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PubMed2000

Measurement of baroreceptor-mediated effects on heart rate variability in fetal sheep.

To determine if alterations in arterial pressure influenced fetal heart rate variability (HRV), experiments were carried out in chronically catheterized fetal sheep aged 128-138 d. Arterial pressure was raised or lowered by intravenous infusion of phenylephrine or sodium nitroprusside, and the effects on heart rate (HR) and HRV were measured (HRV, as the coefficient of variation (CV) in mean pulse interval or by power spectral analysis). Experiments were carried out before and during beta-adrenoceptor blockade with propranolol or before and during cardiac vagal blockade with atropine. There were positive relationships between mean arterial pressure and HRV (slope = 0.074+/-0.001, r = 0.81+/-0.06, p<0.001, measured as the CV of pulse interval) and between mean arterial pressure and power spectral density (slope = 4+/-0.5, r = 0.89+/-0.02, p<0.001) in the frequency range 0.04-0.08 Hz. Beta-adrenoceptor blockade had no effect on these relationships, but they were abolished by cardiac vagal blockade. The sigmoid relationship between fetal HR and mean arterial pressure, i.e. the cardiac baroreflex, was affected, however, by blockade of cardiac sympathetics and abolished by blockade of cardiac vagal activity. Thus, fetal HRV was affected by alterations in arterial pressure, and these effects depended on the integrity of the cardiac vagus, not on alterations in cardiac sympathetic activity. Therefore, although baroreflex control of fetal HR depends on the integrity of both sympathetic and parasympathetic efferent pathways, baroreceptor-induced changes in HRV depend only on the cardiac vagus.

Animals↗
PubMed2006

Painful hand and moving finger treated by wearing a glove.

The authors report a patient with unilateral painful hand and moving finger in whom tactile stimulation interrupted both the movement and the pain. This effect suggests a gating mechanism at a segmental level. The difference between afferent and efferent pathway levels and the delay of several months between trauma and occurrence of symptoms support a central mechanism, most probably involving sensorimotor reorganization at a segmental level.

Female↗
PubMed1996

Abnormalities of torsional fast phase eye movements in unilateral rostral midbrain disease.

In a patient with a unilateral rostral midbrain lesion, three-dimensional scleral search coil eye movement recordings demonstrated slowing of ipsidirectional torsional fast phase eye movements without any abnormalities of torsional slow phases. On high-resolution MRI, the brainstem lesion localized to the area of the efferent pathways from the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF). This supports the experimental finding that unilateral inactivation of the riMLF results in a loss of ipsidirectional torsional fast phase eye movements and the hypothesis that there is lateralization of function throughout the torsional fast eye movement generating system.

Adult↗
PubMed1997

Sensorimotor cerebral activation during optokinetic nystagmus. A functional MRI study.

Self-motion or object motion can elicit optokinetic nystagmus (OKN), which is an integral part of dynamic spatial orientation. We used functional MR imaging during horizontal OKN to study cerebral activation patterns in sensory and ocular motor areas in 10 subjects. We found activation bilaterally in the primary visual cortex, the motion-sensitive areas in the occipitotemporal cortex (the middle temporal and medial superior temporal areas), and in areas known to control several types of saccades such as the precentral and posterior median frontal gyrus, the posterior parietal cortex, and the medial part of the superior frontal gyrus (frontal, parietal, and supplementary eye fields). Additionally, we observed cortical activation in the anterior and posterior parts of the insula and in the prefrontal cortex. Bilateral activation of subcortical structures such as the putamen, globus pallidus, caudate nucleus, and the thalamus traced the efferent pathways of OKN down to the brainstem. Functional MRI during OKN revealed a complex cerebral network of sensorimotor cortical and subcortical activation.

Adult↗
PubMed1993

Fastigial pressor response observed during an operation on a patient with cerebellar bleeding--an anatomical review and clinical significance.

