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PubMed1998

Polysynaptic neuronal pathways from tail cutaneous afferents to hindlimb motoneurons in the spinalized cat.

Postsynaptic potentials (PSPs) were recorded in motoneurons innervating the m. posterior biceps and semitendinosus (PBSt-MN) and m. triceps surae (GS-MN) in 19 spinalized adult cats, after electrical stimulation of the dorsal and ventral tail cutaneous nerves (TDC and TVC). With stimulation at 1,5-5 time threshold, inhibitory PSPs (IPSPs), excitatory PSPs (EPSPs), and mixed PSPs (IPSP/EPSPs, EPSP/IPSPs) were recorded in approximately 90% of PBSt-MN and 70% of GS-MN. IPSPs (IPSPs, IPSP/EPSPs) after stimulation of the contralateral TVC and TDC were observed in 54% and 52% of PBSt motoneurons, respectively. EPSPs (EPSP, EPSP/IPSPs) were recorded after stimulation of ipsilateral TVC in 56% of PBSt motoneurons. IPSPs produced after stimulation of ipsilateral TDC and TVC were observed in 65% and 63%, respectively, of GS-MN showing PSPs after stimulation of tail cutaneous nerves. Measurement of segmental latencies of the earliest PSPs (PBSt-MN, IPSPs: 2.1-7.4 ms, EPSPs: 3.1-18.9 ms, GS-MN, IPSPs: 2.5-17.1 ms, EPSPs: 4.2-19.4 ms) suggested that most of the neural pathways from tail cutaneous afferents to hindlimb motoneurons are at least trisynaptic in the L7 spinal segments. Hemisection of spinal cord at S1-S2 indicated that neural pathways from both the ipsilateral and contralateral low threshold cutaneous afferents pass through the ipsilateral spinal cord at S1-S2. The neural pathways from tail cutaneous afferents to hindlimb motoneurons to maintain the balance of the pelvic girdle were discussed.

Animals↗
PubMed1978

Self-stimulation in the rat: quantitative characteristics of the reward pathway.

Quantitative characteristics of the neural pathway that carries the reinforcing signal in electrical self-stimulation of the brain were established by finding which combinations of stimulation parameters give the same performance in a runway. The reward for each run was a train of evenly spaced monophasic cathodal pulses from a monopolar electrode. With train duration and pulse frequency held constant, the required current was a hyperbolic function of pulse duration, with chronaxie c approximately 1.5 msec. With pulse duration held constant, the required strength of the train (the charge delivered per second) was a hyperbolic function of train duration, with chronaxie C approximately 500 msec. To a first approximation, the values of c and C were independent of the choice either of train duration and pulse frequency or of pulse duration, respectively. Hence, the current intensity required by any choice of train duration, pulse frequency, and pulse duration dependent on only two basic parameters, c and C, and one quantity, Qi, the required impulse charge. These may reflect, respectively, current integration by directly excited neurons; temporal integration of neural activity by synaptic processes in a neural network; and the peak of the impulse response of the network, assuming that the network has linear dynamics and that the reward depends on the peak of the output of the network.

Animals↗
PubMed2005

Synaptic pathways in neural microcircuits.

The functions performed by different neural microcircuits depend on the anatomical and physiological properties of the various synaptic pathways connecting neurons. Neural microcircuits across various species and brain regions are similar in terms of their repertoire of neurotransmitters, their synaptic kinetics, their short-term and long-term plasticity, and the target-specificity of their synaptic connections. However, microcircuits can be fundamentally different in terms of the precise recurrent design used to achieve a specific functionality. In this review, which is part of the TINS Microcircuits Special Feature, we compare the connectivity designs in spinal, hippocampal, neocortical and cerebellar microcircuits, and discuss the different computational challenges that each microcircuit faces.

Animals↗
PubMed1998

Neurophysiologic evaluation of long-term desferrioxamine therapy in beta-thalassemia patients.

