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A patient with unilateral pruritus after a stroke is described. The neural pathways of pruritus and the role of the central nervous system in the initiation and modulation of the itch sensation are discussed. Pathways between the cerebral cortex and the medulla may play important roles in the sensation of pruritus.
The amygdala and orbital cortex are thought to play an important role in the regulation of autonomic functions, hormonal secretion, and behavioral expression in response to sensory stimulation. The responsiveness of neurons in these regions to stimulation of cutaneous and visceral organs indicates that sensory information reaches the amygdala and orbital cortex. In the past, a large number of studies have thoroughly documented multiple neural pathways by which sensory information can reach these regions via relay nuclei in the brainstem and diencephalon. Recent studies reported that the amygdala and orbital cortex also receive direct input from the spinal cord. The aim of this study was to determine the magnitude and the origin of these projections in the rat. Injections of the retrograde tracer Fluoro-Gold (FG), restricted to the amygdala, labeled several hundred neurons bilaterally (60% contralateral) throughout the length of the spinal cord. More than 60% of labeled neurons were found in the lateral reticulated area of the deep dorsal horn and the gray matter surrounding the central canal. Many neurons were also found in the lateral spinal nucleus. Labeled neurons were concentrated in upper lumbar and upper cervical segments. Injections of Fluoro-Gold that were centered in the orbital cortex labeled only a small number of neurons (73% contralateral) within the spinal cord. Most labeled neurons were found in the lateral reticulated area. Neurons located in the intermediate zone and the gray matter surrounding the central canal were found mainly in upper lumbar and upper cervical segments. These findings, together with the anterograde tracing observations, provide evidence for direct projections of spinal cord neurons to the amygdala and orbital cortex. Their laminar distribution in the spinal cord and the involvement of the amygdala and orbital cortex in limbic functions suggest that these pathways may play a role in neuronal circuits that enable somatosensory information, including pain, to affect autonomic, endocrine and behavioral functions.
Thirst and resultant water drinking can arise in response to deficits in both the intracellular and extracellular fluid compartments. Inhibitory influences mediating the satiation of thirst also are necessary to prevent overhydration. The brain regions that underpin the generation or inhibition of thirst in these circumstances can be categorized as sensory, integrative, or cortical effector sites. The anterior cingulate cortex and insula are activated in thirsty human beings as shown by functional brain-imaging techniques. It is postulated that these sites may be cortical effector regions for thirst. A major sensory site for generating thirst is the lamina terminalis in the forebrain. Osmoreceptors within the organum vasculosum of the lamina terminalis and subfornical organ detect systemic hypertonicity. The subfornical organ mediates the dipsogenic actions of circulating angiotensin II and relaxin. Major integrative sites are the nucleus of the tractus solitarius, the lateral parabrachial nucleus, the midbrain raphé nuclei, the median preoptic nucleus, and the septum. Despite these advances, most of the neural pathways and neurochemical mechanisms subserving the genesis of thirst remain to be elucidated.
The respective influence of testosterone and estradiol on the structure of the Common Canary Serinus canaria song was studied by experimentally controlling blood levels of steroid hormones in males and analyzing the consequent effects on acoustic parameters. A detailed acoustic analysis of the songs produced before and after hormonal manipulation revealed that testosterone and estradiol seem to control distinct song parameters independently. The presence of receptors for testosterone and estradiol in the brain neural pathway controlling song production strongly suggests that the observed effects are mediated by a steroid action at the neuronal level.
