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Mandibular motor function is well known to be impaired in the presence of temporomandibular disorders. However, while a vast literature is available concerning accuracy of motor control in limbs, quantitative and objective assessment of mandibular motor control has been seldom performed, also because of the lack of adequate investigative tools. Aim of this work is to present a technique for reliable evaluation of the motor performance of the mandible based on a kinesiography-monitored reach-and-hold task. Nineteen healthy subjects were engaged in a task in which they had to drive a cursor on a screen by corresponding movements of the mandible in the frontal plane and reach 30 random targets sequentially displayed on the screen. The whole task was repeated three times per session in two different days. The individual performance was assessed by different indices evaluating precision and steadiness of target matching. The performance progressively improved in the three trials of the first session, further improved and stabilised in the second session, with an average positioning error of 0·59 ± 038 mm and was slightly correlated with the horizontal dimension of the mandible border movement (r = 0·55). Intraclass correlation coefficient ranged between 0·76 and 0·94 for the different indices indicating good repeatability. The kinesiographic technique allowed for objective and reliable assessment of the voluntary control of the mandible position. Its potential applications include support to the characterisation of temporomandibular disorders and to motor training and progress monitoring in rehabilitation treatments., (© 2011 Blackwell Publishing Ltd.)

This study is the first to report on vascular effect of the chromogranin A derived Vasostatin-I (CgA(1-76)) in vivo. Cardiovascular parameters were recorded in 29 rabbits with sympathetically decentralized right carotid vascular bed. The recombinant human STA CgA(1-78) (VS-1) was infused at 480 μg/kg over 25 min. Group I was kept awake while groups II-V were anesthetized with Ketamine-xylazine. VS-1 was given alone in groups I-II while in presence of either phentolamine, phentolamine plus propranolol or hexamethonium in groups III-V. Serum VS-1 peaked at 2 μg/ml (200 nM) before onset of vascular effects and declined rapidly to ~200 ng/ml within 30 min. In all groups but III and IV VS-1 induced a brief vasoconstriction, being larger in intact than in sympathetically decentralized beds. The VS-1 induced vasoconstriction was not altered by hexamethonium but was abolished by phentolamine. In presence of the α-adrenergic blocker a long lasting vasodilatation, unaffected by propranolol, was apparent on both innervated and decentralized sides. In conclusion, VS-1 induced an α-adrenoceptor-mediated vasoconstriction presumably brought about by noradrenaline release from sympathetic nerves when infused at a dose giving an initial serum concentration of ~200 nM. This initial vasoconstriction masked a persistent adrenoceptor-independent vasodilatation, consistent with previous reports from in vitro models., (Copyright © 2011 Elsevier B.V. All rights reserved.)

Aims: When assessing sympathetic activation in acute stress, the attention is often limited to the sympatho-neural axis, whereas sympatho-adrenal activation, that can only be detected with poor time resolution from the concentration of plasma catecholamines, is often neglected. This study is aimed at re-investigating the role and the relevance of the sympatho-adrenal system in acute stress based on the analysis of haemodynamic responses in conscious rabbits., Methods: Experiments were carried out on 19 rabbits implanted with chronic probes for arterial blood pressure and for blood flow in the facial artery. Cardiovascular responses to a randomized sequence of acute stressors (pinprick, air jet, oscillation of the cage, inhalation of formaldehyde vapours and im injection of hypertonic saline) were recorded before and after α-adrenergic blockade (phentolamine) and unilateral section of the cervical sympathetic trunk (decentralization). Plasma catecholamine concentrations were analysed in four animals., Results: All stressors induced an increase in arterial blood pressure and a reduction of vascular conductance in the facial artery ranging on average from 24% (pinprick) to 55% (box oscillation). Such vasoconstrictor response was abolished by phentolamine. In decentralized arteries, the vasoconstriction was delayed by 10-15 s and decreased in magnitude in a stressor-dependent way, indicating an adrenaline-mediated effect in the late phase of the stress response that was confirmed by changes in plasma adrenaline concentration., Conclusions: In conscious rabbits, rapid release of adrenaline makes a prominent contribution to vasoconstriction in response to different stressors including box oscillation, muscle pain and air jet but not the nasopharyngeal stimulation., (© 2010 The Authors. Acta Physiologica © 2010 Scandinavian Physiological Society.)

