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Biomedical subjects

P Wand

Publications and source records attributed to P Wand.

At least 19 recordsLinked to original sources
PubMed1985

Two types of cat static fusimotor neurones under separate central control?

The effect on the fusimotor system of an injection of the gamma-aminobutyric acid (GABA) antagonist picrotoxin into the reticular part of the substantia nigra (SNR) was studied in muscle spindle primary and secondary endings of pretibial flexors in cats anaesthetized with ketamine. Changes in fusimotor action after drug administration were deduced from changes in bias and sensitivity to sinusoidal stretching of the receptor-bearing muscles when compared to the deefferented preparation. Intranigral injection of picrotoxin (2 micrograms) removed a tonic static fusimotor action from flexor muscle spindle primary endings without affecting the secondary endings in the same muscles. It is concluded that static gamma motoneurones of cat flexors are of more than one functional type, and that the central nervous control of the static fusimotor input to cat flexor muscle spindles has selective access to static bag2 fibres and nuclear chain fibres.

Animals↗
PubMed1985

Responses of Renshaw cells coupled with hindlimb extensor motoneurons to sinusoidal stimulation of labyrinth receptors in the decerebrate cat.

Contraction of ipsilateral limb extensors during side-down roll tilt of the head, leading to selective stimulation of labyrinth receptors, is attributed to an increased discharge of excitatory vestibulospinal (VS) neurons (alpha-responses) and a decreased discharge of medullary inhibitory reticulospinal (RS) neurons (beta-responses), both of which act on ipsilateral extensor motoneurons. Experiments were performed in decerebrate cats, with the de-efferented gastrocnemius-soleus (GS) muscle fixed at a constant length, to find out whether Renshaw (R) cells linked with GS motoneurons responded to labyrinth stimulation elicited by head rotation, while the neck had been bilaterally deafferented. We hoped in this way to clarify the role and the mechanism by which these inhibitory interneurons act on limb extensor motoneurons during the vestibular reflexes. 72.7% of the R-cells, disynaptically excited by group I volleys elicited by single shock stimulation of the GS nerve, weakly responded to head rotation at frequencies of 0.026-0.15 Hz and at a peak amplitude of 10 degrees. For the frequency of head rotation of 0.026 Hz, +/- 10 degrees C, most of the GS R-cells increased their firing rate during side-down head displacement (alpha-responses); some responses were related to head position, but others showed some phase lead or lag with respect to head position. The gain of the first harmonic of these unit responses was very low and corresponded on the average to 0.084 +/- 0.062, S.D. imp./s/deg, while the sensitivity corresponded to 2.14 +/- 2.35, S.D.%/deg (base frequency, 6.85 +/- 5.97, S.D. imp./s). These responses were attributed to the activity of VS neurons, the increased discharge of which during side-down head rotation exerts a weak excitatory influence on a limited number of GS motoneurons and, through their recurrent collaterals, on the related R-cells. The modulation of the firing rate of R-cells coupled with the GS motoneurons increased linearly by increasing the peak amplitude of displacement from 5 degrees to 20 degrees at the frequency of 0.026 Hz, so that the response gain remained almost unchanged. An increase in frequency of head rotation from 0.026 to 0.32 Hz at a fixed amplitude of 10 degrees, thus changing the maximal angular acceleration from 0.26 degrees/s2 to 41.7 degrees/s2, reversed the response pattern of R-cells reported above. The resulting beta-responses, which also showed some phase lead or lag with respect to head position, were attributed to vestibular activation of RS neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Influence of Renshaw cells on the response gain of hindlimb extensor muscles to sinusoidal labyrinth stimulation.

