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Results for “Neural Pathways”

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PubMed1997

Functional relationship between the hypothalamic vigilance area and PAG vigilance area.

The vigilance reaction is characterized by a large bradycardia, a pressor response, and inspiratory apnea in anesthetized rabbits and the inhibition of movement in conscious rabbits. This affective response pattern can be elicited by electrical stimulation of the dorsolateral hypothalamus (the hypothalamic vigilance area) or the ventrolateral periaqueductal gray (the periaqueductal gray vigilance area). The present study sought to advance our understanding of the functional relationship between the hypothalamic vigilance area (HVA) and the periaqueductal gray vigilance area (PVA) by measuring the effects of transverse transections of the caudal portion of the ventrolateral PAG (vlPAG) upon the cardiovascular responses elicited from the dorsolateral hypothalamus and the rostral vlPAG. Selective transverse transections of the caudal vlPAG significantly reduced the magnitudes of the bradycardia and pressor response elicited by stimulation of the PVA rostral to the transection site, but had minimal impact on the cardiovascular responses evoked by stimulation of the HVA. These findings suggest that the cardiovascular responses elicited by stimulation of the vlPAG are mediated by a neural pathway that is parallel, at least in part, to the one that subserves the response elicited from the HVA. The results also provide support for the view that the PAG is not an essential structure in the mediation of the autonomic components of affective behaviors involving behavioral inhibition.

Animals↗

PubMed1999

Inhibition of peripheral NF-kappaB activation by central action of alpha-melanocyte-stimulating hormone.

With the rise in the field of neuroimmunomodulation research, there is increased recognition of the influence of the nervous system and neuropeptides in peripheral disease. The neuropeptide alpha-melanocyte-stimulating hormone (alpha-MSH) is a neuroimmunomodulatory agent that modulates production of proinflammatory cytokines and inhibits peripheral inflammation via actions on CNS receptors. We examined whether central alpha-MSH operates by inhibiting activation of the nuclear factor kappa B (NF-kappaB) that is essential to the expression of proinflammatory cytokines and development of inflammation in the periphery. Electrophoretic mobility shift assays of nuclear extracts from the murine foot pad injected with TNF-alpha demonstrated that centrally administered alpha-MSH does inhibit NF-kappaB activation. Western blot analysis revealed that this inhibition was linked to central alpha-MSH-induced preservation of expression of IkappaBalpha protein in the peripheral tissue. The NF-kappaB and IkappaBalpha effects were inhibited in mice with spinal cord transection. Intraperitoneal (i.p.) injection of the nonspecific beta-adrenergic receptor blocker propranolol, and of a specific beta2-adrenergic receptor antagonist, likewise prevented these effects of central alpha-MSH; blockade of cholinergic, alpha-adrenergic, or beta1-adrenergic receptors did not. Centrally administered alpha-MSH inhibited peripheral NF-kappaB activation and IkappaBalpha degradation even in mice with nonfunctional melanocortin 1 receptors (MC1R). These findings indicate that alpha-MSH can act centrally to inhibit NF-kappaB activation in peripheral acute inflammation via a descending neural pathway. The pathway involves beta2-adrenergic receptors, but does not require activation of MC1R within the brain.

Acute Disease↗

PubMed1991

The influence of contralateral acoustic stimulation on click-evoked otoacoustic emissions in humans.

Contralateral acoustic stimulation has the effect of reducing the amplitude and shifting the phase of click-evoked OAEs. This effect is thought to be mediated via the medial efferent system and, therefore, the presence of this effect could be used to test the integrity of the neural pathway from one cochlea to the other. With a clinical application in mind, a technique for demonstrating the influence of contralateral acoustic stimulation on click-evoked OAEs was designed to overcome fluctuations in patient and environmental noise. The results of this test on three normal subjects and a patient with a posterior fossa lesion are described.

Acoustic Stimulation↗

PubMed1987

Effect of stimulation of the medullary reticular formation on cerebral vasomotor tonus and intracranial pressure.

The authors report the results of a study to evaluate the effect of stimulation of the medullary reticular formation on cerebral vasomotor tonus and intracranial pressure (ICP) after the hypothalamic dorsomedial nucleus and midbrain reticular formation were destroyed. Systemic arterial pressure (BP), ICP, and local cerebral blood volume (CBV) were continuously recorded in 32 cats. To assess the changes in the cerebral vasomotor tonus, the vasomotor index defined by the increase in ICP per unit change in BP was calculated. In 29 of the 32 animals, BP, ICP, and CBV increased simultaneously immediately after stimulation. The increase in ICP was not secondary to the increase in BP, because the vasomotor index during stimulation was significantly higher than the vasomotor index after administration of angiotensin II. The vasomotor index was high during stimulation of the area around the nucleus reticularis parvocellularis. In animals with the spinal cord transected at the C-2 vertebral level, ICP increased without a change in BP. These findings indicate that the areas stimulated in the medullary reticular formation play an important role in decreasing cerebral vasomotor tonus. This effect was not influenced by bilateral superior cervical ganglionectomy, indicating that there is an intrinsic neural pathway that regulates cerebral vasomotor tonus directly. In three animals, marked biphasic or progressive increases in ICP up to 100 mm Hg were evoked by stimulation. The reduction of cerebral vasomotor tonus and concomitant vasopressor response induced by stimulation of the medullary reticular formation may be one of the causes of acute brain swelling.