The fastigial pressor response (FPR) consists of an abrupt rise in blood pressure and tachycardia with hyperpneic response. The FPR is an important sign in posterior fossa surgery for respiration in postoperative patients. The authors experienced a distinct pressor, tachycardiac, and hyperpneic response elicited when controlling bleeding using a bipolar coagulator forceps at the subfastigial white matter in a 72-year-old man with cerebellar hemorrhage. This response was confirmed by bipolar electrodes, which produced a weak current under deeper anesthesia by increasing the concentration of enflurane. The postoperative course of this patient was uneventful. A FPR was suggested to be mediated by axons passing between the nucleus fastigii and the fourth ventricle. These commissural fibers mediating the FPR were suggested to be countercurrent efferent pathways from both sides of the nucleus parabrachialis lateralis, located at the dorsolateral corner of the rostral pons. The authors conclude that the partial destruction of the subfastigial commissural fiber bundle did not result in permanent respiratory deficit. Fatal respiratory disturbance might be anatomically suggested by completely cutting off this fiber bundle.

Aged↗
PubMed1995

Mutism and pseudobulbar symptoms after resection of posterior fossa tumors in children: incidence and pathophysiology.

MUTISM AND A variety of other neurobehavioral symptoms have been reported anecdotally after the removal of posterior fossa mass lesions. To determine the incidence and clinical spectrum of this syndrome, a detailed review was performed of patients undergoing resection of infratentorial tumors at our institution during the last 9 years; 12 of 142 patients (8.5%) manifested this syndrome, the largest series of such patients reported to date. Each child had a lesion that involved the vermis; seven had medulloblastomas, three had astrocytomas, and two had ependymomas. The incidence among children with vermian neoplasms was 13%. Ten children underwent division of the inferior vermis during tumor resection, and three had a superior vermian incision; one child underwent both superior and inferior vermian incisions. In 10 children, mutism developed in a delayed fashion postoperatively. The speech disturbance was associated with poor oral intake in 9 children, urinary retention in 5, long-tract signs in 6, and bizarre personality changes, emotional lability, and/or decreased initiation of voluntary movements in all 12. Neuropsychiatric testing, performed in seven children, confirmed impairments not only in speech but also in initiation of other motor activities. Ten children regained normal speech, bladder control, and neurological functioning, other than ataxia and mild dysarthria, within 1 to 16 weeks; two children had significant residual deficits. Characteristically, affect and oral intake returned to their preoperative baseline before the speech difficulties began to resolve. A detailed radiological review of these cases in parallel with 24 cases of vermian tumors without mutism identified only one factor that was significantly associated with the mutism syndrome, bilateral edema within the brachium pontis (P < 0.01). Neither the size of the tumor nor the length of vermian incision was associated with the development of mutism. The clinical features of this syndrome in the context of these imaging findings suggest that the mutism syndrome results from transient impairment of the afferent and/or efferent pathways of the dendate nuclei that are involved in initiating complex volitional movements. The clinical courses of our patients are presented and compared with those of similar cases in the literature in an attempt to evaluate the validity of this hypothesis.

Adolescent↗
PubMed2000

A role for Pax6 in the normal development of dorsal thalamus and its cortical connections.

The transcription factor Pax6 is widely expressed throughout the developing nervous system, including most alar regions of the newly formed murine diencephalon. Later in embryogenesis its diencephalic expression becomes more restricted. It persists in the developing anterior thalamus (conventionally termed "ventral" thalamus) and pretectum but is downregulated in the body of the posterior (dorsal) thalamus. At the time of this downregulation, the dorsal thalamus forms its major axonal efferent pathway via the ventral telencephalon to the cerebral cortex. This pathway is absent in mice lacking functional Pax6 (small eye homozygotes: Sey/Sey). We tested whether the mechanism underlying this defect includes abnormalities of the dorsal thalamus itself. We exploited a new transgenic mouse ubiquitously expressing green fluorescent protein tagged with tau, in which axonal tracts are clearly visible, and co-cultured dorsal thalamic explants from Pax6(+/+ )or Pax6(Sey/Sey )embryos carrying the transgene with wild-type tissues from other regions of the forebrain. Whereas Pax6(+/+ )thalamic explants produced strong innervation of wild-type ventral telencephalic explants in a pattern that mimicked the thalamocortical tract in vivo, Pax6(Sey)(/Sey) explants did not, indicating a defect in the ability of mutant dorsal thalamic cells to respond to signals normally present in ventral telencephalon. Pax6(Sey)(/Sey) embryos also showed early alterations in the expression of regulatory genes in the region destined to become dorsal thalamus. Whereas in normal mice Nkx2.2 and Lim1/Lhx1 are expressed ventral to this region, in the mutants their expression domains are throughout it, suggesting that a primary action of Pax6 is to generate correct dorsoventral patterning in the diencephalon. Our results suggest that normal thalamocortical development requires the actions of Pax6 within the dorsal thalamus itself.