Seasonally breeding mammals display an annual cycle of fertility that is associated with both structural neuroplasticity and functional changes in the activity of the GnRH neurones in the brain. Sheep are valuable models for understanding the hormonal and environmental cues that regulate seasonal reproduction, as well as the brain circuitry that underlies this response. As a result of the large size of sheep, we can tightly correlate the anatomy of GnRH cells and their patterns of gene expression with direct measurements of their neurosecretory output. Tract tracing studies have begun to reveal the pathways by which seasonal changes in response to oestradiol negative feedback affect the function of the reproductive system. Electron microscopic studies have shown that synaptic inputs on to ovine GnRH cells undergo marked seasonal rearrangements that are independent of hormonal changes and may reflect the intrinsic seasonality of the brain. Recent work indicates that the polysialylated form of neural cell adhesion molecule (PSA-NCAM), a marker of neuroplasticity, is well positioned anatomically to contribute to seasonal structural and functional alterations. Applying state-of-the-art neuroanatomical techniques to this model has allowed us to delineate the neural pathways responsible for the seasonal shut down of reproduction in sheep, as well as to begin to uncover the cellular mechanisms underlying seasonal neuroplasticity in the adult mammalian brain.
Brain structure in health is a dynamic energized equation incorporating chemistry, neuronal structure, and circuitry components. The chemistry "piece" is represented by multiple neurotransmitters such as Acetylcholine, Serotonin, and Dopamine. The neuronal structure "piece" incorporates synapses and their connections. And finally circuits of neurons establish "architectural blueprints" of anatomic wiring diagrams of the higher order of brain neuron organizations. In Alzheimer's disease, there are progressive losses in all of these components. Brain structure crumbles. The deterioration in Alzheimer's is ordered, reproducible, and stepwise. Drs. Braak and Braak have described stages in the Alzheimer disease continuum. "Progressions" through Braak Stages benchmark "Regressions" in Cognitive function. Under the microscope, the Stages of Braak commence in brain regions near to the hippocampus, and over time, like a tsunami wave of destruction, overturn healthy brain regions, with neurofibrillary tangle damaged neurons "marching" through the temporal lobe, neocortex and occipital cortex. In effect the destruction ascends from the limbic regions to progressively destroy the higher brain centers. Rabies infection also "begins low and finishes high" in its wave of destruction of brain tissue. Herpes Zoster infections offer the paradigm of clinical latency of infection inside of nerves before the "marching commences". Varicella Zoster virus enters neurons in the pediatric years. Dormant virus remains inside the neurons for 50-80 years, tissue damage late in life (shingles) demonstrates the "march of the infection" down neural pathways (dermatomes) as linear areas of painful blisters loaded with virus from a childhood infection. Amalgamation of Zoster with Rabies models produces a hybrid model to explain all of the Braak Stages of Alzheimer's disease under a new paradigm, namely "Alzheimer's neuroborreliosis" in which latent Borrelia infections ascend neural circuits through the hippocampus to the higher brain centers, creating a trail of neurofibrillary tangle injured neurons in neural circuits of cholinergic neurons by transsynaptic transmission of infection from nerve to nerve.
The spinal cord was transected in adult New Zealand White rabbits anaesthetized with urethane plus chloralose. The level of transection was in the mid-cervical region. The animals were than ventilated mechanically and the arterial blood pressure was maintained with an intravenous infusion of noradrenaline solution. Stimulation of the hypothalamus 1-2 mm lateral to the third ventricle and 1.5-3 mm dorsal to the mammillary nuclei, in a region known to evoke pressor responses and bradycardia in normal anaesthetized rabbits, never evoked pressor responses in the spinally transected rabbits. Bradycardia was evoked only when the mean arterial blood pressure was maintained above 44-49 mmHg. At higher pressures stimulation evoked a greater bradycardia and the relationship between bradycardia and pressure was approximately linear over much of the range of pressures tested (up to 116 mmHg). Because the threshold mean arterial blood pressure at which hypothalamic stimulation evoked bradycardia was similar to the threshold pressures reported in the literature for baroreceptor activation in the rabbit and because the curve of bradycardia:pressure was similar to published curves of baroreceptor and baroreflex activity against blood pressure, it is concluded that the bradycardia evoked by hypothalamic stimulation in the rabbit is mediated by a neural pathway in the hypothalamus that can increase the gain of the cardio-inhibitory baroreceptor reflex.
