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PubMed1993

Median preoptic neurons projecting to the hypothalamic paraventricular nucleus are sensitive to blood pressure changes.

Twenty-one neurons in the median preoptic nucleus (MnPO) were antidromically activated by electrical stimulation of the hypothalamic paraventricular nucleus (PVN) in male rats under urethane anesthesia. The activity of these identified neurons was tested for a response to activation of peripheral baroreceptors, achieved by rising arterial blood pressure with an intravenous administration of the alpha-agonist metaraminol. Of the neurons tested, 14 displayed a reduction and 2 exhibited an increase in neuronal excitability that accompanied a 30- to 50-mmHg elevation in mean arterial pressure, while 5 were unresponsive. The results show that efferent pathways from the MnPO to the PVN may receive neural inputs from the peripheral baroreceptors, suggesting the involvement of the pathways in the control of cardiovascular function.

Action Potentials↗
PubMed1994

Neurones in the medullary raphe nuclei attenuate the cardiovascular responses evoked from the dorsolateral periaqueductal grey matter.

In rats anaesthetised with alphaxalone/alphadolone, electrical stimulation in the dorsolateral part of the periaqueductal grey matter (PAG; 10 s trains of 1 ms pulses at 80 Hz, 40-80 microA) evoked a pressor response accompanied by tachycardia. Both components of the response were attenuated following microinjection of 200 nl 0.1 M D,L-homocysteic acid into the caudal pole of the nucleus raphe magnus (NRM; n = 12) and into the nucleus raphe obscurus (NRO; n = 22) to selectively activate neuronal perikarya. Microinjection of 200 nl 165 mM NaCl into the same region (n = 15) had no effect. The attenuation of the midbrain-evoked cardiovascular responses lasted for 10-20 min and was independent of changes in resting blood pressure and heart rate. The maximum reduction in the pressor component of the midbrain-evoked responses was similar following stimulation in NRM (-35.4%) and NRO (-36.7%). However, the reduction in the midbrain-evoked tachycardia was greater following stimulation in NRM (-62.8%) compared to NRO (-27.2%). These results indicate that neurones in NRM and NRO may be involved in modulating the level of excitability of the midbrain defence area in the PAG and/or its efferent pathway.

Animals↗
PubMed1995

Reversal of levodopa-induced motor fluctuations in experimental parkinsonism by NMDA receptor blockade.

Dopaminoceptive system alterations in the basal ganglia have been implicated in the pathogenesis of wearing-off fluctuations that complicate levodopa therapy of Parkinson's disease. To evaluate the contribution of glutamatergic mechanisms to the associated changes in striatal efferent pathway function, we examined the ability of N-methyl-D-aspartate (NMDA) receptor blockade to modify the motor response changes produced by chronic levodopa administration to hemiparkinsonian rats. Unilaterally 6-hydroxydopamine lesioned rats, given levodopa/benserazide (25/6.25 mg/kg) twice daily for 3 weeks, developed a progressive shortening in the duration of their motor response to levodopa similar to that occurring in parkinsonian patients with wearing-off phenomenon. The acute systemic administration of MK-801 (0.1 mg/kg) to these animals completely reversed the decrease in turning duration (P < 0.01). Intrastriatal injection of the NMDA antagonist was even more effective in prolonging the levodopa response (P < 0.01), while intranigrally injected MK-801 produced no statistically significant change in the duration of levodopa-induced rotation. Rotational intensity was unaffected by all routes of MK-801 administration. These results suggest that drugs capable of blocking NMDA receptors, especially in striatum, may help ameliorate motor fluctuations in patients with advanced Parkinson's disease.

Animals↗
PubMed1975

Amygdala and masseteric reflex. I. Facilitation, inhibition and diphasic modifications of the reflex, induced by localized amygdaloid stimulation.

