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PubMed1989

[Clinical and etiological study of crossed cerebellar diaschisis. Report of two cases].

With the great progress in the imaging technique of cerebro-cerebellar perfusion and metabolism, it has been revealed that supratentorial cerebrovascular disorders often cause some reduction of contralateral cerebellar blood flow and metabolism. The phenomenon, termed crossed cerebellar diaschisis (CCD), is interpreted to be brought about by transneuronal deactivation of cerebellum via the corticopontocerebellar pathway and usually not to accompanied by limb-incoordination. We have experienced 2 cases presenting ataxia clinically and CCD in positron emission tomography (PET) which are thought to be caused by the interruption of two distinctive neural pathways, the corticopontocerebellar and cerebellorubrothalamic pathways. Case 1 was a 34-year-old housewife with cerebral infarction which magnetic resonance imaging disclosed in the left parietal cortex and subcortical white matter. She showed mild right-sided hemiataxia featured by dysarthria, hypermetria, dysrhythmia, decomposition, dysdiadochokinesis and rebound phenomenon. Cheirooral syndrome, a hand-pronation sign and defects of combined sensation were present on the right but not accompanied by any disturbances of deep sensation. PET with 15O-labeled CO2 and O2 demonstrated the left frontoparietooccipital and contralateral cerebellar hypoperfusion and hypometabolism. Case 2 was a 69-year-old female suffering from aftereffects of old thalamic hemorrhage. Neurological examination revealed moderate degree of right-sided hemiataxia suggesting a cerebellar type of dysfunction like in case 1. Muscle power and sensory system were well-preserved. Brain CT revealed a small and restricted low density area in the left posterolateral thalamus indicating destruction of the Vim nucleus. PET study confirmed reduced blood flow and oxygen metabolism in the left thalamus and contralateral cerebellar hemisphere.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1987

Propagation of vasodilation in resistance vessels of the hamster: development and review of a working hypothesis.

In many tissues, a substantial fraction of total vascular resistance resides in the feed arteries that give rise to the microcirculation. We have explored the thesis that control of tissue blood flow is integrated over several levels of the vascular network, including feed arteries and microvessels. In response to muscular contraction, feed arteries (resting diameter 100-125 microns) of hamster cremaster and gracilis muscles dilated by 20-25%. Acetylcholine applied to distal microvessels of the cremaster induced a dilation that ascended into feed arteries not having direct contact with acetylcholine. In the hamster cheek pouch, iontophoretic application of acetylcholine onto an arteriole (diameter 20-30 microns) triggered a vasodilation that propagated along the arteriole. Propagation was not dependent on blood flow, indicating that the dilator response was conducted along the vessel wall. We found that preventing diameter changes in an arteriole segment along the apparent conducting pathway did not block propagated vasodilation, indicating that propagation was not mediated by a myogenic mechanism requiring changes in smooth muscle length. We investigated whether the conduction of a vasodilatory stimulus may be mediated by either a neural plexus intrinsic to microvessels or cell-cell coupling between the cells composing the arteriole. Tetrodotoxin (10(-6) M) did not block propagated vasodilation, indicating that propagation is not mediated by a neural pathway. Hypertonic sucrose solution applied to an arteriole segment along the apparent conducting pathway attenuated propagation significantly, which is consistent with its reported effect to decouple gap junctions between cells. Thus, propagated vasodilation in arterioles may be mediated by direct cell-cell conduction.

Acetylcholine↗

PubMed2005

Inactivation of the cerebral NFkappaB pathway inhibits interleukin-1beta-induced sickness behavior and c-Fos expression in various brain nuclei.

The behavioral effects of peripherally administered interleukin-1beta (IL-1beta) are mediated by the production of cytokines and other proinflammatory mediators at the level of the blood-brain interface and by activation of neural pathway. To assess whether this action is mediated by NFkappaB activation, rats were injected into the lateral ventricle of the brain with a specific inhibitor of NFkappaB activation, the NEMO Binding Domain (NBD) peptide that has been shown previously to abolish completely IL-1beta-induced NFkappaB activation and Cox-2 synthesis in the brain microvasculature. NFkappaB pathway inactivation significantly blocked the behavioral effects of intraperitoneally administered IL-1beta in the form of social withdrawal and decreased food intake, and dramatically reduced IL-1beta-induced c-Fos expression in various brain regions as paraventricular nucleus, supraoptic nucleus, and lateral part of the central amygdala. These findings strongly support the hypothesis that IL-1beta-induced NFkappaB activation at the blood-brain interface is a crucial step in the transmission of immune signals from the periphery to the brain that underlies further events responsible of sickness behavior.