Alternative Splicing↗
PubMed1978

Peripheral control of responsiveness to auditory stimuli in giant fibres of crickets and cockroaches.

Auditory stimuli initiate ascending activity in large fibres of the ventral nerve cord of the cricket, Acheta domesticus, and the cockroach, Periplaneta americana. This auditory responsiveness is reduced during locomotion. An earlier study concluded that the depression of responsiveness was mediated by descending inhibition. However, the auditory responsiveness is reduced during locomotion even after section of the ventral nerve cord anterior to the abdominal recording electrodes. Further, auditory responsiveness of isolated abdomens attached to intact animals is inhibited during locomotion of their hosts. Laminar wind streams over the cerci depress responsiveness to sound, but only at velocities markedly higher than those encountered by freely walking animals. Although the exact mechanism is not known, the depressed auditory responsiveness can occur independently of any descending influences.

Acoustic Stimulation↗
PubMed1999

Centrally produced neuronal nitric oxide in the control of baroreceptor reflex sensitivity and blood pressure in normotensive and spontaneously hypertensive rats.

We studied the effect of chronic nitric oxide synthase (NOS) blockade in the brain on mean arterial pressure [MAP (mmHg)], heart rate [HR (bpm)] and baroreceptor reflex sensitivity [BRS (mean slope: bpm/mmHg)] in Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Intracerebroventricular (i.c.v.) infusion of the nonselective NOS inhibitor N-Nitro-L-arginine-methylester (L-NAME) (50 microg/kg per day, 11-12 days) increased MAP in WKY and SHR (125+/-2.1 vs 118+/-1.1 controls, P<0.01 and 179+/-3.59 vs 156+/-4.0 controls, P<0.001, respectively) without affecting HR. In L-NAME-treated WKY, BRS to bradycardia was suppressed (-0.79+/-0.09 vs -1.76+/-0.17 controls, P=0.001), whereas in SHR, L-NAME did not affect BRS to bradycardia. BRS to tachycardia remained unaffected in either strain. In WKY, 7-nitroindazole (7-NI x Na+) (34 microg i.c.v./kg per day, 11-12 days), a selective nNOS inhibitor, did not affect MAP or HR, but BRS to bradycardia and tachycardia was decreased (-0.37+/-0.20 vs -0.97+/-0.41 controls, P<0.01 and -1.78+/-0.20 vs -2.52+/-0.40 controls, P=0.05, respectively). In SHR, the same dose of 7-NI x Na+ increased resting MAP (171+/-5.00 vs 150+/-7.00 controls, P<0.05) without affecting HR or BRS to bradycardia or tachycardia. Thus in WKY, BRS to acute changes in systemic blood pressure (BP) is regulated by NO produced by nNOS in the brain, serving as a neurotransmitter in sympathetic and parasympathetic efferent pathways. In SHR, systemic BP is regulated in part by NO released by the type I NOS isoenzyme in the brain.

Animals↗
PubMed1977

ENG analysis of 150 cases of posterior fossa disease.

