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PubMed1994

Endocrine response to brain injury.

The neuroendocrine response (NER) is an essential component of the adaptive process to trauma, brain injury, and major surgery. While receiving additive humoral and neural afferent inputs, the brain nuclei responsible for the NER act mainly by efferent pathways to the hypothalamic-pituitary-adrenal (HPA) axis and the sympathoadrenal system, the activations of which induce subsequent circulatory and metabolic responses. The NER to brain injury is similar to the response observed in patients with extracerebral injury, even if the response after brain injury is extremely variable. Generally, there is a biphasic pattern, with a sympathoadrenal storm associated with variable and altered stimulation of the HPA during the ebb phase. The first phase is followed by a decrease in both responses while other endocrine changes develop, involving mainly the counter-regulatory, gonadal, and thyroid hormones. The outcome after brain injury is closely correlated with the intensity of these changes, particularly with catecholamine plasma levels and the severity of the low triiodothyronine syndrome. Alterations of the thyroid hormones are largely related to a reduction in peripheral deiodination of thyroxin. Recent research shows that increased free-radical production and decreased selenium (an antioxidant) serum levels play an important role in thyroid metabolism. Two major issues remain unsolved: a) the precise definition of cerebral death, since endocrine brain function is not abolished in the state currently defined as brain death; and b) the question of whether substitutive hormone therapy should be applied in severe brain injury.

Animals↗
PubMed1994

Effects of sleep on the responses of single cells in the lateral superior olive.

The effects of behavioral shifts on auditory lateral superior olive neurons were analyzed in guinea-pigs during the sleep-waking cycle with single unit extracellular recordings at the unit characteristic frequency and with low sound intensity. Shifts in the number of spikes in response to pure tones and in spontaneous firing proved to be closely related to waking, slow wave and paradoxical sleep. All of the recorded lateral superior olive (LSO) auditory neurons showed sleep-related firing shifts. Moreover, changes in the pattern of discharge over time were observed in 15% of the LSO cells on passing from waking to sleep. Sleep may determine either an increase or a decrease of the firing number in response to sound. The most important change observed in decreasing firing units was the near-absence of units responding to sound in the paradoxical sleep phase during the last 40 ms of the response. The waking cues for binaural detection, studied with our experimental paradigm, disappeared during slow wave sleep. We thus conclude that the binaural function of some lateral superior olive neurons (11.5%) was impaired during this sleep period in the present experimental conditions. Auditory efferent pathways are postulated to impinge on the auditory processing at LSO nucleus level during the sleep-waking cycle. Thus, auditory unitary activity appears to be dependent on both incoming information, and a CNS descending action closely related to the waking and sleep periods. Functional interactions between pontine sleep-related groups of neurons and auditory system units are suggested.

Acoustic Stimulation↗
PubMed1993

Second messenger systems in brains of patients with Parkinson's or Huntington's disease.

Alterations in protein kinase C (PKC) and myo-inositol 1,4,5-trisphosphate (IP3) receptors were studied in the autopsied human striata from 21 patients with Parkinson's disease (PD) (Yahr III, IV, and V), 8 patients with Huntington's disease (HD), and 23 age-matched and postmortem time-matched nonneurological controls. The concentrations of PKC and IP3 receptors were determined using [3H]4 beta-phorbol 12,13-dibutyrate (PDBu) and [3H]IP3 as respective ligands. Both the specific [3H]-PDBu and [3H]IP3 bindings were significantly reduced in the striata of Yahr V patients with dementia (PDD) and in that of HD patients, as compared to findings in the controls. These bindings were unchanged when all the PD patients without dementia, Yahr (III plus IV) patients, or Yahr V patients without dementia were compared with evidence from the controls. Immunoquantification of four PKC subspecies (alpha, beta I, beta II, and gamma) in the HD putamen revealed a selective reduction in the beta II-PKC immunoreactions. These results are supported by immunohistochemical findings in the rat brain that beta II-PKC is expressed in the striatal gabaergic efferent pathway, while the alpha-PKC is present in the nigrostriatal dopaminergic neurons. The neurochemical pathophysiology of PD differs between patients with and without dementia.

Aged↗
PubMed1993

[Sudomotor dysfunction in Parkinson's disease].