We examined the effects of acute exposure to ozone on the permeability of the tracheal mucosa and the contribution of neural pathways to the effects of ozone using horseradish peroxidase (HRP; mol wt 40,000) as a marker of lumen-to-blood transfer of a macromolecule in guinea pigs in vivo. Each guinea pig was anesthetized and exposed for 30 min to either ozone [0.5 or 3 parts/million (ppm)] or air. Immediately after exposure, a tracheal segment was isolated between two polyethylene cannulas in vivo and filled with HRP solution (50 mg/ml). Blood samples were drawn before and 10, 20, 30, and 40 min after the intratracheal instillation of HRP. The plasma levels of HRP in guinea pigs exposed for 30 min to 3 ppm of ozone, but not to 0.5 ppm of ozone, were significantly greater than those in guinea pigs exposed to air. Although the increased plasma HRP levels after exposure to 3 ppm of ozone were unaffected by propranolol or atropine, they were completely inhibited by pretreatment with capsaicin (50 mg/kg sc, injected in two doses). These results suggest that endogenous neuropeptides mediate the ozone-induced increase in the permeability of the tracheal mucosa in guinea pigs in vivo, but neither an adrenergic nor a cholinergic pathway appears to be involved.
Rats housed in impoverished environments often show greater behavioral deficits after receiving brain lesions than to rats housed in standard or enriched environments. However, the resemblance between the effects of social isolation and those of hippocampal lesions in rats prompted the suggestion that rats socially isolated at weaning rather than grouped counterparts may show less behavioral change after sustaining dorsal hippocampal lesions when adult. In socially reared rats, hippocampal lesions produced increased ambulation and object contact in an open field, reduced passive avoidance in a runway task, and produced faster acquisition of active avoidance in a shuttle box, but there were no such differences in isolation-reared rats. Ambulation and object contact in isolates were intermediate to those of rats with lesions and intact group-housed rats, and the behavior of isolates during passive and active avoidance training was generally similar to that of grouped rats with lesions. The introduction of a distractor during approach training in an alley reduced running speeds more in rats with lesions than in controls. The several significant interactions between housing state and lesion state suggest that neural pathways associated with the hippocampal formation may mediate some behavioral effects of differential housing.
The effects induced by metoclopramide (MCP) were examined in transverse muscular strips from pigeon oesophagus. MCP (0.1 nM-10 microM) induced a concentration-dependent excitatory effect on the EMG activity, characterized mainly by an increase in the spike burst frequency. Such an excitatory effect was fully antagonized by tetrodotoxin and partially antagonized by atropine, by naloxone and by desensitization of the preparation to 5-hydroxytryptamine (5-HT). The atropine-resistant excitatory component was not modified by guanethidine. The combination of naloxone and atropine was more effective than a single antagonist in blocking the response to MCP. The combination of naloxone and 5-HT desensitization failed to further reduce the MCP-induced excitatory effect. The present results indicate that the excitatory effects of MCP are mediated via neural elements. MCP activates both cholinergic and non-cholinergic, non-adrenergic excitatory neurons. Furthermore, results suggest that serotoninergic and opioid neural pathways might be involved in the excitatory effects of MCP.
The purpose of the present study was to examine respiratory-modulated facial nerve activity (FNA) in response to activation of the ventrolateral subarea of the nucleus of the tractus solitarius (vlNTS). The cat was anesthetized with sodium pentobarbital and then vagotomized bilaterally, paralyzed and ventilated artificially. End-tidal fractional concentration of CO2 was maintained at hyperoxic normocapnia. Partial occipital craniotomy was performed to expose the obex. Activities of the phrenic and the facial nerves were simultaneously recorded. The vlNTS was excited by electrical current (80 Hz frequency, 0.5 ms pulse duration and a variety of current from 12.5 to 50 microA) and glutamate (30-100 nl, 0.5 M). Three responsive patterns for both nerves were observed in response to vlNTS activation. First, inspiratory facial nerve activity (iFNA) and phrenic nerve activity (PNA) were decreased (p < 0.01), while expiratory facial nerve activity (eFNA) was not changed. Second, iFNA and PNA were diminished (p < 0.01) but eFNA was enhanced. Third, iFNA was decreased whereas PNA was enhanced. These results suggest that there might be a neural pathway projecting from the vlNTS to the facial nuclei to modulate respiratory-modulated facial nerve activities.