The changes in amplitude of the monosynaptic masseteric reflex (MR), induced by stimulation of the amygdaloid area for the defence reaction (N. basalis, pars magnocellularis) and in other subdivisions of the amygdaloid complex, were studied in cats with spinal section maintained under Flaxedil. Simultaneously, the the effects of stimulation on the tonic activity of the masseteric nerve were observed. A maintained facilitation of the MR was elicited by stimulation of the lateral nucleus, the parvocellular portion of the basal nucleus and the cortical nucleus, while the reflex was inhibited during stimulation of the medial-most portion of the posterior amygdala. Diphasic changes of the MR amplitude (initial facilitation followed by delayed inhibition) were regularly observed when stimulating the magnocellular portion of the basal nucleus. These diphasic changes were closely correlated with the previously described diphasic resporatory and cardiac responses elicited from the same are (Bonvallet and Gary Bobo 1972). The initial facilitation probably corresponds to the "alerting" stage of the defence reaction and the delayed inhibition, associated with cortical, respiratory and cardiac activation, to the "defensive" stage of the reaction. Stimulation of the same area also provokes tonic or rhythmical discharges of the masseteric motoneurons which frequently occur during the delayed inhibition of the MR. The main efferent pathway mediating these motor effects is probably the ansa lenticularis.

Amygdala↗
PubMed1984

Changes of cardiac and respiratory rhythm in non- and tracheostomized rats exposed to nitrogen dioxide.

Cardiac and respiratory changes in non- and tracheostomized rats were examined during exposure to 20 ppm of NO2 for 150 min. The abnormal respiratory pattern consisted of rapid shallow breathing, deep breathing, and apnea, and the bradyarrhythmias were observed in the tracheostomized rats during exposure. Also, similar changes were seen in the nontracheostomized rats. A decrease in the heart rate (HR) was observed in both non- and tracheostomized rats. The decrease in HR was depressed by atropine injection, and the abnormal respiratory patterns were almost abolished by this drug. It was suggested, from these results, that the cardiac and respiratory abnormalities could be induced without the irritation to upper respiratory tracts, and that the vagal efferent pathway had an important role in the appearance of the abnormalities during exposure.

Air Pollutants↗
PubMed1977

Relationship between the ventromedullary clonidine-sensitive area and the posterior hypothalamus.

The connections between the areas 'S' which have been previously described as the ventromedullary sites of the action of clonidine and the posterior hypothalamus have been investigated. Superficial electrocoagulation of the left area 'S' suppresses the pressor response to electrical stimulation of the homolateral part of the posterior hypothalamus. Although such medullary lesions cause a significant reduction of the mean arterial pressure, the contralateral hypothalamic stimulation can still increase blood pressure. Clonidine it self applied topically (8 micrograms/kg) to the ventral face of the brain stem decreases the blood pressure response to liminal hypothalamic stimulation. It is concluded that efferent pathways, which are involved in vasomotor regulation, originate in the posterior hypothalamus and run through the ventrolateral part of the brain stem. The mechanism of the blocking effect of clonidine on these pathways is discussed.

Animals↗
PubMed1994

Motor activation in short- and long-term reserpinized mice: role of N-methyl-D-aspartate, dopamine D1 and dopamine D2 receptors.

The effects of dopamine D1 and dopamine D2 receptor agonists and of subconvulsant doses of N-methyl-D-aspartate (NMDA) and the non-competitive NMDA receptor antagonist, dizocilpine (MK-801), alone and in combination, on the motor activity of short- and long-term reserpinized mice (mice pretreated with 5 mg/kg reserpine 4 h or 20 h before, respectively) were analyzed. With short-term reserpinization, the dopamine D2 receptor agonist, quinpirole (1.5 mg/kg), but not the dopamine D1 receptor agonist, SKF-38393 (15 mg/kg), increased motor activity. The effect of quinpirole in short-term reserpinized mice was potentiated by the simultaneous administration of SKF-38393 (15 mg/kg) and was counteracted by the previous administration of the dopamine D2 receptor antagonist, raclopride (1 mg/kg), or by the simultaneous administration of NMDA (25 mg/kg) or MK-801 (0.5 mg/kg). Neither NMDA (25-100 mg/kg) nor MK-801 (0.5-3 mg/kg) induced motor activation in short-term reserpinized mice. With long-term reserpinization, either quinpirole (1.5 mg/kg) or SKF-38393 (15 mg/kg) increased motor activity. The effect of quinpirole in long-term reserpinized mice was not potentiated by the concurrent administration of SKF-38393 (15 mg/kg), was inhibited by the simultaneous administration of MK-801 (0.5 mg/kg) and was not modified by NMDA (25 mg/kg). The effect of SKF-38393 (15 mg/kg) in long-term reserpinized mice was inhibited by the concomitant administration of MK-801 (0.5 mg/kg) and was slightly antagonized by NMDA (25 mg/kg). NMDA induced motor activation in long-term reserpinized mice at doses which were similar to those causing motor activation in non-reserpinized mice (75 and 100 mg/kg), while MK-801 induced motor activation at a dose which was associated with motor depression in non-reserpinized mice (2 mg/kg). The NMDA-induced motor activation in long-term reserpinized mice was counteracted by the previous administration of a low dose of MK-801 (0.5 mg/kg) and was still present when a stronger dopamine-depleting pretreatment was used. These results are interpreted on the basis of changes in sensitivity of the direct striatal efferent pathway after long-term reserpinization.

