The effects of lesions to the mesolimbic dopamine system on maternal and sexual behaviors in the female rat was assessed. Rat dams that were given ventral tegmental area microinfusions of 6-hydroxydopamine (6-OHDA) during lactation showed a persistent deficit in pup retrieval but were not impaired with respect to nursing, nest building, or maternal aggression. In addition, 6-OHDA-lesioned females failed to respond to amphetamine by showing locomotor hyperactivity. Administration of the dopamine blocker raclopride to neurologically intact dams also inhibited pup retrieval but had no effect on nursing. Females given 6-OHDA during pregnancy appeared completely unresponsive to pups, whereas no maternal deficits were seen in females that received 6-OHDA 8 weeks before parturition. Proceptive (hopping and darting) and receptive (lordosis) components of sexual behavior, assessed after ovariectomy and exogenous steroid hormone treatment, were not affected by mesolimbic 6-OHDA lesions.

No abstract

Prompted by previous reports on muscle thixotropy, we have investigated changes in inherent and reflex stiffness of the finger flexor muscles of human subjects at rest, following transient conditioning manoeuvres involving contractions and/or length changes of the finger flexors. The stiffness measurements were combined with electromyographic recordings from forearm and hand muscles and with microneurographic recordings of afferent stretch responses in finger flexor nerve fascicles. Finger flexor stiffness was evaluated by measuring (a) the flexion angle of the metacarpo-phalangeal joints at which the system during rest balanced the force of gravity and (b) the speed and amplitude of angular finger extensions induced by recurrent extension torque pulses of constant strength delivered by a torque motor. In the latter case, extension drifts in the resting position of the fingers were prevented by a weak flexion bias torque holding the fingers in a pre-determined, semiflexed position against a stop-bar. Stiffness changes following passive large amplitude finger flexions and extensions were studied in subjects with nerve blocks or nerve lesions preventing neurally mediated contractions in the forearm and hand muscles. Inherent stiffness was enhanced following transient finger flexions and reduced following transient finger extensions. The after-effects gradually declined during observation periods of several minutes. Similar results were obtained in subjects with intact innervation who succeeded during the pre- and post-conditioning periods in keeping the arm and hand muscles relaxed (i.e. showed no electromyographic activity). In these subjects it was also found that the after-effects were similar for active and passive finger movements and that isometric voluntary finger flexor contractions loosened the system in a way similar to finger extensions. In some subjects electromyographic reflex discharges appeared in the finger flexors in response to the extension test pulses. When elicited by small ramp stretch stimuli of constant amplitude, the stretch reflex responses were found to vary in strength in parallel with the changes in inherent stiffness following the various conditioning manoeuvres. The strength of the multi-unit afferent stretch discharges in the muscle nerve, used as index of muscle spindle stretch sensitivity, varied in parallel with the changes in inherent stiffness. Post-manoeuvre changes in muscle spindle stretch sensitivity were seen also when the spindles were de-efferented by a nerve block proximal to the recording site. The results can be explained in terms of thixotropic behaviour of extra- and intrafusal muscle fibres.(ABSTRACT TRUNCATED AT 400 WORDS)