The complex interplay of neural, metabolic, myogenic and mechanical mechanisms that regulate blood flow in skeletal muscle (MBF) is still incompletely understood. For the first time, a method is presented for high time-resolution recording of MBF from a purely muscular artery in physiological conditions. Ultrasound perivascular flow probes were implanted (n = 15) mono- or bilaterally around the masseteric branch of the facial artery in nine rabbits and tested up to 16 days after implant. Reliable and stable recordings were achieved in 50% of implants. Blood flow was observed to increase from a resting level of 0.2-0.3 ml min(-1) up to 4.0-6.0 ml min(-1) during spontaneous masticatory activity. In addition, within single masticatory cycles marked back flow transients could be observed (peak flow = -10 ml min(-1)) during powerful masticatory strokes but not during mild mastication. The possibility of (1) surgically removing the sympathetic supply to the relevant vascular bed and of (2) bilaterally monitoring the perfusion of masseter muscles thus allowing to use one side as control side for different types of interventions makes this model a useful tool for disentangling the different mechanisms involved in the control of MBF.

In the complex neurovascular control of the orofacial area, the only vasoconstrictor action is mediated by the sympathetic nervous system; however, its functional role is still unclear as little evidence exists of vasoconstrictor responses to physiological stimuli in both animal and human models. Aim of the present study was to investigate, orofacial vascular responses to acute stress in conscious rabbits. Twenty rabbits, implanted with chronic perivascular flow probes on the facial artery and with a telemetric probe for arterial blood pressure, were subjected to different alerting/stress stimuli, i.e., noise, taps on the rabbit's box, air jet, noxious cutaneous stimuli. Smaller groups of animal also underwent electromyographic (EMG) activity recording from the masseter muscle, unilateral section of the cervical sympathetic nerve (n=8), and alpha-adrenergic blockade with phentolamine (n=6). On average, all stressors evoked a pressor response accompanied by variable changes in heart rate and induced a marked, short-latency reduction in facial artery blood flow, corresponding to a decrease of 37-50% in vascular conductance of the facial artery. Local sympathetic denervation abolished the short-latency (<15s) vasoconstrictor response to all stressors and attenuated the late (>15s) phase of the long-lasting response to the air jet. All vasoconstrictor effects were blocked by phentolamine. Increases in blood flow were observed only in concomitance with masseter EMG activity either during masticatory activity or in the form of brief occasional spontaneous contractions. This study provides evidence of an effective vasoconstrictor control by the sympathetic system in the orofacial area under stress conditions.

The sympathetic nervous system (SNS), that is activated under condition of physical, psychological and psychosocial stress, affects force production and fatigability of muscles by controlling both muscle blood flow and the intracellular contractile mechanism. In addition SNS may affect motor function by modulating afferent activity from muscle spindles that are highly concentrated in jaw-closing muscles. Possible implications of these actions on masticatory function and myofascial pain are discussed.

There is increasing interest about the possible involvement of the sympathetic nervous system (SNS) in initiation and maintenance of chronic muscle pain syndromes of different aetiology. Epidemiological data show that stresses of different nature, e.g. work-related, psychosocial, etc., typically characterised by SNS activation, may be a co-factor in the development of the pain syndrome and/or negatively affect its time course. In spite of their clear traumatic origin, whiplash associated disorders (WAD) appear to share many common features with other chronic pain syndromes affecting the musculo-skeletal system. These features do not only include symptoms, like type of pain or sensory and motor dysfunctions, but possibly also some of the pathophysiological mechanisms that may concur to establish the chronic pain syndrome. This review focuses on WAD, particular emphasis being devoted to sensorimotor symptoms, and on the actions exerted by the sympathetic system at muscle level. Besides its well-known action on muscle blood flow, the SNS is able to affect the contractility of muscle fibres, to modulate the proprioceptive information arising from the muscle spindle receptors and, under certain conditions, to modulate nociceptive information. Furthermore, the activity of the SNS itself is in turn affected by muscle conditions, such as its current state of activity, fatigue and pain signals originating in the muscle. The possible involvement of the SNS in the development of WAD is discussed in light of the several positive feedback loops in which it is implicated.

Previous studies performed in jaw muscles of rabbits and rats have demonstrated that sympathetic outflow may affect the activity of muscle spindle afferents (MSAs). The resulting impairment of MSA information has been suggested to be involved in the genesis and spread of chronic muscle pain. The present study was designed to investigate sympathetic influences on muscle spindles in feline trapezius and splenius muscles (TrSp), as these muscles are commonly affected by chronic pain in humans. Experiments were carried out in cats anesthetized with alpha-chloralose. The effect of electrical stimulation (10 Hz for 90 s or 3 Hz for 5 min) of the peripheral stump of the cervical sympathetic nerve (CSN) was investigated on the discharge of TrSp MSAs (units classified as Ia-like and II-like) and on their responses to sinusoidal stretching of these muscles. In some of the experiments, the local microcirculation of the muscles was monitored by laser Doppler flowmetry. In total, 46 MSAs were recorded. Stimulation of the CSN at 10 Hz powerfully depressed the mean discharge rate of the majority of the tested MSAs (73%) and also affected the sensitivity of MSAs to sinusoidal changes of muscle length, which were evaluated in terms of amplitude and phase of the sinusoidal fitting of unitary activity. The amplitude was significantly reduced in Ia-like units and variably affected in II-like units, while in general the phase was affected little and not changed significantly in either group. The discharge of a smaller percentage of tested units was also modulated by 3-Hz CSN stimulation. Blockade of the neuromuscular junctions by pancuronium did not induce any changes in MSA responses to CSN stimulation, showing that these responses were not secondary to changes in extrafusal or fusimotor activity. Further data showed that the sympathetically induced modulation of MSA discharge was not secondary to the concomitant reduction of muscle blood flow induced by the stimulation. Hence, changes in sympathetic outflow can modulate the afferent signals from muscle spindles through an action exerted directly on the spindles, independent of changes in blood flow. It is suggested that such an action may be one of the mechanisms mediating the onset of chronic muscle pain in these muscles in humans.