Analysis of Variance↗

PubMed1996

Unilateral displacement of lower limb evokes bilateral EMG responses in leg and foot muscles in standing humans.

During upright stance, foot dorsiflexion induced by the movement of a supporting platform elicits a short- (SLR) and a medium-latency response (MLR) in both the soleus and the flexor digitorum brevis muscles; foot plantarflexion elicits a MLR in the tibialis anterior. The SLR is the counterpart of the stretch reflex, but no general agreement exists about the origin of the MLR, though recent results suggest that it is transmitted through group II afferent fibres. Animal studies have shown that group II fibres impinge on interneurones projecting contralaterally as well as ipsilaterally, whereas group I fibres impinge on interneurones which project mainly ipsilaterally. Therefore, we compared the changes in amplitude and latency of the SLRs and MLRs in the right and left limb during postural perturbations induced while subjects maintained both feet on the platform (both-on condition) or while they maintained only one foot on the platform and the other on firm ground (one-on condition). Under the both-on condition, the pattern of EMG responses described above occurred bilaterally. Under the one-on condition, both SLRs and MLRs occurred in the displaced leg. However, whereas the SLRs did not change in amplitude compared with the both-on condition, the MLRs decreased in amplitude to about 50%. MLRs were also present in the non-displaced leg. They were not preceded by any SLR but showed a further decrease in size with respect to the corresponding responses in the perturbed leg. Latency of the MLRs of the perturbed leg increased by about 5 ms passing from the both-on to the one-on condition. In the latter condition, a further increase of 5 ms was observed in the nonperturbed leg with respect to the displaced one. The occurrence of the MLRs but not of the SLRs in the contralateral non-displaced leg is in keeping with the notion that crossed neural pathways fed by spindle group II afferent fibres subserve the MLRs. The changes in latency of the MLRs under the one-on condition compared with both-on give a cue about the synaptic delays along the neural circuit and the time taken by the afferent impulses to cross the spinal cord.

Adult↗

PubMed1995

Identification of spinal interneurons antecedent to adrenal sympathetic preganglionic neurons using trans-synaptic transport of herpes simplex virus type 1.

Control of sympathetic preganglionic neurons appears to be mediated, in part, through polysynaptic pathways using spinal interneurons. To identify spinal interneurons antecedent to adrenal sympathetic preganglionic neurons, we injected herpes simplex virus type 1 into the adrenal gland of hamsters as this virus is an effective trans-synaptic tracer of neural pathways. After a three day survival period, immunocytochemistry was used to visualize virus-infected spinal cord cells. Infected sympathetic preganglionic neurons with somata that were either kite-shaped, elliptical or fusiform and that had extensive dendrite arbors were identified as well as a group of smaller round cells with finer processes. For comparison, in additional hamsters, labelling with the retrograde tracer Fluoro-Gold and histochemical reactions for the enzyme nicotinamide adenine dinucleotide phosphate-diaphorase were used to identify sympathetic preganglionic neurons. Sympathetic preganglionic neurons identified with Fluoro-Gold or herpes virus were present mostly in the nucleus intermediolateralis, pars intermediolateralis and nucleus intermediolateralis, pars funicularis of the spinal cord. The smaller herpes virus-infected cells were found mostly medial to the preganglionic neurons in lamina VII and also dorsally in lamina V of the spinal cord. Assessing immunoreactivity for glial fibrillary acidic protein demonstrated that the smaller herpes virus-infected cells were not reactive astrocytes. Furthermore, these cells were immunoreactive for two neuronal markers, neuron-specific enolase and for microtubule-associated protein 2. These findings suggest that these smaller round cells with finer processes are distinct from sympathetic preganglionic neurons and astrocytes and may be interneurons antecedent to the sympathetic preganglionic neurons.

Adrenal Glands↗

PubMed2003

The neural basis of predicate-argument structure.