Animals↗
PubMed1983

Effect of hypothalamic cooling on the tonic vibration reflex of gastrocnemius muscle in cats.

The tonic vibration reflex (TVR) in a medial gastrocnemius muscle (MG) was analyzed in 28 cats anesthetized with pentobarbital sodium while the preoptic-anterior hypothalamic region (PO-AH) was locally cooled or warmed in a thermoneutral environment. Cooling of the PO-AH did not produce shivering or changes in rectal and skin temperatures, but it brought about facilitation (16/28 cats) or inhibition (9/28) of the TVR in the MG. A few cats (3/28) showed inconsistent alteration of the TVR. Warming of the PO-AH did not produce any changes in the TVR of the MG. Histological identification of thermode placements revealed that in cats having the facilitatory response of the TVR, the thermodes were localized at regions caudal to A 14.0 mm and most of the thermodes in those having the inhibitory response were rostral to A 14.0 mm, except for two cases. Bilateral microinjection of a small quantity of anesthetic agent into the medial forebrain bundle (MFB) at the level of the mamillary body abolished the facilitatory effect of PO-AH cooling on the TVR. The results suggest that the spinal motor system is influenced by the PO-AH's sensitivity to local temperature and that the MFB constitutes part of the efferent pathway of the hypothalamic influence.

Animals↗
PubMed1977

The neurological basis of motor asymmetry following unilateral 6-hydroxydopamine brain lesions in the rat: the effect of motor decortication.

The role of the motor cortex in the mediation of asymmetric movement after unilateral 6-hydroxydopamine (6-OHDA) brain lesions has been examined in the rat. The effect of unilateral and bilateral sensorimotor decortication upon spontaneous and drug (apomorphine and amphetamine)-induced motor asymmetry has been studied following unilateral injection of 6-OHDA into the lateral hypothalamus. Both bilateral decortication and unilateral decortication on the side of the 6-OHDA lesion caused a transient reversal of the spontaneous motor asymmetry normally seen in 6-OHDA lesioned animals. Neither unilateral nor bilateral sensorimotor decortication abolished drug-induced turning behaviour. It is postulated that subcortical basal ganglia efferent pathways may be involved in the mediation of motor asymmetry after unilateral 6-OHDA lesions of the nigrostriatal dopaminergic projection.

Amphetamine↗
PubMed1990

Correlation of somatosensory evoked potentials and long loop reflexes in patients with multiple sclerosis.

Based on the results of somatosensory evoked potentials (SEPs) and long loop reflexes (LLRs) obtained from the 50 upper limbs of 25 normal controls by stimulating the median nerve, four regions were set up in a latency correlation diagram between N20 and LLR, which were assumed to mainly represent the afferent and the efferent functions, respectively. Seventy upper limbs of patients with multiple sclerosis, differently marked according to the presence or absence of pyramidal sign and/or impaired vibration sense, were plotted on the diagram. The regions to which the patient belonged turned out to be reasonably compatible with the neurological status of the patient. Simultaneous measurements of SEPs and LLRs are therefore useful to evaluate the afferent and efferent pathways in the central nervous system.

Adult↗
PubMed1995

Sympathetic skin response: a decade later.