Forty patients with beta-thalassemia major (BTM), between 11 and 19 years of age and maintained on long-term desferrioxamine (DFO) treatment, were examined by evoked potential and nerve conduction velocity studies to investigate a possible involvement of the auditory, visual, somatosensory, or peripheral nervous pathways. Pathologic findings in brainstem auditory-, visual-, and somatosensory-evoked potentials, and nerve conduction velocity studies were demonstrated in 25%, 15%, 7.5%, and 25% of the patients, respectively, whereas 15% demonstrated involvement of multiple neural pathways. Subclinical involvement of the auditory pathway was statistically associated with higher mean daily DFO dose and longer duration of DFO therapy, whereas abnormalities regarding the somatosensory pathways were related to older age, longer mean duration of DFO therapy, and lower serum copper levels. Involvement of the peripheral nervous system was related to lower serum copper levels. Multiple involvement of neural pathways was related to longer mean duration of DFO therapy. We conclude that risk factors related to long-term DFO treatment are only partly responsible for the subclinical involvement of neural pathways demonstrated in beta-thalassemia major patients.

Adolescent↗
PubMed2005

Requirement of the MEK5-ERK5 pathway for neural differentiation in Xenopus embryonic development.

Although previous studies have identified several key transcription factors in the generation process of the vertebrate nervous system, the intracellular signalling pathways that function in this process have remained unclear. Here we identify the evolutionarily conserved mitogen-activated protein kinase kinase 5 (MEK5)-extracellular signal-regulated kinase 5 (ERK5) pathway as an essential regulator in neural differentiation. Knockdown of Xenopus ERK5 or Xenopus MEK5 with antisense morpholino oligonucleotides results in the reduced head structure and inhibition of neural differentiation. Moreover, forced activation of the MEK5-ERK5 module on its own induces neural differentiation. In addition, we show that the MEK5-ERK5 pathway is necessary for the neuralizing activity of SoxD, a regulator of neural differentiation, and is sufficient for the expression of Xngnr1, a proneural gene. These results show that the MEK5-ERK5 pathway has an essential role in the regulation of neural differentiation downstream of SoxD and upstream of Xngnr1.

Animals↗
PubMed2006

Auditory evoked responses in the rat: transverse mastoid needle electrodes register before cochlear nucleus and do not reflect later inferior colliculus activity.

A previously described technique putatively differentiates short-latency auditory evoked potentials in peripheral and central neural pathways of the mouse and rat [Galbraith G, Waschek J, Armstrong B, Edmond J, Lopez I, Liu W, et al. Murine auditory brainstem evoked response: putative two-channel differentiation of peripheral and central neural pathways. J Neurosci Methods 2006;153:214-20]. This technique involves recording from orthogonally oriented subdermal needle electrode pairs, using fast sample rates (100k/s) to accurately measure differences in neural timing and waveform morphology. Electrodes oriented in a transverse plane (mastoid-to-mastoid) register an initial positive-going peak earlier than peaks recorded from electrodes oriented along the scalp midline (anterior and posterior to the interaural line). The absolute latency of the early mastoid component is consistent with an origin in the primary auditory nerve, while delayed midline latencies implicate activity in central neural pathways. We report here the results of recording simultaneously from transverse mastoid (M) needle electrodes and electrodes acutely implanted in cochlear nucleus (CN) and inferior colliculus (IC). The results show a highly consistent pattern in which the initial mastoid component leads CN by an average of 0.16 ms, suggesting an obligatory neural site of origin of the mastoid response that is distal to IC, namely the auditory nerve. Moreover, later IC components (beyond approximately 3.5 ms) are completely absent in mastoid recordings, indicating that the transverse mastoid recordings provide a relatively isolated measure of early auditory neural activity.

Acoustic Stimulation↗
PubMed2004

The pattern of brain c-fos mRNA induced by a component of fox odor, 2,5-dihydro-2,4,5-trimethylthiazoline (TMT), in rats, suggests both systemic and processive stress characteristics.

Predators to rodents and their associated odors are increasingly chosen to study the neural mechanisms of stress and anxiety. Specifically, predatory odors are believed to elicit responses based on the perceived threat (psychological or processive), rather than to any direct systemic effects (pain, blood loss, infection, etc.) of the stimulus, which are mediated by distinct neural pathways. The hypothesis that a chemical component from fox feces, 2,5-dihydro-2,4,5-trimethylthiazoline (TMT), elicits stress responses by specific activation of processive neural pathways was tested. Different amounts of TMT (range: 0-600 micromol) or the control odor butyric acid (0-1200 micromol) were presented to male Sprague-Dawley rats for 30 min. Immediately after odor presentation, rats were sacrificed, blood levels of adrenocorticotropic hormone (ACTH) and corticosterone were measured, and brains were rapidly harvested to measure regional brain c-fos mRNA induction by in situ hybridization. Presentation of TMT (> or =75 micromol), but not butyric acid (up to 1200 micromol), significantly increased ACTH and corticosterone release. TMT presentation, especially with amounts (> or =75 micromol) producing endocrine activation, induced c-fos mRNA in several brain areas, including the olfactory bulb, lateral septal nucleus, septohypothalamic nucleus, anteromedial and oval nuclei of the bed nucleus of the stria terminalis, the central nucleus of the amygdala, the anteroventral, anterodorsal, and medial preoptic nuclei, the anterior, dorsomedial, lateral, supramammillary, dorsal premammillary and paraventricular hypothalamic nuclei, the external lateral parabrachial nucleus, the locus coeruleus, and the nucleus of the solitary tract. Interestingly, these brain regions represent a mix of regional c-fos mRNA induction pattern not reported previously with any other single stressor. These results suggest that TMT elicits stress responses through a relatively unique and complex mix of brain regions associated with both processive and systemic neural pathways, unlike those seen in response to cat odors.

