about 0.4 s, being slower than receptor activation and channel opening. in the resting, active, and even rapidly desensitized state, the alpha polypeptide chains appear to be the primary targets of the photoaffinity reaction. The action spectrum of the photolabeling has a sharp maximum at lambda = 270 nm and a small-side maximum at lambda = 290 nm. It does not resemble the absorption spectrum of the label and may hint at amino acid side chains as the moieties activated by UV light causing the photolabeling. The effector specificity of the observed slow increase of label incorporation into the delta polypeptide chain was investigated. It does not prove that slow desensitization is the underlying event. The agonists acetylcholine and carbamoylcholine as well as treatment of receptor-rich membranes with phospholipase A2 (but not phospholipase D) triggered labeling of delta, but antagonists such as D-tubocurarine and most conspicuously flaxedil had a similar effect.

Affinity Labels↗

Purkinje cells in the cerebellum: their responses to postural stimuli in cats.

The responses of Purkinje cells in the cerebellum produced by various positions of the limbs were studied in decerebrated unanesthetized cats. The majority of units located in the intermediate zone of the anterior lobe selectively reacted to definite postures of the limbs: some of them were active when a given limb was in an extended position and were silent when it was in flexion; the other ones, on the contrary, were active when the limb was flexed and silent when it was extended. The rate of discharges was in both cases the same and amounted to 40 to 80 per second. It did not change with the lapse of time, and remained the same when flaxedil was administered. These results, in connection with some other data, seem to explain the problem of how the cerebellum transforms the information about the tensions of tendons and muscles, delivered by the tendon organs and muscle spindles, respectively, into the information about movements.

Animals↗

Regulation of binding properties of the nicotinic receptor protein by cholinergic ligands in membrane fragments from Torpedo marmorata.

Exposure of receptor-rich membrane fragments from Torpedo marmorata to carbamylcholine causes a slow (half-time of 5--10 min) and reversible change of properties of the cholinergic receptor protein manifested by a decrease of the initial rate of Naja nigricollis alpha-[3H]toxin binding in the presence of carbamylcholine. This change corresponds to a 5- to 20-fold increase of affinity for carbamylcholine. Other agonists, acetylcholine, phenyltrimethylammonium, show the same effect but not the antagonists d-tubocurarine and flaxedil. Decamethonium and hexamethonium show little, if any, agonistic effect in vitro on the same membrane fragments but cause the affinity change. This regulatory property can be lost after aging of the preparation of membrane fragments. Since the affinity increase progresses with a similar time course as the decrease of amplitude of the permeability response consecutive to agonist preincubation, it is proposed that, in the membrane at rest, the receptor protein is present under a state of low affinity for agonists and that the reversible stabilization by the agonists of a high affinity state corresponds to the "pharmacological desensitization" of the system as predicted by one of the models of Katz and Thesleff.

Acetylcholine↗

Time-resolved photolabeling by the noncompetitive blocker chlorpromazine of the acetylcholine receptor in its transiently open and closed ion channel conformations.

A rapid-mixing photolabeling apparatus is developed to resolve the kinetics of association of the noncompetitive channel blocker [3H]chlorpromazine (CPZ) with the membrane-bound acetylcholine (AcCho) receptor from Torpedo marmorata and to photolabel its subunits in the 100-milli-seconds to seconds time range. Rapid mixing of AcCho and [3H]CPZ with the receptor followed by brief (less than 20 msec) UV irradiation results in the selective labeling of the four chains of the AcCho receptor, according to a rapid bimolecular association process close to diffusion-controlled. Rapid association is not observed with the competitive antagonists d-tubocurarine or flaxedil or the snake venom alpha-toxins. Its initial rate increases with agonist concentration, with maxima of 0.6 for carbamoylcholine and 0.2 for phenyltrimethylammonium taking 1 for AcCho, with apparent dissociation constants of 30 microM, 400 microM, and 300 microM for AcCho, carbamoylcholine, and phenyltrimethylammonium, respectively, and with sigmoid shape (Hill coefficients of 1.1-1.3). Under conditions in which the receptor "desensitizes" and the ionic channel closes (preincubation with AcCho), rapid [3H]CPZ association decreases in parallel. It is concluded that the agonist-dependent rapid association of [3H]CPZ takes place at the level of a site common to all five subunits, which lies within the ion channel and becomes accessible when the channel opens.