Sudomotor function was evaluated by using the sympathetic skin response (SSR) and the sweat response to intradermal acetylcholine (ACh) injection in 69 patients with Parkinson's diseases (PD). The incidence of SSR abnormality (34.8%) was as high as that of orthostatic hypotension (30.4%) and increased with the severity of the illness. Anticholinergic drug did not influence the incidence of SSR abnormality. Therefore, the SSR is useful in evaluating sudomotor efferent pathway in PD patients. Moreover, in all patients, sweat response to ACh showed a reduced number of excitable sweat glands and a low volume of sweat. In a patient in whom sweat response to ACh was markedly impaired, however, the density of acetylcholinesterase-positive unmyelinated fibers in biopsied sural nerve was in normal range. Therefore, this is considered to indicate functional disturbance of the postganglionic sympathetic fibers in PD patients, without morphological changes.

Aged↗
PubMed1993

The striopallidal neuron: a main locus for adenosine-dopamine interactions in the brain.

Recent pharmacological data suggest that a receptor-receptor interaction between adenosine A2 and dopamine D2 receptors in the brain underlies the behavioral effects of adenosine agonists and adenosine antagonists, such as caffeine and theophylline. According to this interaction, stimulation of A2 receptors inhibits and their blockade potentiates the effects of D2 receptor stimulation. Furthermore, both A2 and D2 receptors are selectively colocalized on GABAergic striopallidal neurons. In this microdialysis investigation the effect of intrastriatal infusion of adenosine and dopamine agonists and antagonists alone or in combination was studied on the release of GABA from the terminals of the striopallidal neuron in awake, freely moving rats. We report that the GABAergic striopallidal neuron, which is a key component of the indirect striatal efferent pathway, is a main locus for A2-D2 interactions in the brain and possibly a main target for the central actions of adenosine agonists and antagonists.

Animals↗
PubMed1993

Neurogenic pulmonary edema.

The pathogenesis of nervous system-induced pulmonary edema remains incompletely understood. There are two major causes: elevated intravascular pressure and pulmonary capillary leak. Thus, both hemodynamic (cardiogenic) or nonhemodynamic (noncardiogenic) components exist. These components often occur together in settings such as pulmonary edema following epileptic convulsions or intracranial pressure elevation. The hemodynamic component is relatively brief and may unmask a "pure" noncardiogenic pulmonary edema such as that seen in experimental seizures (see Fig. 6). Whether the hemodynamic changes produce a pulmonary capillary leak through pressure-induced mechanical injury to the pulmonary capillaries or whether some direct nervous system control over pulmonary capillary permeability exists remains uncertain. The neuroeffector site for nervous system-induced pulmonary edema appears relatively well established in regions about the caudal medulla, where nuclei regulating systemic arterial pressure and afferent and efferent pathways to and from the lungs are located.

Animals↗
PubMed1993

Orienting head movements resulting from electrical microstimulation of the brainstem tegmentum in the barn owl.

The size and direction of orienting movements are represented systematically as a motor map in the optic tectum of the barn owl (du Lac and Knudsen, 1990). The optic tectum projects to several distinct regions in the medial brainstem tegmentum, which in turn project to the spinal cord (Masino and Knudsen, 1992). This study explores the hypothesis that a fundamental transformation in the neural representation of orienting movements takes place in the brainstem tegmentum. Head movements evoked by electrical microstimulation in the brainstem tegmentum of the alert barn owl were cataloged and the sites of stimulation were reconstructed histologically. Movements elicited from the brainstem tegmentum were categorized into one of six different classes: saccadic head rotations, head translations, facial movements, vocalizations, limb movements, and twitches. Saccadic head rotations could be further subdivided into two general categories: fixed-direction saccades and goal-directed saccades. Fixed-direction saccades, those whose direction was independent of initial head position, were elicited from the midbrain tegmentum. Goal-directed saccades, those whose direction changed with initial head position, were elicited from the central rhombencephalic reticular formation and from the efferent pathway of the cerebellum. Particular attention was paid to sites from which fixed-direction saccadic movements were elicited, as these movements appeared to represent components of orienting movements. Microstimulation in the medial midbrain tegmentum elicited fixed-direction saccades in one of six directions: rightward, leftward, upward, downward, clockwise roll, and counterclockwise roll. Stimulation in and around the interstitial nucleus of Cajal (InC; a complete list of anatomical abbreviations is given in the Appendix) produced ipsiversive horizontal saccades. Stimulation in the ventral InC and near the dorsal and medial edges of the red nucleus produced upward saccades. Stimulation in the reticular formation near the lateral edge of the red nucleus produced downward saccades. Stimulation in the ventromedial central gray produced ipsiversive roll saccades. The metrics and kinetics of fixed-direction saccades, but not their directions, could be influenced by stimulation parameters. As such, direction was an invariant property of the circuits being activated, whereas movement latency, duration, velocity, and size each demonstrated dependencies on stimulus amplitude, frequency, and duration. The data demonstrate directly that at the level of the midbrain tegmentum there exists a three-dimensional Cartesian representation of head-orienting movements such that horizontal, vertical, and roll components of movement are encoded by anatomically distinct neural circuits.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1977

Network of immune-neuroendocrine interactions.