The somatomotor and sympathetic nervous systems are intimately linked. One example is the influence of peripheral sympathetic fibers on the discharge characteristics of muscle spindles. Since muscle spindles play important roles in various motor behaviors, including rhythmic movements, the working hypothesis of this research was that changes in sympathetic outflow to muscle spindles can change rhythmic movement patterns. We tested this hypothesis in the masticatory system of rabbits. Rhythmic jaw movements and EMG activity induced by long-lasting electrical cortical stimulation were powerfully modulated by electrical stimulation of the peripheral stump of the cervical sympathetic nerve (CSN). This modulation manifested itself as a consistent and marked reduction in the excursion of the mandibular movements (often preceded by a transient modest enhancement), which could be attributed mainly to corresponding changes in masseter muscle activity. These changes outlasted the duration of CSN stimulation. In some of the cortically evoked rhythmic jaw movements (CRJMs) changes in masticatory frequency were also observed. When the jaw-closing muscles were subjected to repetitive ramp-and-hold force pulses, the CRMJs changed characteristics. Masseter EMG activity was strongly enhanced and digastric EMG slightly decreased. This change was considerably depressed during CSN stimulation. These effects of CSN stimulation are similar in sign and time course to the depression exerted by sympathetic activity on the jaw-closing muscle spindle discharge. It is suggested that the change in proprioceptive information induced by an increase in sympathetic outflow (a) has important implications even under normal conditions for the control of motor function in states of high sympathetic activity, and (b) is one of the mechanisms responsible for motor impairment under certain pathological conditions such as chronic musculoskeletal head-neck disorders, associated with stress conditions.

Interpretation of transcranial Doppler (TCD) recordings requires assumptions about flow or diameter of the insonated vessel. This study aimed at assessing if activation of the sympathetic system could affect blood velocity (bv) in basal cerebral arteries. In anaesthetized rabbits, stimulation of cervical sympathetic nerve (cervSN) was used selectively to activate the sympathetic pathway to the head while monitoring bv in all major cerebral arteries. cervSN stimulation at 10 Hz produced: 1. in internal carotid artery (ICA) and ICA-supplied arteries (ICA-s), a consistent bv increase ranging between 20 and 70%, 2. in the basilar artery, a transient decrease by 15-30%. These effects were mimicked, in both territories, by injection of phenylephrine into the ICA. Because cerebral blood flow is known to be reduced by cervSN stimulation, the increase in bv in ICA and ICA-s must be ascribed to constriction of the insonated vessels. These effects should be considered when monitoring bv during sympathetic activation tests or exercise.

Previous reports showed that sympathetic stimulation affects the activity of muscle spindle afferents (MSAs). The aim of the present work is to study the characteristics of sympathetic modulation of MSA response to stretch: (i) on the dynamic and static components of the stretch response, and (ii) on group Ia and II MSAs to evaluate potentially different effects. In anaesthetised rabbits, the peripheral stump of the cervical sympathetic nerve (CSN) was stimulated at 10 impulses s(-1) for 45-90 s. The responses of single MSAs to trapezoidal displacement of the mandible were recorded from the mesencephalic trigeminal nucleus. The following characteristic parameters were determined from averaged trapezoidal responses: initial frequency (IF), peak frequency at the end of the ramp (PF), and static index (SI). From these, other parameters were derived: dynamic index (DI = PF - SI), dynamic difference (DD = PF - IF) and static difference (SD = SI - IF). The effects of CSN stimulation were also evaluated during changes in the state of intrafusal muscle fibre contraction induced by succinylcholine and curare. In a population of 124 MSAs, 106 units (85.4 %) were affected by sympathetic stimulation. In general, while changes in resting discharge varied among different units (Ia vs. II) and experimental conditions (curarised vs. non-curarised), ranging from enhancement to strong depression of firing, the amplitude of the response to muscle stretches consistently decreased. This was confirmed and detailed in a quantitative analysis performed on 49 muscle spindle afferents. In both the non-curarised (23 units) and curarised (26 units) condition, stimulation of the CSN reduced the response amplitude in terms of DD and SD, but hardly affected DI. The effects were equally present in both Ia and II units; they were shown to be independent from gamma drive and intrafusal muscle tone and not secondary to muscle hypoxia. Sympathetic action on the resting discharge (IF) was less consistent. In the non-curarised condition, IF decreased in most Ia units, while in II units decreases and increases occurred equally often. In the curarised condition, IF in group II units mostly increased. The results have important functional implications on the control of motor function in a state of 'high' sympathetic activity, like excessive stress, as well as in certain pathological conditions such as sympathetically maintained pain.