Neural correlates exist for a basic component of logical formulae, PREDICATE(x). Vision and audition research in primates and humans shows two independent neural pathways; one locates objects in body-centered space, the other attributes properties, such as colour, to objects. In vision these are the dorsal and ventral pathways. In audition, similarly separable "where" and "what" pathways exist. PREDICATE(x) is a schematic representation of the brain's integration of the two processes of delivery by the senses of the location of an arbitrary referent object, mapped in parietal cortex, and analysis of the properties of the referent by perceptual subsystems. The brain computes actions using a few "deictic" variables pointing to objects. Parallels exist between such nonlinguistic variables and linguistic deictic devices. Indexicality and reference have linguistic and nonlinguistic (e.g., visual) versions, sharing the concept of attention. The individual variables of logical formulae are interpreted as corresponding to these mental variables. In computing action, the deictic variables are linked with "semantic" information about the objects, corresponding to logical predicates. Mental scene descriptions are necessary for practical tasks of primates, and preexist language phylogenetically. The type of scene descriptions used by nonhuman primates would be reused for more complex cognitive, ultimately linguistic, purposes. The provision by the brain's sensory/perceptual systems of about four variables for temporary assignment to objects, and the separate processes of perceptual categorization of the objects so identified, constitute a pre-adaptive platform on which an early system for the linguistic description of scenes developed.

Afferent Pathways↗

PubMed1986

Reflex cardiovascular responses caused by stimulation of pulmonary C-fibers with capsaicin in dogs.

The purpose of these studies was to determine quantitatively the reflex cardiovascular responses to stimulation of the pulmonary C-fibers in dogs. We used a preparation in which the airway, pulmonary artery, and the pulmonary veins to the left lung were cannulated in situ. Ventilation and perfusion of the right lung maintained the animal in relatively normal homeostasis. Capsaicin, a decylenic acid amide of vanillylamine that selectively stimulates nerve endings of unmyelinated fibers (C-fibers), was injected into the left pulmonary artery in 5-ml boluses. Maximal reflex responses were obtained with concentrations as low as 0.8-1.6 X micrograms-1 X kg-1. Heart rate, hindlimb resistance, and left ventricular contractility were lowered transiently (the maximal responses showing declines of 40, 13, and 15.2%, respectively). As a result of these changes, combined with vasodilation in other resistance vessels, cardiac output fell 28% and blood pressure fell 35%. Interrupting the afferent neural pathway by severing the ipsilateral cervical vagus nerve eliminated these responses, confirming the distribution of their reflex origin. Although the role of these reflexes in homeostasis has not been decided, the results of this study suggest that the lungs of dogs, if appropriately stimulated, potentially can exert a major inhibitory influence on the neural regulation of cardiovascular function.

Afferent Pathways↗

PubMed1994

Effect of anterior hypothalamic area lesions on photoperiod-induced shifts in reproductive activity of the ewe.

The areas of the brain involved in photoperiodic control of reproduction are not well defined. The objective of this study was to determine whether anterior hypothalamic area (AHA) lesions in the ewe affected the responses of the reproductive system to shifts in the length of the daily photoperiod and development of photorefractoriness to a constant short day photoperiod. Eleven intact ewes received bilateral radiofrequency lesions of the AHA (AHAX), and five received sham lesions (sham). The ewes then were placed in photochambers and exposed alternately to two approximately 90-day periods of long [16 h of light, 8 h of darkness (16L:8D)] and short (10L:14D) days and then to 10L:14D for an additional 165 days. Blood samples were collected twice weekly to monitor plasma profiles of progesterone, PRL, and total T4, and during the second 16L:8D photoperiod, hourly for one 24-h period to assess melatonin release. Lesions increased (P < 0.001) the interval between the start of long days and cessation of estrous cycles during both long day periods, but did not affect the interval between the start of short days and the onset of estrous cycles for either the first (P = 0.08) or second (P > 0.10) short day period. Consequently, the durations of both anestrous periods were shorter (P < 0.001) for AHAX than for sham ewes. AHA lesions did not affect (P > 0.10) diurnal patterns of melatonin release. No effects (P > 0.10) of lesions were evident on plasma patterns of PRL or total T4 for any short or long day photoperiod. Development of photorefractoriness to constant short days either did not occur or was markedly delayed in five of nine AHAX (P < 0.01) ewes, whereas the other four AHAX ewes became refractory at a time similar (P > 0.10) to that in sham ewes. Responses to inhibitory long day photoperiods and constant short days were highly (P < 0.05) correlated (r = 0.74) and appeared dependent upon the extent of the AHA lesion. These results suggest that AHA lesions disrupt neuronal pathways mediating the effects of shifts in photoperiod on reproductive activity and development of photorefractoriness to constant short days. Our results suggest that the effects of AHA lesions are confined to the termination of reproductive activity, and that different neural pathways participate in photostimulation vs. photosuppression or photorefractoriness.