In order to bring the self-regulated immune system into conformity with other body systems its functioning within the context of an immune-neuroendocrine network is proposed. This hypothesis is based on the existence of afferent--efferent pathways between immune and neuroendocrine structures. Major endocrine responses occur as a consequence of antigenic stimulation and changes in the electrical activity of the hypothalamus also take place; both of these alterations are temporally related to the immune response itself. This endocrine response has meaningful implications for immunoregulation and for immunospecificity. During ontogeny, there is also evidence for the operations of a complex network between the endocrine and immune system, a bidirectional interrelationship that may well affect each developmental stage of both functions. As sequels the functioning of the immune system and the outcome of this interrelation could be decisive in lymphoid cell homeostasis, self-tolerance, and could also have significant implications for pathology.

Animals↗
PubMed1996

[Neurocardiogenic syncope: its pathogenesis, diagnosis and treatment].

Neurocardiogenic syncope seems to be the most common cause of syncope. It is believed to be triggered by paradoxical autonomic reflexes, beginning in the ventricular mechanoreceptors of the heart, modulated by the brain stem and terminating in the autonomic efferent pathways (parasympathetic stimulation with bradycardia or asystole and sympathetic inhibition with severe hypotension). Tilt test has been used recently, as a safety and effective tool to identify subjects prone to syncope. Although the pathophysiology of this syndrome is not completely understood, pharmacological therapeutics seems very effective in resolving symptoms.

Autonomic Nervous System↗
PubMed1995

Electrophysiological changes in substantia nigra after striatal infarction.

The GABAergic efferent pathway from the striatum exerts inhibitory control on the substantia nigra pars reticulata (SNR) neurones. We studied sequential changes in spontaneous single-unit activities in the ipsilateral SNR 1 h, 1 day, 7 days and 14 days after striatal infarction induced by middle cerebral artery occlusion (MCAO) in rats. Compared with a sham-operated group, there was no change in the firing rate 1 h after MCAO, and one day after MCAO the mean firing rate decreased. The firing rate of SNR neurones at 7 and 14 days after MCAO was significantly reduced compared with the sham-operated group. Only two neurones (sham-operated group and 1 h after MCAO group) fired with high frequency. Histological examination revealed degeneration of the ipsilateral SNR 7 and 14 days after MCAO. Our results indicated that SNR neuronal degeneration accompanied by striatal ischaemia does not simply depend on hyperexcitation due to the activation of a disinhibition mechanism.

Animals↗
PubMed1996

Changes in apomorphine pharmacodynamics following repeated treatment in 6-hydroxydopamine-lesioned rats.

Rats with 6-OHDA lesions were repeatedly treated with apomorphine and dose-response relationships compared before and after treatment to better understand the pharmacological mechanisms which result in sensitization. A progressive increase in the magnitude and duration of rotational behavior was observed following repeated treatment and was associated with a nonparallel (upward) shift in apomorphine dose-response curves. These changes are inconsistent with simple shifts in drug potency, and instead are more consistent with changes in the ability of apomorphine to stimulate postsynaptic, striatal efferent pathways which result from repeated drug administration.

Animals↗
PubMed1996

Heart rate responses to intravenous serotonin in rats with acute chagasic myocarditis.

We administered serotonin to rats with experimentally induced chagasic myocarditis in order to study the Bezold-Jarisch reflex. Sixteen 4-month old Wistar rats were inoculated with 200,000 T. cruzi parasites ("Y" strain). Between days 18 and 21 (acute stage), 8 infected rats and 8 age-matched controls received intravenous serotonin as a bolus injection at the following doses: 0.5, 1.0, 2.0, 4.0, 6.0, 8.0, 10.0, 12.0, and 14.0 micrograms/kg. Heart rate was recorded before, during and after each dose of serotonin. The remaining 8 infected animals and 8 controls were subjected to the same experimental procedure during the subacute stage, i.e., days 60 to 70 after inoculation. The baseline heart rate of the infected animals studied during the acute stage (327 +/- 62 beats/min, mean +/- SD) was higher than that of the controls (248 +/- 52, P < 0.01). The heart rate changes were expressed as percent changes to correct for the higher baseline heart rate of the infected animals. A dose-response curve was constructed for each group of animals. The slope for the acutely infected animals (r = -0.95, b = -3.98) was not different from that for the control animals (r = -0.92, b = -3.50). The infected animals studied during the subacute stage (r = -0.92, b = -4.33) were not different from the age-matched controls (r = -0.87, b = -4.03). These results suggest that the afferent and efferent pathways which mediate the Bezold-Jarisch reflex are functionally preserved in rats with histologically proved chagasic myocarditis.