The neural projection of the lateral septum (LS) to the rostral mesencephalic central gray (MCG) is sexually dimorphic and plays an important role in inhibiting female reproductive behavior. In this experiment, development of the LS-MCG connection from birth to 15 days after birth was examined in female rats by a tract-tracing method with DiI. On the birth day (D1 rat), and 5, 10 or 15 days after birth (D5, D10 or D15 rat, respectively) or 8 weeks after birth (adult), the brain was fixed by perfusion of a mixture of 4% PFA and 0.1% glutaraldehyde. DiI was pasted on the coronally cut-surface of the LS and the sample was incubated in PFA at 40 degrees C for up to 4 months. After incubation, 200-microm frozen parasagittal sections were prepared and observed by fluorescence microscopy. As a result, numerous DiI labeled fibers were found in the preoptic area, the anterior and posterior hypothalamus, and the MCG in adult rats. In D1 rats, several labeled axons extended caudal to the anterior hypothalamic area. In D5 rats, a few labeled fibers reached the MCG. Some labeled fibers were observed in the rostral MCG of D10 rats. In D15 rats, a considerable number of labeled fibers were seen to reach the rostral MCG and relative density of the fibers was comparable to that of adult. These results suggest that the neural pathway from the LS to the rostral MCG develops acutely during the period from 5-10 days up to more than 15 days after birth.
This study investigated the regulation of reflex excitability in normal and midthoracic contusion-injured animals. Recent observations revealed that rate depression, a rate-modulatory process that decreases reflex excitability, was significantly decreased following experimental midthoracic contusion injury. The present experiments were performed to extend those studies and to determine if posttetanic potentiation (PTP), a rate-modulatory process that increases reflex excitability, also was altered in lumbar monosynaptic reflexes (MSRs) following midthoracic contusion injury. In normal animals, a mean PTP of 160% of the pretetanus control was observed at 30 sec following tetanus of the tibial MSR. The decay of the PTP in normal animals followed a rapid initial, then a more gradual pattern, before returning to pretetanus values by 5 min posttetanus. Following midthoracic contusion injury, the maximal (unpotentiated) MSRs were significantly increased in amplitude, whereas the percent potentiation of the PTP of the tibial MSRs was significantly decreased. PTP decay in postcontusion animals was significantly more gradual than observed in normal animals and followed a single decay process. Further analysis of rate depression of tibial MSRs in normal animals revealed that the attenuation pattern produced by stimulation within the lower range of test frequencies was different from that produced by stimulation at the higher test frequencies. Following contusion, rate depression of tibial MSRs was significantly reduced at all test frequencies. These physiological changes in the stretch reflex neural pathway are discussed relative to the development of spasticity.
We measured foveal flicker sensitivity with and without external added temporal noise at various levels of retinal illuminance and described the data with our model of flicker sensitivity comprising: (i) low-pass filtering of the flickering signal plus external temporal and/or quantal noise by the modulation transfer function (MTF) of the retina (R): (ii) high-pass filtering in proportion to temporal frequency by the MTF of the postreceptoral neural pathways (P): (iii) addition of internal white neural noise; and (iv) detection by a temporal matched filter. Without temporal noise flicker sensitivity had a band-pass frequency-dependence at high and medium illuminances but changed towards a low-pass shape above 0.5 Hz at low luminances, in agreement with earlier studies. In strong external temporal noise, however, the flicker sensitivity function had a low-pass shape even at high and medium illuminances and flicker sensitivity was consistently lower with noise than without. At low luminances flicker sensitivity was similar with and without noise. An excellent fit of the model was obtained under the assumption that the only luminance-dependent changes were increases in the cut-off frequency (fc) and maximum contrast transfer of R with increasing luminance. The results imply the following: (i) performance is consistent with detection by a temporal matched filter, but not with a thresholding process based on signal amplitude; (ii) quantal fluctuations do not at any luminance level become a source of dominant noise present at the detector; (iii) the changes in the maximum contrast transfer reflect changes in retinal gain, which at low to moderate luminances implement less-than-Weber adaptation, with a 'square-root' law at the lowest levels; (iv) the changes of fc as function of mean luminance closely parallels time scale changes in cones, but the absolute values of fc are lower than expected from the kinetics of monkey cones at all luminances; (v) the constancy of the high-pass filtering function P indicates that surround antagonism does not weaken significantly with decreasing light level.