Most of the transcranial Doppler (TCD) experimental studies on cerebral haemodynamics have been performed in the rabbit because of the similarity between its Willis circle and that of the human, but these studies have mainly been limited to the basilar artery. The present study was aimed at extending the use of TCD sonography to all other large cerebral arteries. In anaesthetised rabbits, these arteries were insonated from three different recording sites, i.e. top-cranial, suboccipital and orbital, using a two-channel pulsed Doppler device equipped with 4 and 8 MHz probes. First, discrimination between intra- and extracranial arteries was achieved through a standard 'rebreathing' test (hypercapnic-hypoxic stimulation). The distinctive blood velocity response patterns, reflecting the different extents of metabolic reactivity in intra- and extracranial territories, are described and discussed. Intracranial arteries were then identified on the basis of their response to ipsi- and contralateral common carotid artery occlusion. This procedure allowed recording from the following arteries: anterior common trunk, anterior cerebral, internal carotid, middle cerebral and basilar; the latter could be simultaneously monitored with any of the others. This study provides an experimental model allowing investigation of regional differences in the haemodynamic response to neurogenic and pharmacological stimuli.

The changes in sympathetic outflow may be evaluated from the amplitude of the antidromic compound action potential (ACAP) according to the collision technique described by Douglas and Ritchie (Douglas, W.W. and Ritchie J.M., A technique for recording functional activity in specific groups of medullated and non-medullated fibers in whole nerve trunks. J. Physiol., 138(1957) 19-30). This technique was revised, taking into account the depressant action exerted by antidromic stimulation on sympathetic preganglionic neurones (SPNs). Cervical sympathetic nerve (CSN) of rabbits was used as experimental model. Stimulation frequencies of 0.2-0.5 Hz were found to be sufficiently low to avoid depressant actions on CSN spontaneous activity; they were employed to test the sensitivity of the technique during different experimental manoeuvres, such as changes in pulmonary-ventilation, baroreceptor unloading and arousal stimuli. In addition a procedure was devised to calibrate the ACAP amplitude: high frequency antidromic stimulation was used to induce a complete and transient inhibition of SPNs which allows to record the ACAP maximum amplitude. ACAPs recorded in various experimental conditions can then be expressed as percentage of this value.

There is no general agreement regarding several aspects of the role of the sympathetic system on cerebral haemodynamics such as extent of effectiveness, operational range and site of action. This study was planned to identify the effect of a generalised sympathetic activation on the cerebral haemodynamics in healthy humans before it is masked by secondary corrections, metabolic or myogenic in nature. A total of 35 healthy volunteers aged 20-35 underwent a 5 min lasting cold pressor test (CPT) performed on their left hand. The cerebral blood flow (CBF) velocity in the middle cerebral arteries and arterial blood pressure were recorded with transcranial Doppler sonography and with a non-invasive finger-cuff method, respectively. The ratio of arterial blood pressure to mean blood velocity (ABP/Vm) and Pulsatility Index (PI) were calculated throughout each trial. CPT induced an increase in mean ABP (range 2-54 mmHg depending on the subject) and only a slight, though significant, increase in blood velocity in the middle cerebral artery (+2.4 and +4.4% on ipsi- and contralateral side, respectively). During CPT, the ratio ABP/Vm increased and PI decreased in all subjects on both sides. These changes began simultaneously with the increase in blood pressure. The increase in ABP/Vm ratio is attributed to an increase in the cerebrovascular resistance, while the concomitant reduction in PI is interpreted as due to the reduction in the compliance of the middle cerebral artery. The results suggest that generalised increases in the sympathetic discharge, causing increases in ABP, can prevent concomitant increases in CBF by acting on both small resistance and large compliant vessels. This effect is also present when a slight increase in blood pressure occurs, which suggests a moderate increase in the sympathetic discharge, i.e. when ABP remains far below the upper limit of CBF autoregulation.