Acetylcholine↗

Covalent labeling of functional states of the acetylcholine receptor. Effects of antagonists on the receptor conformation.

Photoaffinity labeling of membrane-bound nicotinic acetylcholine receptor from Torpedo marmorata electric tissue with the ion-channel blocker [3H]TPMP+ reveals various functional states of the receptor protein if labeling is performed with ms time resolution. In the resting and in the activated state most of the label is incorporated into the alpha-polypeptide chains of the receptor complex. When equilibrated with agonists and antagonists, predominantly the delta-polypeptide chain (and to a lesser extent the beta-chain) reacts with the photolabel. Reactivity of the delta-chain increases after exposure to cholinergic effectors with a half-life slower than the kinetics of receptor activation or rapid desensitization. Agonists and antagonists stimulate photolabelling of the delta-chain with different kinetics. For acetylcholine, carbamoylcholine and suberyldicholine the half-life of the reactivity increases is 400 - 500 ms; for the antagonists hexamethonium, d-tubocurarine and flaxedil it is about 10 s. The latter slow kinetics are also observed when the receptor is preequilibrated with agonists or antagonists prior to mixing with [3H]TPMP+ and starting the photoreaction. We conclude that time-resolved photoaffinity labeling can convalently mark protein structures involved in receptor functions. Of special interest is the observation that antagonists also induce a conformational change in the receptor protein.

Acetylcholine↗

The incorporation of acetylcholinesterase from the electric organ into liposomes.

Several methods have been used to bind electric organ aetylcholinesterase to the walls of phosphatidylcholine liposomes. One of these methods [Brunner, J., Skrabal, P. & Hauser, H. (1976) Biochim. Biophys. Acta, 455, 322-331] achieved complete incorporation, although some enzyme was shown to be sequestered inside the vesicles. The association was established either in the presence of high salt media or altered liposomal membrane fluidity. The reconstitution process impaired the allosteric transition of acetylcholinesterase which is thought to occur when Flaxedil (gallamine triethiodide) is present in a low ionic strength medium. It is suggested that the cholinesterase is capable of being incorporated into liposomes, possibly via hydrophobic forces. Such a system may be an adequate one for further study of the functioning of the enzyme in a defined membrane environment.

Acetylcholinesterase↗

Circulatory depression following low frequency stimulation of the sciatic nerve in anesthetized rats.

Earlier experiments have shown that afferent electrical stimulation of the sciatic nerve for 30 min induces a long-lasting post-stimulatory endorphin-dependent decrease in blood pressure in awake spontaneously hypertensive rats (SHR). In the present study we have examined whether this depressor response can be observed also in anesthetized SHR. The sciatic nerve was stimulated for 30 min with low-frequent (3 Hz) trains of impulses and the changes in blood pressure, heart rate and renal nerve activity were observed during the stimulation and in the post-stimulatory period. Animals anesthetized with Nembutal, Althesin and N2O did not show any post-stimulatory depression. In contrast, during chloralose anesthesia combined with muscle paralysis with Flaxedil, sciatic nerve stimulation induced a long-lasting post-stimulatory decrease in blood pressure due to central inhibition of sympathetic activity. The decrease in blood pressure could be prevented by naloxone and was therefore likely to be mediated via activation of central endorphin systems.

Alfaxalone Alfadolone Mixture↗

Blockade of intrafusal neuromuscular junctions of cat muscle spindles with gallamine.

This is a report on the resistance to block of the motor terminals on intrafusal fibres of cat soleus muscle spindles using the drug gallamine triethiodide (Flaxedil). To minimize diffusion barriers and to permit accurate measurements of time courses, rather slow rates of gallamine infusion were used (0.15 mg min-1). The main finding made was that after gallamine infusion, when extrafusal tension had dropped to half, all dynamic fusimotor effects and eight of twenty static effects had fallen to 40% or less of their control value. The remaining static effects persisted at 60-80% of their control value. Where fusimotor fibres were stimulated together with one or two skeletomotor fibres, the influence of the skeletomotor axons was significant only after spindle biasing had fallen to low levels. When gallamine infusion was stopped extrafusal tension returned to control levels within 20-75 min, depending on the length of the block, while fusimotor responses did not fully recover within the recording period of up to 150 min. The combination for some fusimotor responses of an early fall and a late recovery when compared with extrafusal tension, suggested a greater sensitivity of these endings to the drug. A comparison of spindle responses to the drug succinyl choline (SCh) and to fusimotor stimulation in the presence of gallamine showed that SCh responses were rapidly reduced by gallamine and had a long recovery time course, as were some fusimotor responses. From this it is argued that fusimotor effects with a high sensitivity to gallamine blockade were associated with nuclear bag fibre contractions and the more resistant effects with nuclear chain fibre contraction. It is generally believed that intrafusal neuromuscular junctions are more resistant to neuromuscular blockers than extrafusal junctions. The present experiments provide evidence to the contrary for some intrafusal junctions. Since muscle relaxants are often used in general anaesthesia it is interesting to speculate about the recovery of function of proprioceptive reflexes and of kinaesthesia during the immediate post-anaesthetic period, in view of the large difference in recovery time for transmission at intrafusal and extrafusal junctions.