SUMMARY1. A local anaesthetic drug was injected around the peroneal nerve in healthy subjects in order to investigate whether the resulting loss in foot dorsiflexion power in part depended on a y-fibre block preventing 'internal' activation of spindle end-organs and thereby depriving the a-motoneurones of an excitatory spindle inflow during contraction. The motor outcome of maximal dorsiflexion efforts was assessed by measuring firing rates of individual motor units in the anterior tibial (t.a.) muscle, mean voltage e.m.g. from the pretibial muscles, dorsiflexion force and range of voluntary foot dorsiflexion movements. The tests were performed with and without peripheral conditioning stimuli, such as agonist or antagonist muscle vibration or imposed stretch of the contracting muscles.2. As compared to control values of t.a. motor unit firing rates in maximal isometric voluntary contractions, the firing rates were lower and more irregular during maximal dorsiflexion efforts performed during subtotal peroneal nerve blocks. During the development of paresis a gradual reduction of motor unit firing rates was observed before the units ceased responding to the voluntary commands. This change in motor unit behaviour was accompanied by a reduction of the mean voltage e.m.g. activity in the pretibial muscles.3. At a given stage of anaesthesia the e.m.g. responses to maximal voluntary efforts were more affected than the responses evoked by electric nerve stimuli delivered proximal to the block, indicating that impaired impulse transmission in a motor fibres was not the sole cause of the paresis.4. The inability to generate high and regular motor unit firing rates during peroneal nerve blocks was accentuated by vibration applied over the antagonistic calf muscles. By contrast, in eight out of ten experiments agonist stretch or vibration caused an enhancement of motor unit firing during the maximal force tasks.5. The reverse effects of agonist and antagonist vibration on the ability to activate the paretic muscles were evidenced also by alterations induced in mean voltage e.m.g. activity, dorsiflexion force and range of dorsiflexion movements.* To whom correspondence and reprint requests should be sent.

SUMMARY1. Different techniques were used to generate sudden ramp extension movements of the wrist while the subjects were either relaxed or maintaining a weak voluntary contraction in the wrist flexors. Afferent responses to the displacements were recorded with a tungsten micro-electrode inserted into a fascicle of the median nerve supplying one of the wrist flexor muscles, and e.m.g. responses were recorded with needle electrodes inserted into the same muscle.2. With the wrist flexors either relaxed or contracting, extensions at 100-200'/sec for 60-70 msec (generated by either an hydraulic motor or a torque motor) produced segmented afferent responses with two to four afferent bursts, separated by intervals of 20-30 msec. The successive neural peaks, occuring during the stretch phase, were correlated to mechanical vibrations sensed by a strain gauge and sometimes also by a wrist goniometer. With the flexor muscles contracting, the successive peaks in the neurogram were followed by similar peaks in the e.m.g, the delay between neural and e.m.g. peaks being 20-25 msec.3. Small abrupt extension movements of 1-2°lasting only 10-15 msec often produced segmented afferent responses with one neural burst occuring during the stretch phase and another 15-20 msec later, corresponding to a mechanical oscillatory event succeeding the stretch. The oscillation and the second neural burst were not present with small extension movements of smooth onset and halt. With the flexor muscles contracting, stimuli producing one afferent burst produced only one e.m.g. peak, whereas double-peaked afferent discharges produced double-peaked e.m.g. responses, the delay between individual neural e.m.g. peaks being 20-25 msec.4. Similar segmentation of the neural stretch responses was seen when abrupt displacements were produced by electrically induced muscle twitches, by manual pulls on a spring attached to the hand or by the subject making fast voluntary wrist extensions. This grouping of afferent discharges was seen in both multi-unit and in single-unit recordings from fibres identified as group Ia afferents. 6. For imposed movements with a duration of 60-70 msec the successive e.m.g. peaks caused a fused reflex contraction, appearing as a torque trace deflexion, starting at about the time when the movement ended and reaching its peak within about 40 msec. With longer-lasting movements the mechanical reflex response accompanying the successive e.m.g. bursts, appeared as a decelerative force, starting to oppose the ongoing movement about 60 msec after its start. Mechanical consequences of stretch reflex contractions starting after, rather than during, the stretch movement are discussed.