Stimulation of the cervical sympathetic nerve at 10/s increases by 12.9 +/- 0.7% peak tension of maximal twitches in the directly stimulated jaw muscles and markedly depresses (41.6 +/- 1.3%) the tonic vibration reflex (TVR) elicited in the same muscles by vibration of the mandible. Both effects are not significantly influenced by administration of beta-adrenoceptor antagonists. When both alpha- and beta-adrenergic receptors are blocked, sympathetic stimulation induces a very small increase in twitch tension (3.8 +/- 0.7%), while no detectable change in the TVR is observed. Close arterial injection of alpha 1-adrenoceptor agonist phenylephrine mimics the effects induced by sympathetic stimulation on twitch tension and TVR, dose-dependently. The noradrenaline co-transmitter neuropeptide Y also produces a long-lasting, dose-dependent increase in the twitch tension which is unaffected by blockade of adrenergic receptors as well as of the neuromuscular junctions. Contribution of neuropeptide Y to the sympathetically-induced reduction of the stretch reflex is not clearly demonstrated. These data suggest that co-operation between noradrenaline and neuropeptide Y may be effective in determining sympathetic modulation of skeletal muscle function.

The effect of bilateral cervical sympathetic nerve stimulation on microvascular cerebral blood flow, recorded at various depths in the parietal lobe and in ponto-mesencephalic areas, was investigated by laser-Doppler flowmetry in normotensive rabbits. These areas were chosen as representative of the vascular beds supplied by the carotid and vertebro-basilar systems, which exhibit different degrees of sympathetic innervation, the former being richer than the latter. Sympathetic stimulation at 30 imp/s affects cerebral blood flow in 77% of the parietal lobe and in 43% of the ponto-mesencephalic tested areas. In both cases the predominant effect was a reduction in blood flow (14.7 +/- 5.1% and 4.1 +/- 2.4%, respectively). The extent of the reduction in both areas was less if the stimulation frequency was decreased. Sometimes mean cerebral blood flow showed a small and transient increase, mainly in response to low-frequency stimulation. The morphology was analysed of low-frequency spontaneous oscillations in cerebral blood flow, attributed to vasomotion. Present in 41% of the tested areas (frequency 4-12 cycles/min, peak-to-peak amplitude 10-40% of mean value), these waves decreased in amplitude and increased in frequency during sympathetic stimulation, irrespective of changes in mean flow. The possibility has been proposed that the sympathetic action on low-frequency spontaneous oscillations may contribute to the protective influence that this system is known to exert on the blood-brain barrier in hypertension.

The effect of sympathetic activation on the spindle afferent response to vibratory stimuli eliciting the tonic vibration reflex in jaw closing muscles was studied in precollicularly decerebrate rabbits. Stimulation of the cervical sympathetic trunk, at frequencies within the physiologic range, consistently induced a decrease in spindle response to muscle vibration, which was often preceded by a transient enhancement. Spindle discharge was usually correlated with the EMG activity in the masseter muscle and the tension reflexly developed by jaw muscles. The changes in spindle response to vibration were superimposed on variations of the basal discharge which exhibited different patterns in the studied units, increases in the firing rate being more frequently observed. These effects were mimicked by close arterial injection of the selective alpha 1-adrenoceptor agonist phenylephrine. Data presented here suggest that sympathetically-induced modifications of the tonic vibration reflex are due to changes exerted on muscle spindle afferent information.

This paper describes a non-invasive, very inexpensive method of estimating tissue displacements of various origin that is easy and fast to set up. This technique utilizes an inductive proximity sensor (IPS), which is a non-contact length transducer measuring the distance between its probe and a metal target. Its working principle is based on the electromagnetic coupling originating between the sensor probe, a source of high-frequency magnetic field, and the metal target where parasitic currents take place. The linear working range of the IPS model used here is 0.1 to 6 mm probe-target distance, its resolution is about 2 microns. The IPS has been employed on rabbits and humans to measure the displacement of a target glued to the skin of various body areas with respect to the fixed probe of the sensor. Its high resolution, together with an extensive working range, allows the evaluation of numerous physiological events which produce displacements ranging from 2 microns -- to 9 mm, reflecting either tissue volume changes or movements. In particular, an interesting application is to monitor, through volume variations, the extent and the time course of local vascular modifications induced by manoeuvres which elicit changes in vasomotor tone; vascular filling, tissue swelling etc. Therefore, this measure may be considered a 'surface plethysmography' record. In addition, the contractions of skeletal muscles, under either isotonic or isometric conditions, can be estimated through this sensor. This system may therefore find applications for research purposes and practical demonstrations to students.

The action of bilateral cervical sympathetic nerve (CSN) stimulation on mean cerebral blood flow (CBF) and on its rhythmical fluctuations was studied in normotensive rabbits by using laser-Doppler flowmetry (LDF). A reduction in mean CBF, mediated by alpha-adrenoceptors, was the predominant effect; it was more often present and larger in size in the vascular beds supplied by the carotid than in those supplied by the vertebro-basilar system. This suggests that the sympathetic action facilitates a redistribution of blood flow to the brain stem. The effect induced by CSN stimulation on CBF spontaneous oscillations was a consistent decrease in amplitude and an increase in frequency, irrespective of the changes produced on the mean level of CBF. The possible implications of the sympathetic action on the state of the blood-brain barrier (BBB) are discussed. Experimental and clinical data dealing with the influence of sympathetic activation on the cerebrovascular system have been compared. As a result the possibility of analysing the spontaneous oscillations of CBF for clinical purposes is suggested.