The contraction of limb extensor muscles during side-down roll tilt of the animal depends upon an increased discharge of excitatory vestibulospinal (VS) neurons (alpha-response) and a reduced discharge of inhibitory reticulospinal (RS) neurons of the medulla (beta-response), both acting on ipsilateral limb extensor motoneurons. In the decerebrate cat, a modulation of the multiunit EMG activity was clearly present in forelimb extensors, but was extremely weak or absent in hindlimb extensors. Experiments performed in decerebrate cats with the deefferented GS muscle fixed at a constant length have shown that Renshaw (R)-cells, monosynaptically coupled with gastrocnemius-soleus (GS) motoneurons, were either unresponsive or displayed only very weak, small amplitude alpha-responses to sinusoidal stimulation of labyrinth receptors elicited during slow head rotation after bilateral neck deafferentation. This effect was attributed to excitatory VS volleys acting on GS motoneurons and, through their recurrent collaterals, on the related R-cells. In these instances the recurrent inhibition of the GS motoneurons contributed to the very low gain of the EMG response of the corresponding muscles to labyrinth stimulation. Intravenous injection of an anticholinesterase (eserine sulphate, 0.05-0.1 mg/kg) at a dose that in previous experiments increased the firing rate of medullary RS neurons, while decreasing the decerebrate rigidity, slightly increased the discharge rate of R-cells linked with the GS motoneurons in the animal at rest; these findings suggest that the RS system inhibits the extensor motoneurons by exciting the related R-cells. All the R-cells, which prior to the injection were either unresponsive or showed an alpha-response to head rotation (at 0.026-0.15 Hz, +/- 10 degrees), after eserine sulphate showed a beta-response for the same parameters of labyrinth stimulation. In particular, a reduced discharge of the R-cells linked with the GS motoneurons occurred during side-down head rotation as shown for the majority of the RS neurons. It appears therefore that the same R-cells, which in the normal decerebrate cat responded to the excitatory VS volleys acting through the GS motoneurons, were now decoupled from their input motoneurons during head rotation, thus behaving as if they underwent the most efficient direct excitatory control of the RS system. The reduced discharge of the R-cells linked with the GS motoneurons during side-down head rotation would lead to disinhibition of these motoneurons, thus enhancing the response gain of the corresponding muscle to labyrinth stimulation.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

Non-dopaminergic neurones of the reticular part of substantia nigra can gate static fusimotor action onto flexors in cat.

The effect on the fusimotor system of electrical stimulation of the reticular part of the substantia nigra or of the injection of the gamma-aminobutyric acid (GABA)-antagonist picrotoxin into this structure was studied in spindle receptors of pretibial flexors in cats anaesthetized with ketamine. Afferent activity of muscle spindle primary endings was recorded before and during these two forms of intranigral stimulation. Dynamic spindle sensitivity was assessed during both small- (100 microns) and large-amplitude (2 mm) sinusoidal stretching of the receptor-bearing muscles. From changes in spindle sensitivity after nigral electrical stimulation (eleven out of fourteen primary endings) or intranigral injection of picrotoxin (fifty-one out of sixty-seven primary endings) it is deduced that functional activation of neurones of the reticular part of substantia nigra, in this preparation, removed a normally present tonic static fusimotor action from the primary sensory endings of pretibial flexor muscle spindles. This effect, induced by picrotoxin (2 micrograms in 1 microliter), was reversed by a subsequent intranigral injection of the GABA-agonist muscimol (0.4 microgram in 1 microliters), but remained unchanged after subsequent intracaudate injections of haloperidol (12.5 micrograms in 5 microliters) or apomorphine (5 micrograms in 5 microliters). It is concluded that the C.N.S. can gate static fusimotor action onto flexor muscle spindle primary endings through non-dopaminergic output neurones of the reticular part of substantia nigra.

Animals↗
PubMed1982

Effect of fusimotor stimulation on ia discharge during shortening of cat soleus muscle at different speeds.

1. In barbiturate-anaesthetized cats, the L7 and S1 dorsal and ventral roots were dissected to isolate functionally single afferents identified as primary endings of soleus muscle spindles, and motor filaments which exerted a fusimotor action on the afferents with limited action on extrafusal muscle. Up to seven filaments, with an action on a given primary ending, could be isolated and each was classified as exerting either a predominantly dynamic or static action.2. Combined stimulation of these filaments, at rates up to 200 impulses/s could maintain afferent firing during muscle shortenings at speeds up to 200 mm/s.3. Fusimotor stimulation could also maintain afferent firing at a target frequency of 100 impulses/s during muscle shortenings up to 200 mm/s. The timing, in relation to the onset of shortening, and the rates of fusimotor stimulation were found to be critical in achieving the target frequency.4. Sinusoidal modulation of the frequency of fusimotor stimulation was used to study the conditions required to achieve constant afferent firing in the face of imposed sinusoidal length changes.5. For given depths of modulation, the phase advance of fusimotor stimulation needed to produce minimum modulation of afferent firing (best compensation) increased with increasing frequency of the sinusoids. The compensation deteriorated with an increase in the frequency of the sinusoids and a change in the mean muscle lengths, although in some cases it could be restored by adjustments to the depth of modulation of fusimotor rate. This suggests that for movements of varying speeds and amplitudes, settings which are appropriate for shortening at a given velocity and mean muscle length, do not apply if either of these two variables are altered.6. These findings demonstrate that the fusimotor system is potentially capable of eliciting constant afferent firing as envisaged in the ;servo-assistance' hypothesis (Matthews, 1964, 1972; Stein, 1974). This, and the fact that constant afferent firing is not seen during normal unobstructed shortenings at velocities greater than 0.2 resting length/s (Prochazka, 1981), are used to argue that it is by choice rather than necessity that ;servo-assistance' (as defined above) is not employed during normal movements. However, servo-assistance of a different form (involving modulated spindle afferent feed-back from both agonists and antagonists) remains a viable alternative.