Sympathetic skin response (SSR) is a simple, reproducible test of function of a polysynaptic reflex having diverse afferents, a common efferent pathway through the spinal cord, pre and post-ganglionic sympathetic fibers and with sweat glands as effectors. The reflex is co-ordinated in the posterior hypothalamus or upper brainstem reticular formation. It has been used in a variety of disorders of peripheral and central nervous system. Methodology, possible anatomic substrates, changes in SSR in various diseases and their correlation with clinical features of dysautonomia, bed side tests for dysautonomia and other electrophysiological parameters are critically evaluated. Almost a decade after the start of its widespread clinical utilization, several aspects of SSR remain inconclusive. A consensus as to what change in SSR to consider abnormal is yet to be reached. Though its ease of application supersedes a variety of other autonomic function tests, relying only on SSR changes for prognostication or therapeutic decisions appears impracticable. A battery of tests is thus a necessity.

Axons↗
PubMedDate not supplied

Role of opioid receptors in the substantia nigra in morphine-induced muscular rigidity.

Uni- or bilateral injection of morphine (MO) (3-13 nmoles) into the substantia nigra pars reticulata (SNR) produced tonic activity in the electromyogram (EMG) recorded from the gastrocnemius-soleus (GS) muscle of non-anesthesized rats. This activity was antagonized by naloxone (NAL) (10 nmoles) coadministered with MO into the SNR. Bilateral lesion of the caudate nucleus (CN) with kainic acid did not prevent the tonic EMG activity occurring after the injection of MO into the SNR. Unilateral injection of MO (40 nmoles) into the CN also induced tonic EMG activity in the GS-muscle, which was antagonized by NAL (10 nmoles) administered into the SNR ipsilaterally and simultaneously to the intrastriatal injection of MO. The results suggest that enkephalinergic mechanisms in the SNR seem to play a crucial role in the function of striatal efferent pathways relayed in the SNR.

Animals↗
PubMed1990

Rotation in response to selective dopamine receptor agonists in rats with electrolytic substantia nigra lesions.

Rats with unilateral, electrolytic substantia nigra (ESN) lesions were tested for rotation following systemic injections of the D1 dopamine receptor agonist SKF38393 or the D2 agonist quinpirole. Only quinpirole produced significant levels of rotation, which was ipsilateral in direction. This rotation was potentiated by coadministration of the D1 agonist, and was significantly reduced by injections of either a D1 or D2 receptor antagonist. Other groups of lesioned animals were treated with reserpine for 5 days and were then tested for rotation in response to the agonists. In this case, SKF38393 produced significant levels of contralateral rotation, while quinpirole-induced rotation remained ipsilateral; coadministration of the D1 and D2 agonists resulted in pronounced ipsilateral rotation. These results stress a role for D1 receptor mechanisms in producing rotation, and suggest that different striatal efferent pathways mediate rotation in response to selective agonists following ESN lesions.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1992

Role of afferent information in the timing of motor commands: a comparative study with a deafferented patient.

The accuracy of the motor system in synchronizing simultaneous movements initiations was tested in two conditions: (1) when the motor commands were triggered by an external signal (reactive condition), and (2) when subjects self-paced their movement onsets (self-paced condition). The task consisted of initiating simultaneously ipsilateral finger extension and heel raising. Eight normal subjects and a deafferented patient were tested. In the reactive condition, both normal subjects and the deafferented patient exhibited a precession of finger initiation over heel raising. This delay corresponds to the difference observed in the reaction time of the two limbs when measured independently. It reflects the difference in conduction times of the efferent pathways, as if the two motor commands were released simultaneously through a common triggering signal in the motor cortex. In contrast, in the self-paced condition normal subjects showed precession of heel over finger onsets, suggesting that synchrony is based upon the evaluation of afferent information. Unlike normal subjects, the patient showed no heel precession in the self-paced condition. These findings suggest that reactive and self-paced responses are produced through two different control modes and that afferent information contributes to the timing of motor commands in the self-paced mode.

Adult↗
PubMed1977

Effect of preoptic administration of angiotensin on lateral hypothalamic unit activity.