Animals↗

PubMed1996

The afferent pathways of discogenic low-back pain. Evaluation of L2 spinal nerve infiltration.

The afferent pathways of discogenic low-back pain have not been fully investigated. We hypothesised that this pain was transmitted mainly by sympathetic afferent fibres in the L2 nerve root, and in 33 patients we used selective local anaesthesia of this nerve. Low-back pain disappeared or significantly decreased in all patients after the injection. Needle insertion provoked pain which radiated to the low back in 23 patients and the area of skin hypoalgesia produced included the area of pre-existing pain in all but one. None of the nine patients with related sciatica had relief of that component of their symptoms. Our findings show that the main afferent pathways of pain from the lower intervertebral discs are through the L2 spinal nerve root, presumably via sympathetic afferents from the sinuvertebral nerves. Discogenic low-back pain should be regarded as a visceral pain in respect of its neural pathways. Infiltration of the L2 nerve is a useful diagnostic test and also has some therapeutic value.

Adolescent↗

PubMed1997

New concepts of the neuroendocrine regulation of gonadotropin surges in rats.

In species that ovulate spontaneously, two key events mediate the stimulation of preovulatory gonadotropin surges: 1) neurosecretion of a preovulatory LHRH surge and 2) an acute increase in responsiveness of the pituitary gland to the LHRH neurosecretory trigger. These processes, in turn, depend upon both the positive feedback actions of preovulatory estrogen secretions and specific neural signals for initiation of the surge. In female rats, the neural signals for the surge are principally derived from the 24-h neural clock, thereby limiting the timing of surges to the afternoon of proestrus. It remains unclear, however, how neural signals converge with endocrine signals (estrogen) in specific brain cells and how their cellular integration leads to appropriate secretion of gonadotropin surges. Previous work has suggested that estrogen may exert its facilitatory actions by opening a neural "gate," thereby allowing transmission of the daily neural signal to surge-initiating neuronal groups. How may estrogen act to render a neural pathway patent? A conventional view holds that steroid hormones can exert permissive effects on signaling efficacy by modulating neurotransmitter receptor expression, intracellular second messenger production, and protein kinase activity. However, recent evidence has suggested that estrogen may also have the capacity to permit cross-talk between neurotransmitter signaling pathways and parallel transcriptional regulatory pathways. The progesterone receptor is an estrogen-inducible transcription factor that has been shown to be transactivated--even in the absence of its cognate ligand--after stimulation of neurotransmitter receptors coupled to adenylate cyclase stimulation. Thus, the convergence of neural and endocrine signals for the stimulation of gonadotropin surges could occur at the level of the progesterone receptor: estrogen may stimulate expression of progesterone receptors, which in turn may be initially transactivated by synaptic signals. Activated progesterone receptors may thereafter regulate transcription of target genes that control transmitter synthesis and release in neural circuitries governing LHRH gene expression and/or pulsatile LHRH release. An analogous mechanism may operate in pituitary gonadotrophs, in which ligand-independent transactivation of progesterone receptors mediates integration of neurosecretory and estrogen positive feedback signals, leading to increased pituitary responsiveness to LHRH. It is proposed that the "seeding" of specific neuronal groups and pituitary gonadotrophs with progesterone receptors, and perhaps other inducible transcription factors, comprises an important basis of estrogen's permissive role in the stimulation of gonadotropin surges. The validity of this integrative model remains to be confirmed, as does its possible importance in generating gonadotropin surges in other species.

Animals↗

PubMed2001

Differential extrageniculostriate and amygdala responses to presentation of emotional faces in a cortically blind field.