Animals↗
PubMed1981

Nigral output neurons are engaged in regulation of static fusimotor action onto flexors in cat.

Picrotoxin and muscimol were unilaterally injected into the postero-lateral part of the reticular zone of substantia nigra (plSNR) through chronically implanted guide cannulae in ketamine-anesthetized cats. Afferent activity of pretibial flexor muscle spindle primary and secondary endings was recorded before and after drug administration, and spindle sensitivity monitored during both sinusoidal and ramp stretch of the receptor-bearing muscle. From changes in spindle sensitivity after drug injection it is deduced that unilateral block by picrotoxin of the action of GABA on postsynaptic receptors in plSNR removes tonic static fusimotor action from flexor muscle spindle primary endings. Secondary endings seemed largely unaffected. The effect on primary endings is reversed by a subsequent injection of muscimol. It is concluded that the central nervous system, through GABA-modulated nigral output neurons, can control static fusimotor action onto flexor muscle spindle primary and secondary endings separately to some extent.

Animals↗
PubMed1979

Drug-induced stereotypes and asymmetric behaviour after substantia nigra pars posterior (SNPP) lesions in cats.

Apomorphine- (Apo) and amphetamine- (Amph) induced behavioural phenomena were studied in cats which received either 6-hydroxydopamine (6-OHDA) or electrothermic lesions of the posterior part of the substantia nigra (SNPP). In this species, as in rats, both drugs evoked sterotypies (sniffing and head nodding) and an enhancement of locomotor activity. However, distinct differences between the reactions of cats and rats to both drugs were found, the most evident effect being the lack of sterotyped gnawing and licking. By correlating the data on behaviour, the histological examination showing the size and location of the lesions, and the dopamine (DA) content of the corresponding caudate nuclei, it is concluded that the fewer DA-specific neurons lesioned in the SNPP, the more pronounced was the ipsilateral asymmetric behaviour. We suggest, therefore, that the ipsilateral asymmetric behaviour in cats following APO- and AMPH-treatment is due to the destruction of a non-catecholaminergic output.

Animals↗
PubMed1979

The effects of intranigral injections of picrotoxin and carbachol in cats with a lesioned nigrostriatal pathway.

Picrotoxin, carbachol and atropine were injected intranigrally through chronically implanted crannulae in cats. The drug-induced behavioural syndromes, mainly asymmetric behaviour, were analyzed. The changes in these syndromes after 6-hydroxydopamine (6-OHDA) lesion of the substantia nigra (SN) indicate that, in addition to the dopaminergic (DA), a non-catecholaminergic (non-CA) nigral output exists, both being responsible for asymmetric behaviour. It is further suggested that gamma-aminobutyric acid (GABA) receptors are present on both dopaminergic and non-CA nigral output neurons, while acetylcholine (ACh) receptors, responsible for asymmetric behaviour, are almost exclusively located on non-CA nigral output neurons.

Animals↗
PubMed1979

Muscle spindle discharge in normal and obstructed movements.

1. The discharge activity of muscle spindle endings located in tail and hind limb muscles was recorded during voluntary movements in the cat. 2. During active shortening of the receptor-bearing muscles, both primary and secondary endings tended to fall silent. This was more pronounced, the higher the rate of muscle shortening. We suggest that in unobstructed movements in which muscle velocities exceed 0.2 resting lengths per second (lr/sec), the firing patterns of spindle afferents are dominated by their responses to the length variations. At velocities lower than 0.2 lr/sec, fusimotor action may predominate. 3. When active muscle shortening was unexpectedly halted, both primary and secondary endings resumed firing, but the increases in discharge rate were not as abrupt as might have been expected had there been strong co-activation of fusimotor and skeletomotor neurones. Rather, for the types of movements studied, fusimotor action appears to have been quite modest.