1. In precollicular decerebrate rabbits we investigated the effect of sympathetic stimulation, at frequencies within the physiological range, on the tonic vibration reflex (TVR) elicited in jaw closing muscles by small amplitude vibrations applied to the mandible (15-50 microns, 150-180 Hz). The EMG activity was recorded bilaterally from masseter muscle and the force developed by the reflex was measured through an isometric transducer connected with the mandibular symphysis. 2. Unilateral stimulation of the peripheral stump of the cervical sympathetic by the TVR, and a marked decrease or disappearance of the ipsilateral EMG activity. No significant changes were detected in the EMG contralateral to the stimulated nerve. Bilateral CSN stimulation reduced by 60-90% the force reflexly produced by the jaw closing muscles and strongly decreased or suppressed EMG activity on both sides. This effect was often preceded by a transient TVR enhancement, very variable in amplitude and duration, which was concomitant with the modest increase in pulmonary ventilation induced by the sympathetic stimulation. 3. During bilateral CSN stimulation, an increase in the vibration amplitude by a factor of 1.5-2.5 was sufficient to restore the TVR reduced by sympathetic stimulation. 4. The depressant action exerted by sympathetic activation on the TVR is mediated by alpha-adrenergic receptors, since it was almost completely abolished by the I.V. administration of either phentolamine or prazosin, this last drug being a selective antagonist of alpha 1-adrenoceptors. The sympathetically induced decrease in the TVR was not mimicked by manoeuvres producing a large and sudden reduction or abolition of the blood flow to jaw muscles, such as unilateral or bilateral occlusion of the common carotid artery. 5. The effect of sympathetic stimulation was not significantly modified after denervation of the inferior dental arch and/or anaesthesia of the temporomandibular joint, i.e. after having reduced the afferent input from those receptors, potentially affected by CSN stimulation, which can elicit either a jaw opening reflex or a decrease in the activity of the jaw elevator muscle motoneurons. 6. These data suggest that, when the sympathetic nervous system is activated under physiological conditions, there is a marked depression of the stretch reflex which is independent of vasomotor changes and is probably due to a decrease in sensitivity of muscle spindle afferents.

The effect of sympathetic stimulation on the jaw jerk reflex has been studied in precollicular decerebrate rabbits. This reflex was elicited by a downward mandibular movement applied to the lower jaw through a servo controlled puller. Unilateral stimulation of the cervical sympathetic nerve at 10/s consistently induced a decrease in the JJR, i.e. a marked reduction of the EMG activity in the ipsilateral masseter muscle, accompanied by a 30-40% decrease in the reflexly developed force. In these trials EMG of the contralateral muscle, recorded as control, was not significantly affected. Bilateral stimulation of cervical sympathetic nerve strongly reduced or suppressed the EMG activity in both sides and produced a parallel decrease in the developed force which reached values ranging from 12.5% to 37.0% of controls (with an average of 28.9% +/- 8.9, S.D.). The effect of sympathetic stimulation was also tested on the contraction of the masseter muscle elicited by direct electrical stimulation. Sympathetic activation induced a modest increase in both amplitude and duration of muscle twitch, thus showing that the reduction in the reflex response can not be attributed to an action exerted by the adrenergic mediator on the muscular contraction. All these effects were almost completely abolished by the blockade of alpha-adrenergic receptors. They were proved not to be secondary to the sympathetically-induced vasomotor changes. Therefore the marked JJR reduction produced by activation of the sympathetic nervous system is suggested to be due to the sympathetically-induced decrease in neuromuscular spindle sensitivity to muscle length changes, previously reported.

Stimulation of the cervical sympathetic trunk, at frequencies within the physiological range, consistently elicits a partial recovery of the contractile force in the fatigued digastric muscle. This action, together with the tension potentiation induced by the sympathetic system in the non-fatigued muscle, could improve the muscular performance under the physiological conditions associated with increase in the sympathetic outflow.

The sympathetic system can influence skeletal muscle function through an action exerted at the peripheral level, namely on muscle spindle afferent information and muscular contraction. Data supporting such a conclusion are briefly reviewed. Also, the results described in the present paper suggest that the sympathetic nervous command affecting muscle function is tonic in nature and that it can be modulated by inputs which are known to influence other sections of the sympathetic system.