Patient G.Y. is able to discriminate emotional facial expressions presented in his blind (right) hemifield despite an extensive lesion of the corresponding (left) striate cortex. One proposal is that this residual ability (affective "blindsight") depends on a subcortical visual pathway comprising the superior colliculus, posterior (extrageniculate) thalamus and amygdala. Here we report differential amygdala responses in G.Y. to presentation of fearful and fear-conditioned faces in his blind (right) hemifield. These amygdala responses exhibited condition-dependent covariation with neural activity in the posterior thalamus and superior colliculus. Our results provide further evidence that an extrageniculostriate (colliculo-thalamo-amygdala) neural pathway can process fear-related stimuli independently of both the striate cortex and normal phenomenal visual awareness.

Adult↗

PubMed1995

Study on vomiting related to the vestibulo-autonomic reflex.

The purpose of this study was to investigate the neural pathway from the vestibular labyrinth to the medullary vomiting center in the cat, using electrophysiological techniques. During electrical stimulation of the canal nerve, we found conflicting results: the pressure in the stomach sometimes increased, and sometimes decreased. There might be several neural structures between the semicircular canal nerve and the vomiting center in the dorsolateral portion of the reticular formation of medulla oblongata. Retching or vomiting-like behavior during both respiration and movement of the stomach was recorded during stimulation at several sites in the lateral medullary reticular formation. However, the evoked unit activities were not always induced by stimulation of the canal nerve.

Animals↗

PubMed2004

Basic advances and new avenues in therapy of spinal cord injury.

The prospects for successful clinical trials of neuroprotective and neurorestorative interventions for patients with acute and chronic myelopathies depend on preclinical animal models of injury and repair that reflect the human condition. Remarkable progress continues in the attempt to promote connections between the brain and the sensory and motor neurons below a spinal cord lesion. Recent experiments demonstrate the potential for biological therapies to regenerate or remyelinate axons and to incorporate new neural cells into the milieu of a traumatic spinal cord injury. The computational flexibility and plasticity of the sensorimotor systems of the brain, spinal cord, and motor unit make functional use of new circuitry feasible in patients. To incorporate residual and new pathways, neural repair strategies must be coupled to rehabilitation therapies that drive activity-dependent plasticity for walking, for reaching and grasping, and for bowel and bladder control. Prevention of pain and dysautonomia are also clinical targets. Research aims to define the temporal windows of opportunity for interventions, test the safety and efficacy of delivery systems of agents and cells, and provide a better understanding of the cascades of gene expression and cell interactions both acutely and chronically after injury. These bench-to-bedside studies are defining the neurobiology of spinal cord injury rehabilitation.

Animals↗

PubMed1981

Renin release after furosemide and ethacrynic acid in man. Evidence for neural reflex control mechanisms.

The mechanisms of renin release after furosemide (F) and ethacrynic acid (EA) in man were examined. We evaluated whether acute volume shifts within the low pressure system after F induce renin release via neural pathways. Immersion in a water-bath or beta-blockade reduced the increase of plasma renin concentration after F but not after EA. It is concluded that acute renin release after F but not after EA in man is partially due to neurally mediated reflexes originating from volume receptors in the cardiopulmonary area.

Adult↗

PubMed1995

Pattern and time course of immediate early gene expression in rat brain following acute stress.

The pattern and time course of brain activation in response to acute swim and restraint stress were examined in the rat by in situ hybridization using complementary RNA probes specific for transcripts encoding the products of the immediate early genes c-fos, c-jun and zif/268. A widespread pattern of c-fos messenger RNA expression was detected in response to these stressors; surprisingly, the expression patterns were substantially similar following both swim and restraint stress. A dramatic induction of c-fos messenger RNA was observed in numerous neo- and allocortical regions, the lateral septal nucleus, the hypothalamic paraventricular and dorsomedial nuclei, the anterior hypothalamic area, the lateral portion of the retrochiasmatic area, the medial and cortical amygdaloid nuclei, the periaqueductal gray, and the locus coeruleus; however, a prominent induction of c-fos was also seen in numerous additional subcortical and brainstem regions. Although not as widely expressed in response to stress as c-fos, induction of zif/268 messenger RNA was also detected throughout many brain areas; these regions were largely similar to those in which c-fos was induced, although in a number of regions zif/268 was expressed in regions devoid of c-fos messenger RNA. Few brain areas showed increased expression of c-jun following stress; these regions also showed induction of c-fos and/or zif/268. The time courses of expression of all three immediate early genes were similar, with peak levels observed at the 30 or 60 min time point, and a markedly reduced signal evident at 120 min post-stress. However, in a number of cases a delayed and/or prolonged induction was noted that may be indicative of secondary neuronal activation. A number of recent studies have attempted to define neural pathways which convey stress-related information to the hypothalamic-pituitary-adrenal axis. The present results reveal a widespread pattern of neuronal activation in response to acute swim or restraint stress. These findings may aid in the identification of stress-specific neural circuits and are thus likely to have important implications for our understanding of neuronal regulation of the stress response.