Analysis of the ENG records of 150 patients with well substantiated neurologic disease involving the structure of the posterior fossa revealed a high incidence of diminished optic fixation inhibition (DOFI) of caloric induced nystagmus. DOFI is defined as less than 50 percent decrease of speed of the slow phase when eyes are open and fixated. The whole group was subdivided into seven subgroups according to type and location of disease and the incidence of DOFI was found to vary significantly in the different subgroups. The highest incidence was found in the group of cerebellar mass lesions and in the group of degenerative diseases, most of which had cerebellar involvement. A review of the literature reveals work done by others showing that suppression of vestibular reflexes induced by high speed turning and also habituation of caloric induced nystagmus is dependent on optic fixation inhibition (opto-vestibular reflex.). It has been shown that the flocculonodular lobe of the cerebellum has an inhibitory effect on the effects of vestibular activity by both destructive and stimulating techniques. Afferent and efferent pathways between the cerebellum and primary vestibular reflex arcs have been extensively described. It has been shown that cerebellar nodulectomy severely interferes with acquisition of habituation and retention of previously acquired habituation. Since habituation and suprression of vestibular nystamus depend on optic fixation inhibition and equally on the cerebellum, it is reasonable to infer that the opto-vesitubular inhibitory reflex is mediated by the crebellum. The clinical data of the 150 cases were analyzed for correlation of DOFI and other cerebellar signs. This analysis gives a high incidence of correlation: 66 percent of the cases having DOFI also had other cerebellar signs, whereas only 19 percent of cases that did not have DOFI had other cerebellar signs. These data lend further support to the inference that the cerebellum is involved in mediation of the opto-vestibular inhibitory reflex. Under most circumstances visual perception of the environment during movement depends on an inter-reaction between the vestibulo-oculomotor and the opto-vestibular reflexes. Eye movements during head movements are entirely different with eyes closed than with eyes open and fixating. In fact, it can be shown that ocular fixation is far more efficient during head movements than it is during movement of an object with head stationary. It is probable that fixation in the former case is the result of vestibulo-oculomotor slow phase activity modified by the opto-vestibular inhibitory reflex and elimination of the fast phase. A defect in the latter should result in a sense of spatial insecurity during movement by virtue of altered visual perception. The opto-vestibular inhibitory reflex is a central descending reflex probably mediated through the cerebellum. It is easy to test during and ENG. It is essential to normal visual perception during head movement...

Brain Diseases↗
PubMed1998

Glutamate-like immunoreactivity in axon terminals from the olfactory bulb to the piriform cortex.

A highly specific anti-glutamate monoclonal antibody, mAb2D7, was used together with light and electron microscopy to elucidate the role played by the amino acid glutamate in the projection from the olfactory bulb to the piriform cortex in the rat. By light microscopy, glutamate-like immunoreactivity was observed in neuronal cell bodies and in the neuropil of the piriform cortex. Double labelling experiments which involved injections of wheat germ agglutinin-horse--radish peroxidase into the olfactory bulb and a post-embedding immunogold method for electron microscopy revealed anterogradely labelled terminals making asymmetric synaptic contacts on dendrites in the piriform cortex which contained high levels of glutamate as assessed by quantification. These results further support a role for glutamate as a neurotransmitter in the efferent pathway of the rat olfactory bulb.

Animals↗
PubMed1997

Neural reflex regulation of arterial pressure in pathophysiological conditions: interplay among the baroreflex, the cardiopulmonary reflexes and the chemoreflex.

The maintenance of arterial pressure at levels adequate to perfuse the tissues is a basic requirement for the constancy of the internal environment and survival. The objective of the present review was to provide information about the basic reflex mechanisms that are responsible for the moment-to-moment regulation of the cardiovascular system. We demonstrate that this control is largely provided by the action of arterial and non-arterial reflexes that detect and correct changes in arterial pressure (baroreflex), blood volume or chemical composition (mechano- and chemosensitive cardiopulmonary reflexes), and changes in blood-gas composition (chemoreceptor reflex). The importance of the integration of these cardiovascular reflexes is well understood and it is clear that processing mainly occurs in the nucleus tractus solitarii, although the mechanism is poorly understood. There are several indications that the interactions of baroreflex, chemoreflex and Bezold-Jarisch reflex inputs, and the central nervous system control the activity of autonomic preganglionic neurons through parallel afferent and efferent pathways to achieve cardiovascular homeostasis. It is surprising that so little appears in the literature about the integration of these neural reflexes in cardiovascular function. Thus, our purpose was to review the interplay between peripheral neural reflex mechanisms of arterial blood pressure and blood volume regulation in physiological and pathophysiological states. Special emphasis is placed on the experimental model of arterial hypertension induced by N-nitro-L-arginine methyl ester (L-NAME) in which the interplay of these three reflexes is demonstrable.