Animals↗

Somato-sensory paths to the second cortical projection area of the group I muscle afferents.

1. Cats anaesthetized with chloralose and paralysed with Flaxedil were used. The projections of muscle, joint and skin afferents to the cortical fold hidden in the anterior suprasylvian sulcus were investigated with micro-electrode recording techniques.2. Electrical stimulation of Group I muscle afferents from the contralateral forelimb evoked a negative focal potential (latency 5 msec) in a locus of 1-2 mm diameter found in the lower bank of the fold. In one experiment a response to Group I muscle afferents from the contralateral hind limb was observed. The Group I potentials disappeared after sectioning of the dorsal columns at C3.3. Groups II and III muscle afferents, low threshold skin afferents and joint afferents also evoked potentials in the Group I locus. It was concluded that the joint afferents originated mainly in the Ruffini endings of the joint capsule.4. Groups II and III muscle afferents, low threshold skin and low threshold joint afferents projected to the upper bank of the suprasylvian fold. A certain somatotopic arrangement was observed.5. The possibility of connexions between the cortex of the anterior suprasylvian fold and the primary somato-sensory projection areas was discussed, as well as the organization of the loci in the fold in terms of cell colonies with different properties.

Animals↗

Inhibition by efferent nerve fibres: action on hair cells and afferent synaptic transmission in the lateral line canal organ of the burbot Lota lota.

1. Intracellular recordings were made from morphologically identified hair cells in the lateral line canal organs of the burbot Lota lota. 2. I.p.s.p.s were recorded from hair cells when the efferent fibres were excited by electrical stimulation of the lateral line nerve. The i.p.s.p.s were abolished when the fish was injected with immobilizing concentration of Flaxedil which is known to block the efferent synapses. 3. The i.p.s.p.s are accompanied by a decrease in the resistance of the hair cell membrane and an increase in the intracellular receptor potential. 4. Spontaneous and mechanically evoked e.p.s.p.s which were recorded intracellularly from the post-synaptic afferent nerve terminals were reduced in amplitude for the duration of the i.p.s.p.

Animals↗

Gallamine triethiodide-induced modifications of sodium conductance in Myxicola giant axons.

1. Internal gallamine triethiodide (Flaxedil) modifies Na+ channel kinetics in Myxicola axons but does not alter K+ conductance. The drug has no effect externally. 2. Gallamine initially increases the leakage-conductance, but this effect completely reverses within 30 min despite the maintained presence of drug. 3. During step depolarizations to membrane potentials less than -10 mV, gallamine slows the rate of Na+ inactivation, but all channels which have opened can still inactivate. During depolarizations to more positive potentials, gallamine-modified Na+ currents show a biphasic decline, and at VM greater than -10 mV, Na+ inactivation is incomplete as evidenced by the large Na+ tail currents which follow pulses sufficiently long to have allowed complete inactivation of normal Na+ channels. The tail currents are slower than normal Na+ tails, and exhibit a pronounced hook. With gallamine, the fraction of Na+ channels which do not inactivate increases sigmoidally over the range 0 mV to +80 mV. 4. For VM greater than ENa, gallamine almost completely blocks outward Na+ currents. The block is determined by the direction of Na+ current, rather than the absolute membrane potential. 5. Gallamine has no effect upon the rate of Na+ channel activation, the maximum Na+ conductance, the steady-state Na+ inactivation curve, or the rate of development or removal of inactivation by prepulses. 6. Gallamine eliminated physiological immobilization of intramembrane charge movements (QOFF and QON) and does not itself induce immobilization. Thus, in the presence of gallamine, QOFF following long pulses is the same as QOFF following short pulses.