The Fourth International Cough Symposium took place in London between the 29th of June and 1st of July 2006. There were overall 22 posters presented during the meeting. These posters were divided into the following sections: methods of cough investigations, definitions of cough, receptor mechanisms, neural pathways, animal experiments and clinical aspects of cough. This review will focus on the discussions related to the posters.
The neural pathways involved in the milk ejection reflex have been studied with the aid of the 2-deoxyglucose (2DG) method. All the experiments were carried out on Wistar female rats, 9-11 days post-partum, which had been separated from their pups (except for one) overnight. The effect of suckling on the relative metabolic activity (RMA) of the brain was studied in conscious rats and in rats anaesthetized with urethane. Control animals were similarly treated but were not suckled. In addition, the effect of mammary nerve stimulation on RMA was studied in animals anaesthetized with urethane; sham-operated animals served as controls for this group. Suckling (minimum of 10 pups) in conscious animals had no apparent effect on the RMA of any of the brain areas measured. However, in anaesthetized rats, suckling produced a significant increase in the RMA of the paraventricular and supraoptic nuclei (PVN and SON), but had no effect on the RMA of any other brain area or the pituitary gland. Stimulation of the mammary nerve, with a stimulus that causes milk ejection and an increase in prolactin release, produced a significant increase in the RMA of the PVN, SON, the pars distalis and pars nervosa and the spinothalamic tract, and a significant decrease in the ventromedial and mediodorsal nuclei of the thalamus, the zona incerta, the red nucleus and the ventral nucleus of the lateral lemniscus. These results show that suckling significantly increases the metabolic activity of afferent terminals in the PVN and SON. Activation of the cell bodies of the PVN and SON, as assessed by increased RMA of the pituitary gland, could be evoked by the more intense stimulus of mammary nerve stimulation. The ascending pathway from the mammary nerve involves the spinothalamic tract but could not be traced beyond the midbrain. The lack of effect of suckling in conscious animals may have been due to the inhibitory influence of stress mediated by forebrain structures.
We investigated the white matter structure in children (n = 14) with a wide range of reading performance levels using diffusion tensor imaging (DTI), a form of magnetic resonance imaging. White matter structure in a left temporo-parietal region that had been previously described as covarying with reading skill in adult readers also differs between children who are normal and poor readers. Specifically, the white matter structure measured using fractional anisotropy (FA) and coherence index (CI) significantly correlated with behavioral measurements of reading, spelling, and rapid naming performance. In general, lower anisotropy and lower coherence were associated with lower performance scores. Although the magnitude of the differences in children are smaller than those in adults, the results support the hypothesis that the structure of left temporoparietal neural pathways is a significant component of the neural system needed to develop fluent reading.
Neuroimaging research has shown localised brain activation to different facial expressions. This, along with the finding that schizophrenia patients perform poorly in their recognition of negative emotions, has raised the suggestion that patients display an emotion specific impairment. We propose that this asymmetry in performance reflects task difficulty gradations, rather than aberrant processing in neural pathways subserving recognition of specific emotions. A neural network model is presented, which classifies facial expressions on the basis of measurements derived from human faces. After training, the network showed an accuracy pattern closely resembling that of healthy subjects. Lesioning of the network led to an overall decrease in the network's discriminant capacity, with the greatest accuracy decrease to fear, disgust and anger stimuli. This implies that the differential pattern of impairment in schizophrenia patients can be explained without having to postulate impairment of specific processing modules for negative emotion recognition.