Animals↗
PubMed1998

Schizophrenia and glutamatergic transmission.

Schizophrenia is a human brain disease with well-defined symptoms and a lifelong disease course, but without a current biological explanation. Several observations implicate brain glutamatergic abnormalities in the pathophysiology of this illness. This evidence includes both human neurochemical and clinical pharmacologic data. Furthermore the psychotomimetic action of phencyclidine, the noncompetitive NMDA-sensitive glutamate receptor antagonist, suggests the association between human psychosis and NMDA receptor blockade. This paper reviews basic aspects of glutamatergic transmission in animal and human brain with particular attention to its putative role in schizophrenia. Consideration is given to other glutamate-related human brain diseases and their purported mechanisms. Evidence of glutamatergic abnormalities in schizophrenia is critically reviewed, including data using postmortem neurochemistry, in vivo human brain imaging, clinical pharmacology, and animal models. The current theoretical formulations based on these studies are articulated. We propose a "working" glutamate hypothesis of schizophrenia which postulates a diminished glutamatergic transmission in the hippocampal glutamate-mediated efferent pathways and cerebral dysfunction in the hippocampus and its target areas, especially the anterior cingulate cortex. Considerable work remains to be done in this area to formulate and test a comprehensive hypothesis.

Brain Chemistry↗
PubMed1995

Similar fine structural localization of immunoreactive glutamate in the frog pineal complex and retina.

The distribution of immunoreactive glutamate was compared in the pineal complex (pineal and frontal organs) and retina of frogs (Rana esculenta, R. arvalis, R. ridibunda, R. catesbeiana, Bufo viridis, Bombinator igneus) by postembedding immuno-electron microscopy. Similar to retinal photoreceptors (rods and cones), bipolars and ganglion cells, the rod- and cone-like photoreceptors and the neurons of the pineal and frontal organs exhibited glutamate immunoreactivity. Synaptic terminals of photoreceptor cells on secondary neurons of the pineal complex and retina were strongly immunoreactive. The pineal tract and the fibers of the frontal nerve also displayed glutamate immunoreactivity. There was no essential difference in the immunoreactivity of the retinal and pineal elements among the species studied. The similar histology of the pineal complex and retina of the frog and the high correlation of their binding sites of antiglutamate immunosera allow us to assume that glutamate performs a similar role in the pineal complex as is already known for the retina. The high immunoreactivity of the presynaptic region of pinealocytic processes and axons of secondary neurons suggests the role of a neurotransmitter for this excitatory amino acid in the efferent pathways of the pineal complex.

Animals↗
PubMed1979

Significance of skin pressure in body heat balance.

It has been demonstrated by Takagi and his colleagues that pressure on a specified area of the body surface causes depression of sweating in a certain body division and changes in the relative sweat rates between body divisions. Furthermore, skin pressure has been assumed to suppress the central thermoregulatory activity, thus bringing about a rise or fall in body temperature in a hot or cool environment, respectively. We examined the effect of skin pressure applied to the bilateral subaxillary regions on body heat balance by means of continuous recordings of evaporative weight loss (total sweat rate), local sweat rates at various areas and rectal and skin temperatures and measurements of metabolic rate. Most experiments were carried out at a room temperature of 36 degrees C with 40% rh and a few were done at 27 degrees C in the absence of thermal sweating. Various strengths of pressure up to 5 kg/50 cm2 were employed. It was observed that the total sweat rate was either unchanged, decreased or occasionally even increased. There was an apparent tendency that the stronger the pressure was, the more depressed was the total sweating. A weaker pressure, on the other hand, often caused facilitation of total sweating. Changes in rectal and mean body temperatures and in metabolic rate were minimal in the majority of cases, and bore no relationship to the changes in the total sweat rate. These results offer no evidence that skin pressure of up to 5 kg/50 cm2 affects human central thermoregulatory activity but suggest that it may exert a sweat-inhibitory effect, primarily through the interaction of sudomotor impulses somewhere along the efferent pathways, possibly at the spinal segmental level.