Animals↗
PubMed2001

Cardiovascular regulation of vasopressin neurons in the supraoptic nucleus.

This paper reviews the regulation of hypothalamic vasopressin and oxytocin neurosecretory cells in the neural response to plasma volume expansion. Many questions remain unanswered regarding how an increase in volume affects neurohypophysial hormone secretion, what receptors are important in mediating this response, and which neural pathways are responsible for conveying the signal from those receptors to the hypothalamus. Plasma volume expansion activates regions of the central nervous system associated with inhibition of vasopressin release, oxytocin secretion, and inhibition of sympathetic nerve activity. Cardiac receptors, not arterial baroreceptors, are primarily responsible for activation of the regions associated with regulation of vasopressin secretion and sympathetic outflow. Other stimuli that as yet are undefined account for activation of oxytocin-secreting neurons. Electrophysiology experiments have measured the inhibition of vasopressin-secreting magnocellular neurons in the supraoptic nucleus by select stimulation of cardiac receptors in the caval-atrial junction. Further experiments suggest that the perinuclear zone, a population of neurons surrounding the supraoptic nucleus, is a necessary part of the pathway by which caval-atrial stretch decreases the excitability of vasopressin neurons. The perinuclear zone is also a necessary synapse for arterial baroreceptor-mediated inhibition of vasopressin neurons. This suggests that the neural pathways that inhibit vasopressin release in response to an increase in blood pressure and an increase in blood volume may overlap at the perinuclear zone of the supraoptic nucleus. Finally, the integration of various neural pathways activated by multiple receptors to ultimately determine the activity of magnocellular neurons and vasopressin secretion is discussed.

Animals↗
PubMed2005

Nociceptive scores and endorphin-containing cells reduced by low-level laser therapy (LLLT) in inflamed paws of Wistar rat.

OBJECTIVE: This study aimed to investigate how local pain relief is mediated by laser therapy and how dose affects the relationship. METHODS: Inflammation was induced in the hind-paws of Wistar rats. Two groups of rats received 780-nm laser therapy (Spectra-Medics Pty Ltd.) at one of two doses (2.5 and 1 J/cm(2)). One group acted as a control. Scores of nociceptive threshold were recorded using paw pressure and paw thermal threshold measures. RESULTS: A dose of 1 J/cm(2) had no statistically significant effect on antinociceptive responses. A dose of 2.5 J/cm(2) demonstrated a statistically significant effect on paw pressure threshold ( p < 0.029) compared to controls. There was no difference in paw thermal threshold responses and paw volumes at either dose. Immunohistochemistry in control animals demonstrated normal beta-endorphin containing lymphocytes in control inflamed paws but no beta-endorphin containing lymphocytes in rats that received laser at 2.5 J/cm(2). CONCLUSION: The results confirm previous findings that the effect of laser therapy is dose-related. The mechanism of effect may occur via a differentiated pressure-sensitive neural pathway rather than a thermal-sensitive neural pathway. The significance of the immunohistochemistry findings remains unknown.

Animals↗
PubMed2006

Activation of the adenylyl cyclase/protein kinase A pathway facilitates neural release of beta-nicotinamide adenine dinucleotide in canine mesenteric artery.