The effect of administering angiotensin II to the preoptic region on lateral hypothalamic single unit activity was studied in unanesthetized, freely-moving rats. Angiotensin (100 ng) reliably initiated drinking behavior and caused an increase in the discharge frequency of single neurons located in the perifornical area but had no effect on units in the zona incerta, ventromedial hypothalamus or farlateral hypothalamus. These results suggest that efferent pathways from preoptic receptors for angiotensin pass through the midlateral hypothalamus.

Action Potentials↗
PubMed1994

Neural regulation of bronchial blood flow.

The neural regulation of the bronchial vasculature differs from that of the general systemic circulation in that vasodilator reflexes play a major part in determining blood flow. These reflexes originate in the upper or lower airways, in carotid chemoreptors or in cardiac chemosensitive nerves; those arising in the lower airways are most potent and may increase bronchial blood flow several-fold and cause swelling of the airway mucosa. Lower airway reflexes have afferent and efferent pathways in the vagus nerves, the former including sensory C-fibers and rapidly adapting receptors, the latter involving both cholinergic and non-cholinergic transmitters. In addition, neuropeptides released from the C-fiber terminals provide a local mechanism for vasodilation independent of central reflex control. This so-called axon-reflex plays the major part in bronchial vasodilation in rodents but makes only a small contribution in larger animals. In larger animals centrally-mediated reflexes and vagal vasodilator pathways appear more important. Nevertheless, local neural vasodilation may be important in airway disease; the factors that favor its operation in animals other than rodents deserve to be explored.

Animals↗
PubMed1990

Mediation of reflex tachycardia becomes exclusively beta-adrenergic in old Fischer 344 rats.

To study how baroreflex regulation changes with age we compared reflex heart rate responses elicited in awake Fischer 344 rats of different ages during intravenous infusions of phenylephrine or sodium nitroprusside. Underlying neural mechanisms were assessed by repeating baroreflex tests following cholinergic blockade with methylatropine or beta-adrenergic blockade with propranolol. Basal heart rates always tended to be lower in old than in young rats, but the differences became statistically significant only after beta-adrenergic or combined cholinergic and beta-adrenergic blockade. Most reflex heart rate responses (i.e. except reflex tachycardia in males during depressor responses to sodium nitroprusside) were initially weaker in old than in younger rats. Reflex bradycardia and tachycardia were reduced equally in both age groups after cholinergic blockade, but were reduced more in old than in young rats after beta-adrenergic blockade. beta-adrenergic blockade alone reduced reflex tachycardia as much as did combined blockade thereby suggesting that the predominant neural mechanism was beta-adrenergic. Taken altogether these results are compatible with the interpretation that efferent pathways for mediating heart rate reflexes in Fischer 344 rats are altered with age such that as parasympathetic mediation diminishes, residual mediation particularly of reflex tachycardia, becomes almost exclusively beta-adrenergic or sympathetic.

Aging↗
PubMed1979

Changes in body temperature after administration of amino acids, peptides, dopamine, neuroleptics and related agents.

Drugs may alter body temperature by acting on any component of the thermoregulatory system. These components include heat production, heat conservation and heat loss effectors and their efferent pathways, thermosensors and their afferent pathways and neurons within the central nervous system that coordinate thermoregulatory effector activities. A thermostat is often thought to be involved although thermoregulation can be explained by models that do not incorporate a thermostat. An action on a particular component can be assessed by determining the effect of a drug on body temperature over a range of environmental temperatures and by observation and measurement of associated changes in effector activities. A scheme for such assessment is presented along with examples of its use. The study of drug-induced changes in body temperature has expanded greatly within the past decade. The primary purpose of this review is to provide a readily available source of information on interactions between certain drugs and the thermoregulatory system. Extensive tables are presented of body temperature changes after administration of amino acids, peptides, dopamine and related agents, phenothiazine neuroleptics and also phenothiazines that lack neuroleptic activity, butyrophenones, diphenylbutylpiperidines such as pimozide and miscellaneous neuroleptics. The information tabulated includes the species used, route of administration and dose of drugs, the environmental temperature at which the experiments were performed, the number of tests, the direction and magnitude of body temperature change and remarks on the presence of special conditions, such as age or lesions, or on the influence of other drugs, such as antagonists, on the response to the primary drug. Most of the cited literature was published since 1965.

Amino Acids↗