Adult↗
PubMed1999

The neural mechanism of rectal motility response induced by the epicardial application of lactic acid.

The epicardial application of lactic acid induced a biphasic rectal motility response in lightly anaesthetised, open-chested and artificially ventilated cats. This rectal biphasic response is reflexogenic in nature as epicardial lignocaine abolished such response. This rectal biphasic response is abolished by cardiac sympathectomy and reprecipitated by left inferior cardiac afferent nerve stimulation. Such response is also abolished by sacral ventral rhizotomy and reproduced by stimulation of the peripheral cut end of split sacral ventral roots. This indicates that the afferent and efferent pathways for such reflex are lying in the cardiac sympathetic and sacral pelvic nerves, respectively. The higher centers involved for such reflex are lying above the mid-collicular level of the brain as decerebration at the mid-collicular level completely abolished such type of rectal response. Furthermore, the relaxation phase and contraction phase of such rectal response are mediated through nitric oxide release and cholinergic neurones, respectively, as NG-nitro-L-arginine and atropine abolished relaxation and contraction phase of the rectal response, respectively.

Animals↗
PubMed2003

The role of nitric oxide (NO) in control of LHRH release that mediates gonadotropin release and sexual behavior.

Nitric oxide (NO) plays a crucial role in reproduction at every level in the organism. In the brain, it activates the release of luteinizing hormone-releasing hormone (LHRH). The axons of the LHRH neurons project to the mating centers in the brain stem and by efferent pathways, evoke the lordosis reflex in female rats. In males, there is activation of NOergic terminals that release NO in the corpora cavernosa penis to induce erection by generation of cyclic guanosine monophosphate (cGMP). NO also activates the release of LHRH which reaches the pituitary and activates the release of gonadotropins by activating neural NO synthase (NOS) in the pituitary gland. Follicle stimulating hormone (FSH)RH selectively releases FSH also by activating NOS. Leptin releases LHRH by activating NOS to release FSH and LH with the same potency as LHRH. These actions are mediated by specific receptors on the gonadotropes for LHRH, FSHRH and leptin. The responsiveness of the pituitary is controlled by gonadal steroids. In the gonad, NO plays an important role inducing ovulation and in causing luteolysis; whereas in the reproductive tract, it relaxes uterine muscle via cGMP and constricts it by prostaglandins.

Animals↗
PubMedDate not supplied

[Aetiological factors in left-handedness].

Lateralisation associates the extremities and senses of one side of the body, which are connected by afferent and efferent pathways, with the primary motor and sensory areas of the hemisphere on the opposite side. Dominant laterality denotes the appearance of a dominant extremity or sense in the performance of complex psychomotor activities. Laterality is manifested both as right-handedness or left-handedness, which are functionally equivalent and symmetrical in the performance of activities. Right-handedness is significantly more common than left-handedness. Genetic theory is most widely accepted in explaining the onset of lateralisation. According to this theory, the models of brain organisation asymmetry (anatomical, functional, and biochemical) are strongly, genetically determined. However, the inability to clearly demonstrate the association between genetic factors and left-handedness has led researchers to investigate the effects of the environment on left-handedness. Of particular interest are the intrauterine environment and the factors influencing foetal development, of which hormones and ultrasound exposure are the most significant. It has been estimated that an extra five cases of nonright-handed lateralisation can be expected in every 100 males who were exposed to ultrasound in utero compared to those who were not. Socio-cultural pressure on left-handed individuals was much more severe in the past, which is confirmed by scientific findings that left-handedness is present in 13% of individuals in their twenties, while in less than 1% of individuals in their eighties.

Functional Laterality↗