Animals↗

Cardiovascular and respiratory responses to slow ramp carotid sinus pressures in the dog.

The respiratory and mean arterial pressure (MAP) responses to slow ramp pressure stimulation of carotid baroreceptors were compared in pentobarbital-anesthetized vagotomized dogs breathing 100% O2. Carotid sinus pressure (CSP) was raised from 50 (control) to 220 mmHg and then returned to control as linear ramps (+/- 1 mmHg/s) in isolated sinuses. MAP, heart rate (HR), ventilation (VE), frequency (f), and tidal volume (VT) were expressed as percent of control. The maximum difference between responses to positive and negative ramps at a given CSP (MAX) and the average difference (AVG) served as indicators of the hysteresis for each response. In 27 dogs MAP changed monotonically with varying CSP with insignificant (P = 0.27, MAX) or barely significant (P = 0.03, AVG) hysteresis, monotonic function being one that is continuously nondecreasing or continuously nonincreasing. Similar responses were obtained for HR. VE decreased as CSP increased, but the change was not monotonic. During negative ramp, VE increased back to control with an overshoot. Hysteresis for VE was pronounced (P less than 0.0001, both measures). The VE response was primarily determined by f; VT increased with CSP. To eliminate secondary respiratory effects due to alterations in MAP, in seven dogs similar experiments were performed after ganglionic blockade with hexamethonium. Hysteresis in VE and f persisted. To assess the role of changing arterial PCO2 (PaCO2) on VE, the CSP was held constant (after a ramp rise) at 140, 150, or 180 mmHg before reducing it at -1 mmHg/s to 50 mmHg; however, a significant hysteresis in VE was still observed. Further experiments, to eliminate secondary reflexes due to altered PaCO2, were performed in seven dogs after ganglionic blockade and paralysis with Flaxedil, with phrenic nerve activity as an indicator of ("neural") respiration. The hysteresis in VE and f were no longer significant. In summary, the results indicate that 1) slow ramp carotid baroreceptor stimulation elicits both VE and cardiovascular responses, the VE response showing a dramatically higher hysteresis than the cardiovascular responses; 2) the ventilatory hysteresis is partially explained by the secondary changes in PaCO2 and perhaps by cardiovascular variables; and 3) the central processing of the baroventilatory reflex appears to be rate sensitive at a slower rate of pressure change than that which causes rate sensitivity in the baropressure reflex.

Animals↗

Reticulospinal neurons with and without monosynaptic inputs from cerebellar nuclei.

An account is given of the responses of 557 medial reticular neurons with axons projecting down the spinal cord. All 30 experiments were on decerebrated unanesthetized cats paralyzed by Flaxedil. Recording from single neurons was by extracellular glass microelectrodes. Identification was first by location (confirmed by subsequent histology) in the medial reticular nucleus of medulla or pons, and second by antidromic activation from cord stimulation at C2 and L2 segmental levels. Axonal conduction velocities were calculated from the latency differential between L2 and C2 antidromic responses, and were usually in the range of 90-140 m/s; but about 25% were slower, ranging down to 30 m/s. Stimulation by electrodes in the ipsilateral and contralateral fastigial nuclei differentiated reticulospinal neurons into two classes according to whether they did or did not receive monosynaptic inputs, the respective populations of fully investigated neurons being 270 and 174. The fastigioreticular neurons were distinguished by a higher background frequency with mean values of 28 as against 15/s. There were also significant diffences in both the excitatory and inhibitory responses to afferent volleys from forelimb and hindlimb nerves. Comparison of the respective latency histograms showed that the responses of neurons with a fastigial input had an excess of latencies in the ranges that can be correlated with the latency histograms observed for fastigial responses. Thus, there is evidence for the effectiveness of the fastigial input and so for the pathway with monosynaptic linkage: Purkinje cells of cerebellar vermis yields fastigial neurons yields medial reticular neurons projecting down the spinal cord. Adequate stimulation of cutaneous receptors by pad taps and air-jet stimulation of hairy skin in a disppointingly small action when compared with fastigical responses. Explanations of this deficiency are suggested. Another discrpancy from the fastigial responses is that the medial reticular neurons have much wider receptive fields with little discrimination between ipsilateral and contralateral and between forelimb and hindlimb. Stimulation of the ipsilateral tegmental tract was tested on 183 reticulospinal neurons, 112 being with fastigial inputs. In about half there was a powerful monosynaptic excitation, which would identify such neurons as being on the pathway from mesencephalic and diencephalic centers to the spinal cord. There is a general discussion of transmission across successive synaptic relays, where specificity is sacrificed to integration.