SUMMARY1. Experiments were performed to check the validity of previous claims concerning the 'long-loop' aetiology of 'late' reflex electromyogram (e.m.g.) responses to muscle stretch in man. The primary aim was to investigate whether observations previously presented in favour of the 'long-loop hypothesis' are explicable also in terms of the 'resonance hypothesis', according to which the 'late' reflex components represent spinal, short-latency responses to intramuscular oscillations initiated by the impact.2. The contracting wrist flexors of healthy subjects were exposed to trains of recurrent 25-50 Hz stretch stimuli (wrist torque pulses). Each of the initial two or three pulses in the train was followed by e.m.g. peaks with a latency of 20-25 msec. The e.m.g. peaks driven in this way had the following characteristics in common with the successive two or three e.m.g. peaks which were induced by single ramp stretches or tendon taps. (a) Changes in stimulus parameters which altered the strength of the initial e.m.g. peak often had an opposite effect on the strength of the succeeding peak(s). Muscle vibration which attenuated the initial peak often enchanted the succeeding one(s). (b) The initial e.m.g. peak was less affected than the succeeding peak(s) by the subjects' attempts to respond with rapid 'resist' or 'let go' reactions.3. Intramuscular oscillations (monitored by a needle accelerometer) and e.m.g. responses evoked by single ramp stretches and/or tendon taps were also studied in the long thumb flexor, the calf muscles and the masseter muscle. In the thumb flexor, the initial accelerometer deflexion was only rarely succeeded by a short latency e.m.g.peak, but the succeeding wave in the needle accelerogram was followed by such a peak, appearing about 40 msec after stimulus application. By contrast, the calf muscles and the jaw elevators exhibited a high amplitude, short-latency e.m.g. response to the first but only rarely to the second intramuscular oscillation wave.4. The interval between initial and second e.m.g. peaks following tendon taps was longer for calf muscles than for wrist flexors and longer for wrist flexors than for jaw elevators. Similar differences were observed with respect to the intervals between the damped intramuscular oscillations initiated by the impacts.5. Without denying the existence of 'long-loop reflexes' it is concluded that the characteristics of the 'late' reflex responses to muscle stretch in man are explicable also in terms of the 'resonance hypothesis'.

The purpose of the present work is to examine the causes of the Piper rhythm, i.e. the tendency towards rhytmical 40-60 Hz grouping of motor unit potentials in steadily contracting human muscles. At weak or moderate contraction strength individual motor units exhibited preferred firing rates which were subharmonically related to the Piper rhythm in the gross EMG. Microelectrode muscle nerve recordings provided no support for the hypothesis that the Piper rhythm is dependent on resonance-induced rhythmical volleys of afferent spindle impulses causing reflex entrainment of motor impulses. This hypothesis also seems inconsistent with the findings that Piper rhythms of similar frequency appear in muscles with widely different mechanical properties and that the rhythms are about equally prominent in muscles with brisk as in muscles with weak or absent stretch reflexes. The results suggest that the Piper rhythm is dependent on some kind of pace-maker in the spinal cord or the cerebrum which tends to entrain and synchronize motor impulses.

3. Damped muscular oscillations in the 30-50 Hz range were also initiated by sudden halts of voluntary wrist movements, by electrically induced twitches, and by voluntary brisk contractions. In these instances too, the mechanical oscillations were reflected in the shape of the succeeding e.m.g. response.4. The interval between the two initial peaks in the accelerometer records was always shorter with tendon taps than in ramp stretch experiments. A corresponding difference was noted in the intervals between the following two peaks in the reflex e.m.g. response.5. The initial peak in the accelerometer records could be ascribed to a wave propagated at about 40 m/sec in the wrist flexor muscles. Inconclusive results were obtained in attempts to determine whether the subsequent oscillations represented reflexions of the propagated wave at the ends of the muscle.6. The muscles were also exposed to recurrent stretch stimuli (torque pulses) with a repetition rate varying between 15 and 100 Hz. At 30-50 Hz the intramuscular oscillations reached their maximal amplitude, and such repetition rates were also 3 PHY 326 6. EKLUND AND OTHERS most efficient in producing synchronized e.m.g. bursts, time-locked to the oscillations. The mechanical responses of the wrist flexors to single or recurrent perturbations were to a large extent mimicked by a rubber band model with a longitudinal resonance frequency of about 40 Hz.7. It is concluded that segmentation of reflex e.m.g. responses to sudden joint displacements and other types ofbrisk muscle perturbations to a large extent depends on the inherent resonance characteristics of musculo-tendinous structures. Primary spindle endings with their high vibration sensitivity and their segmental projections to a-motoneurones are believed to be the receptors primarily responsible for reflex entrainment of the motor impulses.