Action Potentials↗
PubMed1977

Effects of 1,3-dimethyl-5-aminoadamantane hydrochloride (DMAA) on the stretch-induced reflex tension of flexor muscles and the excitability of the gamma-loop in decerebrate and spinal cats.

The effects of 10 mg/kg i.v. 1,3-dimethyl-5-aminoadamantane hydrochloride (memantine, DMAA) on the stretch-induced reflex tension of flexor muscles extensor digitorum longus and tibialis anterior (EDL/TA) and on the excitability of the neurons relaying transmission in the gamma-loop have been investigated in decerebrate and spinal cats. DMAA essentially reduced the relfex excitability of flexors EDL/TA induced by fusimotor activity in the decerebrate preparation. The drug did not stimulate the reflex activity in acute spinal cats. In the concentration used, DMAA suppressed largely the transmission of the fusimotor reflex in the decerebrate as well as in the spinal preparation, although in spinal cats DMAA increased the average firing rate of muscle spindle primaries originating from EDL/TA muscles. The possible mechanism of action of the compound on dopaminergic and serotonergic systems as well as its basic effects on neuronal membranes is discussed.

Amantadine↗
PubMed1976

The response of alpha-motoneurons of different size to stretch and vibration of extensor muscles after injection of 5-hydroxytryptophan in spinal cats.

1. Vibration of the GS muscle at 100/sec, and the peak-to-peak amplitude of about 100 mu, produced slight reflex activity of homonymous and heteronymous alpha-motoneurons in the spinal, unanesthetized cat. 2. Intravenous injection of the 5-HT precursor 5-HTP (25 mg/kg, L-form) performed in the spinal preparation facilitated the responses of single extensor alpha-motoneurons to both vibration and stretch of the corresponding muscle. The 5-HT antagonist methysergide (0-5 mg/kg i. v.) blocked almost completely the facilitation of the vibration and stretch induced motoneuronal discharges produced by 5-HTP in the spinal cat, indicating that the facilitation was 5-HT specific. 4. A comparison of the types of alpha-motoneurons participating in the reflex responses elicited by the different stimuli in the spinal cat following injection of 5-HTP showed that both small-tonic and large-phasic alpha-motoneurons take part in both stretch and vibration reflexes. 5. It is concluded that the alpha-motoneuron pool of the GS muscle represents an homogenous population, no matter what kind of synaptic drive is used for its activation, and that the susceptibility of a motoneuron to discharge depends on the amount of the afferent excitatory input rather than on the modalities of sensory stimulation.

5-Hydroxytryptophan↗
PubMed1975

The proprioceptive activation of stretch tension in pretibial flexor muscles induced by stimulation of antagonistic muscle afferents.

1. The effect of tetanic stimulation of ipsilateral group I afferents from the GS muscle on a synchronous stretch of the flexor EDL/TA muscles has been investigated in precollicular decerebrate cats. 2. The stretch-induced tension of the EDL/TA muscles increases remarkably during simultaneous stimulation of the GS nerve with maximal intensities corresponding to 1.5 times the threshold for the group 1 afferents. This increas appears above all in the dynamic part of stretch. 3. Under our experimental conditions there is no activation fo flexor-alpha-motoneurones during tetanic stimulation of the GS afferents without muscle stretch, as measured by the resting tension of the EDL/TA muscles. 4. Desptie an increase in the stretch-induced tension during fusimotor stimulation of antagonistic group I afferents, a transmission loss in the excitation via the psi-loop to the flexor-alpha-motoneurones occurs. This could be demonstrated by the ratio: increase in the tension T /increase in the number of Ia spikes. This is explained by snychronous convergence of the discharges of Ia inhibitory interneurones to the flexor-alpha-motoneurones. 5. The system studied demonstrates an input-output relation of the stretch reflex during conditions in which both reciprocal inhibition and autogenetic excitation via the psi-loop occur. It appears however, that the reciprocal inhibition is partly overwhelmed by the autogenetic excitation which results from the increase in the Ia discharge rate during fusimotor reflex. 6. It is postulated that static rather than dynamic psi-moto-neurones are involved in the investigated reflex arc.

Action Potentials↗