Action Potentials↗

Taste responses in the parabrachial pons of decerebrate rats.

1. Behavioral studies have shown that chronic decerebrate rats retain the capacity to react appropriately to gustatory stimuli (12), but do not form taste-illness associations (13). Little is known, however, about the effects of decerebration on the processing of gustatory information. The present experiment was designed to investigate this issue in the parabrachial nucleus of the pons (PbN). 2. Rats were decerebrated at the supracollicular level under ketamine and ether anesthesia and were prepared for electrical recording in the PbN. Thereafter, animals were maintained under Flaxedil, and wound edges were frequently treated with lidocaine. Heart rate, core temperature, and CO2 were monitored throughout each experiment. Control subjects were treated identically, except that they were not decerebrated. 3. Sapid solutions of NaCl (0.1 M), HCl (0.01 M), sucrose (0.5 M), saccharin sodium (0.004 M), and quinine HCl (.01 M) were used as taste stimuli. After a 10-s base line, each stimulus was bathed over the tongue for 10 s followed by a 10-s wait and a 20-s rinse of distilled water. The intertrial interval was at least 2 min. 4. Gustatory responses from 32 parabrachial units in 13 decerebrate rats were recorded. These were compared with responses in 31 units from the PbN of 16 intact rats. 5. Analysis of response profiles of PbN units in decerebrate rats showed that these units produced smaller responses to NaCl and HCl and larger responses to saccharin sodium compared with units in intact rats. 6. Despite changes in response magnitude, the temporal patterns of response (phasic-tonic relationships) were not different in PbN units in decerebrate rats compared with controls. Differences in the length of responses were, however, apparent. Responses to saccharin sodium were longer, response to NaCl, HCl and sucrose were shorter, and responses to quinine HCl were unchanged. 7. Results of a multidimensional scaling analysis of the response profiles across units showed that "taste spaces" for decerebrate and intact rats were similar. Units in each group were meaningfully placed near stimuli that evoked the best response in a given unit. Units that did not respond well to any stimulus were placed close together regardless of their best stimulus in both taste spaces. 8. Responses to the termination of the taste stimulus (OFF-responses) were observed in PbN units in the decerebrate rat but not in units from the intact rat. Twenty-one OFF-responses were recorded in 14 units; 6 of these occurred in the absence of a response to the stimulus.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Neck muscle spindle activity in the decerebrate, unparalyzed cat: dynamics and influence of vestibular stimulation.

1. Using floating electrodes, we recorded from neck-muscle spindle afferents in the C2 dorsal root ganglion of the decerebrate cat. Nerves to dorsal neck muscles were cut so that the afferents presumably originated mainly from ventral and ventrolateral perivertebral muscles and sternocleidomastoid. One goal of our experiments was to study possible vestibular influence exerted on these spindles via the fusimotor system. Unparalyzed preparations were therefore used. 2. Stimuli consisted of sinusoidal rotations in vertical planes. Neck tilt stretched neck muscles, whereas whole-body tilt stimulated vestibular receptors. 3. For each afferent we first determined the most effective direction of neck tilt, then used stimuli oriented close to this direction to study response dynamics, particularly gain of responses to stimuli of different amplitudes (0.5-7.5 degrees). 4. Three-quarters of the afferents failed to respond to 0.5 degrees, 0.2-Hz neck rotations. Stimuli that were effective usually elicited responses that had low gain and were linear over the whole range of amplitudes. Only a few afferents had behavior typical of spindle primary afferents: high-gain responses to small sinusoidal stimuli, gain decreasing as stimulus amplitude increases. This prevalence of static spindle responses in the unparalyzed cat is in striking contrast to results obtained on neck-muscle spindles in paralyzed, decerebrate cats, and on hindlimb extensor muscle spindles in decerebrate, unparalyzed cats. 5. Paralysis produced by injection of Flaxedil changed the behavior of 2/4 spindle afferents tested, causing the appearance of high-gain responses to 0.5 degrees stimuli and of nonlinear behavior.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