Using high performance liquid chromatography techniques with fluorescence detection we demonstrate that overflow of beta-nicotinamide adenine dinucleotide evoked by electrical field stimulation (16 Hz, 0.3 ms) in the canine isolated mesenteric artery is increased by the activators of adenylyl cyclase (AC) forskolin and calcitonin gene-related peptide (CGRP), by dibutyryl cAMP, and by the inhibitors of phosphodiesterases III and IV milrinone and rolipram. The enhancing effect of forskolin is abolished by the AC inhibitor MDL 12,330A and by protein kinase A (PKA) inhibitors peptide 14-22 amide and 4-cyano-3-methylisoquinoline. Therefore, activation of the AC/cAMP/PKA pathway enhances the release of beta-NAD+ from perivascular nerve terminals.

Adenylyl Cyclase Inhibitors↗
PubMed2006

Major depressive disorder: remission of associated symptoms.

Major depressive disorder (MDD) is a highly prevalent disease often associated with significant medical comorbidity. However, limited data are available examining the associated symptoms of MDD, especially the painful physical symptoms that frequently occur in patients. The presence of these physical symptoms greatly reduces a clinician's ability to recognize and diagnose MDD, ultimately leading to poor treatment outcome. While the treatment goal of MDD is complete remission of all symptoms and the patient's return to full-functioning capacity, if physical symptoms persist, the patient does not achieve functional recovery. Severe consequences have been associated with incomplete remission and residual symptoms, including greater disability and health care costs, plus the increased risk of relapse, morbidity, and mortality. In the treatment of MDD, the noradrenergic, serotonergic, and dopaminergic neural pathways have been found to be affected by depression. More specifically, these neural pathways may correlate with certain psychological and physical symptoms of depression. By studying the effects of antidepressant medications on specific neurotransmitters, antidepressant therapies could be matched to treat specific symptoms of depression. To achieve the goal of remission, clinicians must first determine the best rating method to identify and accurately evaluate the physical symptoms of depression in addition to the core mood symptoms. Therefore, further studies are needed to aid our assessment of physical symptoms and to meet the challenge of effectively matching treatments to a patient's specific symptoms.

Antidepressive Agents↗
PubMed1992

Effect of hearing loss of cochlear origin on the auditory brain stem response.

Auditory brain stem response (ABR) testing is widely used to detect lesions of the auditory neural pathways. The ABR waves depend not only on the integrity of the neural pathways, but also on the condition of the cochlea. To properly interpret the ABR response, it is necessary to understand the effects of cochlear hearing loss on the ABR wave latencies. We studied two populations of subjects with cochlear hearing loss: one with varying degrees of high-frequency hearing loss and the other with varying degrees of flat configuration hearing loss. The degree of cochlear hearing loss was quantified in several different ways and subjected to one linear and three nonlinear regression analyses to test for accuracy in predicting ABR wave latencies and interpeak intervals (waves I, III, V, I-V, I-III, and III-V) for three click intensities. Hearing loss levels from 2 to 6 kHz, in particular 4 kHz, were superior to other audiometric test frequencies as predictors of ABR wave latencies for the group with the high-frequency losses. No particular characterization was found to be superior for the flat hearing loss configurations. From these results, modeled predictions of wave latencies as a function of degree and configuration of hearing loss were made. The modeled predictions are then used to suggest guidelines for interpretations of ABR results where hearing impaired patients are involved.

Adult↗
PubMed1993

Involvement of L-arginine-nitric oxide pathways in neural relaxation of the sphincter of Oddi.

To evaluate if L-arginine-nitric oxide-pathways are involved in the neural relaxation of the sphincter of Oddi, we studied the effect of nitric oxide synthase inhibition on electrical field stimulation-induced relaxation of the sphincter of Oddi in the guinea pig in vitro. After incubation with atropine (1 microM), phentolamine (1 microM) and propranolol (1 microM), histamine (50 microM) and cholecystokinin-octapeptide (25 nM) produced similar increases in sphincter tone. Subsequent field stimulation induced sphincteric relaxation, that was significantly greater when the initial tone had been raised by cholecystokinin (5 Hz, 59 +/- 9%; 10 Hz, 79 +/- 9%) compared to histamine (5 Hz, 27 +/- 3%; 10 Hz, 40 +/- 7%). N-omega-Nitro-L-arginine methyl ester (L-NAME, 100 microM), which competitively inhibits nitric oxide synthase, markedly suppressed this relaxation. The subsequent addition of L-arginine (1 mM), but not D-arginine (1 mM), restored the relaxation. Hexamethonium (100 microM) did not affect the relaxation, but tetrodotoxin (1 microM) completely abolished it. Sodium nitroprusside caused a dose-dependent relaxation of the sphincter (ED50 13 nM), which was unaffected by L-NAME. In conclusion, endogenous nitric oxide synthase products represent a major transmitter of non-adrenergic non-cholinergic relaxation of the sphincter of Oddi in the guinea pig. This relaxation is partially facilitated by cholecystokinin.