Acute Disease↗
PubMed1997

Xenopus Brn-3.0, a POU-domain gene expressed in the developing retina and tectum. Not regulated by innervation.

PURPOSE: To study the effect of denervation on the expression of the POU-domain gene Brn-3.0 in the Xenopus visual system. METHODS: An oligonucleotide probe was used to identify homologs of the murine gene Brn-3.0 in the retina. In situ hybridization was used to determine the spatial distribution of the mRNA within the developing embryo. To study the effects of denervation on Brn-3.0 expression and cell fate, embryonic eyes were transplanted to an ectopic location on the animal (the flank) before the onset of retinal ganglion cell (RGC) axonogenesis. Gene expression in ectopic eyes and denervated tecta was analyzed over time using in situ hybridization. RESULTS: The deduced, partial amino acid sequence for Xenopus Brn-3.0 shows 100% identity with the mouse Brn-3.0 and the human Brn-3a gene products. It is expressed during early embryonic development in distinct populations of the neural crest and later in specific cranial ganglia. It also is expressed in RGCs and in the optic tectum, beginning before the first RGC axons have reached the tectum and continuing without interruption throughout the period when retino-tectal connections are established and refined. If the retino-tectal projection is kept from forming by transplanting one eye to an ectopic location, Brn-3.0 expression is unaffected in both the ectopic eye and the denervated side of the tectum. CONCLUSIONS: Coordinate expression of Brn-3.0 in afferent and efferent pathways suggests mutual regulation. However, the authors' evidence shows that expression in the retina is not regulated by target-derived factors nor is expression in the tectum regulated by retinal innervation.

Animals↗
PubMed1997

[Involuntary movements caused by basal ganglia-disorders and their age dependency: introductory remarks].

The basal ganglia modulate voluntary movements involving the neural circuit of the cortex-basal ganglia-thalamus-cortex. The basal ganglia receive all of the afferents at the striatum and project the efferents from two output structures, the medial segment of the globus pallidus and pars reticulata of the substantia nigra. Besides the cortex, the basal ganglia receive inputs from pars compacta of the substantia nigra (SNc) and centromedian nuclei of the thalamus. The afferent from the SNc is the nigrostriatal (NS) dopamine (DA) neuron and has important roles in functional modulation of the basal ganglia. As for efferents, the basal ganglia also have output projections to the superior colliculus and pedunculo-pontine nuclei. In the basal ganglia, the striatum has two efferent pathways; one is the direct projection which projects directly to the output structure and the other is the indirect pathway which projects to the output structures via the lateral segment of the globus pallidus and the subthalamic nuclei, changing synapses at these nuclei. The lesions in the basal ganglia show various movement disorders or involuntary movements depending on their foci. Basal ganglia lesions also develop symptoms age dependently; a certain lesion develops dystonia in younger brains, while revealing parkinsonism in adult or older brains. This age dependency depends on the difference in the course of the functional maturation of each component and pathway of the basal ganglia. At this symposium we tried to show the basic pathophysiologies of age dependency by discussing basal ganglia disorders in children compared to those in adults and referring to the basic science of the basal ganglia.

Adult↗
PubMedDate not supplied

[The cholinergic system of the striatum: its participation in the motor and sensory components of motor behavior].

This review deals with the recent data on participation of the dorsal striatum cholinergic system in orientation behavior and in regulation of attention to significant stimuli, which was realized via the range of subcortical structures, among them the intralaminar thalamic nuclei (CM-Pf) and pedunculopontine nuclei (PPN) play an especially important role. On the basis of our own experimental data it was suggested that by using an adequate pharmacological effects upon striatal cholinergic system, it was possible to change the sensory and motor components of movement behavior. Whereas the unilateral microinjections of cholinergic receptor agonists lead to behavioral changes only on the day of injection, the bilateral injections change the formed type of the movement behavior for a long time. An important role of the dorsal striatal cholinergic system in switching and modulation of the indirect efferent pathway was substantiated. By this mechanism, inhibition of nonspecific sensory afferentation at different subcortical levels and an increase of significant sensory signals can take place. A manifestation of this mechanism can be the sharp improvements of differentiation of sensory stimuli after activation of the striatal cholinergic system. On the other hand, the cholinergic striatal limitation of movement activity (a decrease of locomotion, an increase of tonic component of movement and streamlining of posture) may be the important factors for making a decision in a difficult situation.