The mesencephalic trigeminal nucleus was studied in anaesthetized and curarized rabbits by recording the unitary activity through extracellular microelectrodes and identifying the constituent cell types. Two types of units were found, namely primary afferents supplying jaw raising muscle spindles and periodontal or gingival mechanoreceptors. These two groups of neurons exhibited a rostrocaudal somatotopy: the former occupied the entire rostral portion of the nucleus (A7-P2.3; trochlear decussation being taken as an arbitrary 0 level), the latter was located caudally (P3-P4.5) while the somata of both types of afferent fibres were present between P2.2 and P3. No evidence was found for representation of both tendon organs of jaw muscles and joint receptors. Among the units innervating muscle spindles, secondary afferents were largely more numerous than the primary ones. Among periodontal and gingival mechanoreceptor afferents, incisors were the most widely represented, followed by interalveolar gingiva and molars; the axonal conduction velocity ranged between 9 and 40 m/sec and between 8 and 16 m/sec for ipsilaterally and contralaterally projecting neurons, respectively. The motor responses obtained by electrical stimulation of discrete areas of the MTN confirmed the presence of a high degree of segregation between the two different populations of neurons. In fact, jaw raising movements are obtained when stimulating the area within A7 and P2 containing the somata of spindle afferent neurons, while only jaw opening movements are elicited by stimulation of the caudal levels of the nucleus. These data also show that the periodontal neurons whose somata are located in the MTN participate in the jaw opening reflex, just as the more numerous periodontal mechanoreceptors whose somata are located in the Gasser ganglion. Soma-somatic and soma-axon hillock gap junctions were found among the neurons of the MTN, particularly in the caudal third of the nucleus.

The effect of the electrical stimulation of the peripheral stump of the cervical sympathetic nerve, at physiological frequencies, was studied on the activity of mechanoreceptors with sensory field around the teeth, in anaesthetized and paralysed animals. In the 33% of the tested units either an increase of the resting discharge rate or an activation of the receptors occurred. The latency of this response ranged between 0.3 and 6 sec; the maximum discharge frequency, which varied widely in different units, was reached within the subsequent 2 to 4 sec and usually outlasted the duration of the stimulation. The possible mechanisms of this sympathetic effect are discussed on the basis of its latency and pattern and of the following further observations: i) its presence after denervation of carotid sinus and glomus, ii) its dependence on the stimulation of preganglionic sympathetic fibres belonging to the groups S1 and S2, iii) the absence of response in the mechanoreceptor units by the temporary occlusion of the ipsilateral common carotid artery.

In rabbits, cats and rats anaesthetized, curarized, with the skull fixed in a stereotaxic apparatus, the peripheral stump of the cervical sympathetic nerve (c.s.n.) was electrically stimulated at frequencies within the physiological range and the isometric tension was recorded at the lower jaw. In a group of experiments the afferent discharge from the jaw elevator muscle spindles was also recorded, in the mesencephalic nucleus of the fifth cranial nerve. Unilateral stimulation of the c.s.n. induced in jaw elevator muscles of rabbits an increase of tension of 5.5 +/- 0.5 g (latency: 0.5-2 s, time constant: 2.5-5 s) maintained with little or no decrement until the end of stimulation. This response proved not to be secondary to vasomotor changes since: i) approximately half of it was mediated by the fastest conducting component of the c.s.n. fibres, ii) it was not mimicked by a sudden reduction of blood supply to the muscles, iii) it was unaffected by 10 min bilateral occlusion of both the external and the internal carotid arteries. During c.s.n. stimulation the afferent discharge from spindles belonging to jaw elevator muscles exhibited an increase of firing (often preceded by a transient decrease) lasting throughout the stimulation. Also, the position sensitivity of all the spindle afferents tested was modified by the sympathetic stimulation. The results presented are interpreted to suggest that the sympathetic system may induce an intrafusal muscle fibre contraction in jaw elevator muscles. The possible functional implications are also discussed.

1. The effects of epileptogenic stimulation of the cerebral masticatory area on the somata of the first-order neurons of masticatory proprioception localized in the mesencephalic trigeminal nucleus (MTN) were studied in curarized, lightly anaesthetized rabbits. 2. Low-frequency stimulations inducing modest cortical after-discharges fired the silent MTN units with latencies of 0.3-0.8 sec, and induced alternate excitatory and inhibitory effects on the active units. On some occasions the tonic afferent discharge was changed into rhythmic bursts, which occurred at the constant frequency of 2.5-3.5/sec for the entire range of stimulation frequencies used, i.e. from 0.3 to 10/sec. 3. High-frequency cortical stimulations eliciting true epileptic seizures induced a transient increase in discharge of the MTN units, followed by a prolonged inhibition. 4. All these effects were attributed to activation of reticular pathways acting on the some of the recorded proprioceptive neurons. Such a modulation of the proprioceptive input elicited by the epileptic masticatory cortex may contribute to the motor effects and to the changes of the masseteric reflex which occur during convulsive seizures.