Amino Acid Oxidoreductases↗
PubMed2006

The role of the nervous system in rhinitis.

The nose provides defensive and homeostatic functions requiring rapid responses to physical and chemical stimuli. As a result, it is armed with a complex nervous system that includes sensory, parasympathetic, and sympathetic nerves. Sensory nerves transmit signals from the mucosa, generating sensations, such as pruritus; motor reflexes, such as sneezing; and parasympathetic and sympathetic reflexes that affect the glandular and vascular nasal apparatuses. Reflexes directed to the nose are also generated by inputs from other body regions. Hence all symptoms that constitute the nosologic entity of rhinitis can be triggered through neural pathways. In addition, neural signals generated in the nose can influence distal physiology, such as that of the bronchial tree and the cardiovascular system. Neural function can be chronically upregulated in the presence of mucosal inflammation, acutely with an allergic reaction, or even in the absence of inflammation, as in cases of nonallergic rhinitis. Upregulation of the nasal nervous system can occur at various levels of the reflex pathways, resulting in exaggerated responses (neural hyperresponsiveness), as well as in increased capacity for generation of neurogenic inflammation, a phenomenon that depends on the release of neuropeptides on antidromic stimulation of nociceptive sensory nerves. The molecular mechanisms of hyperresponsiveness are not understood, but several inflammatory products appear to be playing a role. Neurotrophins, such as the nerve growth factor, are prime candidates as mediators of neural hyperresponsiveness. The many interactions between the nervous and immune systems contribute to nasal physiology but also to nasal disease.

Humans↗
PubMed1989

A study of the extracellular matrix protein as the migration pathway of neural crest cells in the gut: analysis in human embryos with special reference to the pathogenesis of Hirschsprung's disease.

Immunocytochemical studies on the human embryo were made using antineuronal cell antibody and a panel of anti-extracellular matrix protein antibodies such as fibronectin, laminine, collagen type IV, and hyaluronic acid. All the enteric ganglia are shown to be from a single, vagal neural crest source, although the recent dual gradient migration theory of neural-crest-derived cells in the gut can be challenged. Neural-crest-derived cells first appear in the mesenchyme of the developing esophagus at 4 weeks, and then migrate down along the gut in a craniocaudal direction. The observed distribution of fibronectin and hyaluronic acid indicates the presence of these matrices providing a migration pathway for neural-crest-derived cells in the developing gut. The appearance of neural-crest-derived cells in the gut is always preceded by the appearance of these matrices. On the other hand, substrate or laminine and collagen type IV appears to promote outgrowth of neurites from settled neural-crest-derived cells and their maturation. The distribution of these matrices within the pathway seems consistent with their role in navigating the neural-crest-derived cells toward their final destination. Enteric neurogenesis is dependent on these matrices, and their alteration in early embryonal stage may be a significant factor in the pathogenesis of Hirschsprung's disease.

Cell Movement↗
PubMed1998

Alternative pathways of neural control of the immune process.

Less well established alternative neuromodulatory pathways are neuropeptide-mediated axon reflexes of sensory neurons, gut immunotrafficing, gut transmucosal transport of endogenous bacterial toxin, and the direct secretion of immunoregulatory cytokines by the brain. TNF-alpha and IL-1ra enter peripheral blood after their intracerebroventricular (i.c.v.) injection. Closed head injury or stroke increases blood IL-6 and the acute phase response; neuroblastomas immunosuppress by secreting TGF-beta. The IL-6 that appears in the blood after i.c.v. IL-1 in the rat is partly derived by secretion from the brain into the superior sagital sinus (Romero et al.; 1996. Am. J. Physiol. 270: R518) and is not dependent on peripheral sympathetic activation. Central endothelium and choroid plexus are potential sources of sagital sinus IL-6. TNF-alpha, which appears in blood after i.c.v. LPS, but not IL-1 beta, is due largely to toxin leaving the brain compartment and activating peripheral immunoreactive tissues. Antigens and cytokine immunoregulators drain into cervical lymph. Changes in glial milieu induced by intrinsic neuronal activity could by secretion from brain to blood modulate peripheral immunoreactivity.

Animals↗