Animals↗
PubMed1997

Changes in central motor-sensory system following voluntary movement of stimulated finger.

OBJECTIVE: We examined which components of somatosensory evoked potentials (SEP) were modulated during the voluntary movement of stimulated fingers and discuss our findings with respect to the decrease in SEPs in terms of both centrifugal and centripetal mechanisms. METHODS: The study was performed in the Laboratory of Physiology, Institute of Health and Sport Sciences, University of Tsukuba. Experiments were performed on 10 healthy young male subjects, aged 19-21 years. All subjects were right-handed and were free of neurological disease. RESULTS: We found that N20-P25 (P22 at frontal area) -N35-(N30 at frontal) P45 (P40 at frontal area) components at the F3, the C3' and the P3 were consistently evoked, but N35 was increased at P3 and N30 attenuation at F3 during a sustained voluntary movement. Furthermore, the present experiments showed that frontal N30 was markedly decreased during a sustained voluntary movement. We also found that all SEPs components, except for parictal N35, were significantly decreased during sustained voluntary movement tasks. CONCLUSIONS: We concluded that the suppression of SEPs appeared to be due to the interaction of both centrifugal and centripatal mechanisms. Namely, in a particular type of movement task, more prenounced afferent mechanisms may contribute to the decrease in SEPs, while in the other types of tasks, more pronounced afferent activities may contribute to the decrease in SEPs.

Adult↗
PubMed1997

Reorganization of somato-urethral reflexes following spinal cord injury in the rat.

PURPOSE: It is known that reflex activity of the urinary bladder can be inhibited or facilitated by perineal cutaneous stimulation. This study was undertaken to examine the urethral striated (EUS) and smooth muscle responses evoked by perineal cutaneous stimulation in the rat. MATERIALS AND METHODS: Urethral perfusion pressure and EUS-EMG were monitored in urethane-anesthetized normal and chronic spinal rats (4-5 weeks after T(8-9) spinalization) of either sex. Somatic perineal stimulation was performed by tactile or pinch stimulation to the perineum. RESULTS: In both normal and chronic spinal rats, perineal stimulation elicited a transient increase in EUS-EMG activity which was abolished following neuromuscular blockade with alpha-bungarotoxin i.v. In normal rats treated with alpha-bungarotoxin perineal stimulation did not elicit a detectable urethral smooth muscle response. However, in chronic spinal rats perineal stimulation increased urethral pressure by smooth muscle contraction in males and decreased urethral pressure by smooth muscle relaxation in females. The evoked urethral smooth muscle contraction in males was significantly reduced or abolished by atropine i.v., but not by sympathetic nerve transection or prazosin i.v., whereas the relaxation in females was significantly reduced or abolished by N-nitro-L-arginine methyl ester (a nitric oxide synthase inhibitor, i.v.). CONCLUSIONS: These data indicate that spinal cord injury unmasks somato-urethral smooth muscle reflexes mediated by lumbosacral parasympathetic efferent pathways. The reflexes consist of a nitric oxide-mediated urethral relaxation in females and an atropine-sensitive urethral contraction in male rats.

Animals↗
PubMed1997

Evoked potentials in diabetes mellitus.

Abnormalities of central afferent and efferent pathways have been revealed by evoked potential studies in diabetic patients. Central conduction time is only slightly prolonged; in afferent pathways the primary sensory neuron is more affected than in the subsequent stages, probably as an expression of a central-peripheral distal axonopathy. Central nervous system abnormalities are more frequent in patients with peripheral neuropathy, but evoked potential can be abnormal even in patients without neuropathy. Brainstem auditory evoked potential (BAEP), somatosensory evoked potentials (SEPs) and visual evoked potentials (VEPs) can be affected together, but isolated abnormalities are more frequently observed. Diffuse neuropathological changes have been found in the optic nerves, periventricular regions, brainstem and spinal cord in postmortem pathological studies. Similar changes have been found in animals with experimental diabetes. The pathophysiology of central nervous system (CNS) abnormalities is uncertain, many causes are probably active in including neural damage: chronic hyperglycemia, hypoglycemic episodes, angiopathy, blood-brain barrier dysfunction and others, still unknown.

Diabetes Mellitus↗