In anaesthetized and curarized cats electrical stimulation of the lumbar sympathetic trunk, at frequencies within the physiological range, induces the development of a small tension in superficial lumbrical muscles (50-100 mg in different preparations). This effect can be reproduced in anaesthetized and curarized cats by stimulating the peripheral stump of the tibial nerve with parameters adequate to activate the entire C-fibre group, and therefore postganglionic sympathetic fibers. The collision technique was used to evaluate in the tibial nerve possible changes in afferent activity from the skinned foot. It was found that an increase of non-cutaneous activity consistently occurs in A beta and, occasionally, in A alpha fibre groups. Secondary and primary spindle afferents, respectively, belong to these fibre groups. It was also found that: (1) the tension development in lumbrical muscles and the increase of the afferent activity of non-cutaneous origin exhibit similar time courses; (2) the two events are affected in parallel by the same stimulus parameters; (3) both events are abolished by alpha-adrenoceptor antagonists. Therefore the possibility of a sympathetic fusimotor action affecting mainly secondary afferents is suggested and discussed.

Pure stimulation of carotid chemoreceptors induces, as a primary effect, the general spontaneous activation of both the cardioexcitatory and the cardioinhibitory medullary centres. These effects have been shown by keeping constant those parameters which, when modified, produced secondary effects hiding the investigated primary ones.

Swiss male albino mice were treated subcutaneously with the main cannabinoids (CBN, CBD, delta9-THC) at the dosage of 1 mg/kg per day for 30 days, and with the crude resin. At the end of the treatment, after supramaximal stimulation of the sciatic nerve, a significant decrease of both maximal twitch and tetanus tensions was observed in delta9-THC-treated animals; CBD and resin treatment produced some decrease in active tension, while CBN treatment induced an enhancement of the contractile strength. Histology showed lesions interpretable as due to muscular dystrophy. Analysis of protein and hydroxyproline muscular content showed a marked reduction in protein in all treated animals, with a corresponding high increase in hydroxyproline content.

In anaesthetized and paralyzed rabbits, electrical stimulation of the cervical sympathetic nerve at physiological frequencies induces in jaw muscle spindle afferents a short-latency decrease or suppression of discharge. This effect is very stereotyped in pattern and is attributed to direct sympathetic innervation of spindles. It is mediated by preganglionic S1-S2 sympathetic fiber groups. A longer-latency facilitatory effect follows, probably vasomotor in origin and mediated by S3-S4 groups. Both responses are eliminated by administration of alpha-adrenergic blocking agents. The latencies, patterns, thresholds, durations and reproducibility of these responses have been studied and the mechanisms possibly involved are discussed.

In anaesthetized and curarized rabbits, the cervical sympathetic nerve (CSN) stimulation induces in jaw elevator muscles a tension response which can be mimicked by the intravenous injection of adrenaline, noradrenaline and phenylephrine. This response, previously described and attributed to the contraction of muscle spindle fibres, is entirely mediated by alpha-adrenoceptors. The administration of phenoxybenzamine (2.5-3.5 mg/kg) markedly inhibits the responses to the sympathetic stimulation and to the injection of adrenergic agonists. Rauwolscine (1 mg/kg) reduces the development of tension induced by both CSN stimulation and noradrenaline injection without significantly affecting the response to phenylephrine. These data suggest the presence of postsynaptic alpha 1- and alpha 2-adrenoceptors in intrafusal muscle fibres. Moreover, the possibility that alpha 2-adrenoceptors may also have an extrasynaptic location is entertained.

Electric stimulation of the peripheral stump of cervical sympathetic nerve (0.5-5.0 sec trains at 1 msec, 6-10 V, 0.5-30 HZ) induced in jaw muscle spindle afferents: (1) decrease of discharge frequency with 0.6-2.5 sec latency, lasting 8-13 sec (in 40% of the units) possibly due to direct sympathetic innervation of spindles; and (2) subsequent modest increase of frequency, probably secondary to muscular vasoconstriction.

The action exerted by the sympathetic system on skeletal muscle is briefly reviewed with regard to the effects induced by the adrenergic mediator on extra-fusal muscle fibre contractility and on muscle spindle receptor organs. In particular, the different responses of slow - and fast - contracting muscles to catecholamine administration and to sympathetic stimulation are reported. Also, the sympathetically--induced effects on muscle spindle afferent activity are discussed on the basis of recent anatomical and functional data suggesting the existence of a direct action exerted by noradrenergic axons on intrafusal muscle fibres. Some of the possible implications of these data are then briefly mentioned.

In anaesthetized cats the electrical stimulation of the cervical sympathetic nerve induces a considerable increase (150-250%) in the nociceptive jaw opening reflex elicited by tooth pulp stimulation (JOR). The mechanisms potentially responsible for this effect are discussed and the possibility is suggested, that a portion of the response is due to a modulatory action exerted by the sympathetic on the nociceptive input.