Animals↗

PubMed1994

Integration of postprandial function in the proximal gastrointestinal tract. Role of CCK and sensory pathways.

Cholecystokinin (CCK) stimulates vagal afferent fiber discharge, both gastric and intestinal, which seems to result in reflex decrease in gastric motility, gastric acid secretion, and stimulation of pancreatic protein secretion. Endogenous release of CCK by fat or soybean trypsin inhibitor also alters function by way of a capsaicin-sensitive pathway. We suggest that CCK is released locally from the intestine and acts locally or systemically to stimulate vagal afferent fiber discharge to alter proximal gastrointestinal function (Fig. 14). In this way, in addition to its effect on food intake, CCK and the neural pathway integrate function in the proximal gastrointestinal tract, regulating the entry of food into the duodenum to ensure effective digestion and absorption.

Afferent Pathways↗

PubMed2003

Ascending visceral regulation of cortical affective information processing.

Over a century ago, William James proposed that strong emotions represent the perceptual consequences of somato-visceral feedback. Although the strong form of this conception is no longer viable, considerable evidence has accumulated indicating a range of visceral influences on higher neurobehavioural processes. This literature has only recently begun to consolidate, because earlier reports generally remained at the demonstration level, and pathways and mechanisms for such influences were uncertain. Recently, specific effects of visceral feedback have become apparent on cortical activity, cerebral auditory-evoked responses, anxiety, memory and behavioural aspects of immunological sickness. Moreover, considerable progress has been made recently in determining the specific neural pathways and systems underlying these actions, especially the role of noradrenergic projections from the nucleus of the tractus solitarius and the locus coeruleus to the amygdala in memory processes, and to the basal forebrain in the processing of anxiety-related information. The present paper highlights selected recent findings in this area, and outlines relevant structures and pathways involved in the ascending visceral influence on higher neurobehavioural processes.

Affect↗

PubMed1992

ON- and OFF-pathways form separate neural substrates for motion perception: psychophysical evidence.

We have tested the hypothesis that in humans the signals carried by ON- and OFF-pathway respectively are processed for the perception of motion by two distinct physiological substrates. In vertebrates, onset of a bright visual stimulus is signaled to the CNS by ON-center retinal ganglion cells; onset of a dark stimulus is transmitted by OFF-center cells. We chose apparent motion generated by successive presentation of two adjacent lines as a stimulus. Lines presented on a bright background were either darker or brighter than this background. Delayed onset of a pair of bright or dark lines elicits apparent motion at the same time fulfilling the constraint of stimulating either ON- or OFF-center ganglion cells, respectively. We determined the threshold delay needed for subjects to perceive the temporal order of the onset of the two lines for various angular separations. The threshold delay for a pair of bright lines stayed low for separations from 2' to 7'. The threshold delay for a pair of dark lines was low only within a narrow range of separations centered around 3'. The variation of thresholds with line distance must reflect the existence of a limited processing zone for the perception of motion. The diameter of the processing zone for bright lines is about twice as large as that for dark lines. This suggests that in humans the separation of ON- and OFF-pathways extends to the early stages of motion perception. To test this hypothesis independently, thresholds were determined when a bright and a dark line were presented in succession. This was done for a separation of 3' where thresholds for a pair of lines with equal contrast are similarly low. Temporal order was perceived correctly only when the delay was at least two to four times as high as the threshold delays found for the equal contrast stimuli.

Humans↗