Animals↗

PubMed1995

[Brain plasticity. New possibilities in the treatment of nerve damage?].

The article briefly reviews current views on the formation of neural pathways and appropriate connectivity between neurons during the development of the nervous system. The importance of axonal guidance and neurotrophic factors is pointed out. The relevance of these processes to clinical applications is illustrated by a few examples of recent attempts to develop new strategies for the treatment of certain neurological disorders. The prediction is that appreciable progress can be expected in the foreseeable future.

Axons↗

PubMed1984

Diminished bronchial reactivity to cold air in diabetic patients with autonomic neuropathy.

To investigate the role of neural pathways in the nonasthmatic response to eucapnic hyperventilation with below freezing air five diabetic patients with severe symptomatic autonomic neuropathy were studied. Their responses were compared with those shown by five diabetic patients without autonomic neuropathy and five non-diabetic controls. After bronchial provocation testing with cold air the diabetic patients with autonomic neuropathy did not show a significant fall in specific airways conductance (mean (SE) maximum percentage fall 2.0 (3)%), whereas conductance fell in the diabetic patients without neuropathy by 30.8 (2.0)% (p less than 0.001) and in the non-diabetic controls by 22.7 (4.6)% (p less than 0.02). In subjects who do not have asthma the bronchial response to cold air is mediated largely via neural mechanisms.

Adult↗

PubMed1993

Erectile mechanism in paraplegia.

Erection is generally viewed as a reflex mechanism that can receive higher CNS influences. Paraplegic men who have lost reflex activity from the genital area are, therefore, treated as irreversibly impotent. However, the innervation of the male reproductive system suggests that two neural pathways innervate the genitals. In theory, the second (thoracic-lumbar) pathway should compensate for the loss of the first (sacral) pathway in cases of low spinal lesions. Clinical practice, however, ignores the TL pathway as a basis for treatment of spinal cord-injured men. This study used an animal model to demonstrate that the TL pathway could mediate penile responses in paraplegic rats. Eighty-five percent (85%) of spinal animals showed penile responses following hypothalamic (MPOA) stimulation despite a complete loss of peripheral erectile reflexes. These results not only have important implications from a clinical perspective, they further document the physiology of erection and support the view that erection is not a primary parasympathetic activity, but probably results from a sequence of sympathetic processes.

Animals↗

PubMed2003

Connecting the eye to the brain: the molecular basis of ganglion cell axon guidance.

In the past several years, a great deal has been learnt about the molecular basis through which specific neural pathways in the visual system are established during embryonic development. This review provides a framework for understanding the principles of retinal ganglion cell axon guidance, and introduces some of the families of axon guidance molecules involved. In addition, the potential relevance of retinal axon guidance to human visual developmental disorders, and to retinal axon regeneration, is discussed.

Axons↗

PubMed1993

Pharmacological analysis of fear-potentiated startle.

1. The potentiated startle paradigm measures conditioned fear by an increase in the amplitude of a simple reflex (the acoustic startle reflex) in the presence of a cue previously paired with shock. This paradigm offers a number of advantages as an alternative to most animal tests of fear or anxiety because it involves no operant and is reflected by an enhancement rather than a suppression of ongoing behavior. 2. A variety of drugs which block anxiety in people block fear-potentiated startle in rats. Although the 5-HT1A agonist buspirone is especially effective in blocking fear-potentiated startle, more selective 5-HT1A agonists have been less consistently effective. However, when these drugs are combined with only partially effective doses of the D1 antagonist, SCH23390, a full blockade of fear-potentiated startle is achieved. Hence, synergistic actions appear to occur between serotonin and dopamine in modulating the expression of fear-potentiated startle. 3. In addition to pharmacological studies, physiological studies are being used to define the neural pathways necessary for a visual conditioned stimulus to alter the acoustic startle reflex. The current working hypothesis is that the conditioned stimulus activates the central nucleus of the amygdala through a pathway involving the lateral geniculate nucleus, perirhinal cortex, and lateral and basolateral amygdaloid nuclei. The central nucleus of the amygdala then projects directly to the acoustic startle pathway so as to modulate the startle response. Chemical or electrolytic lesions of either the central nucleus or the lateral and basolateral nuclei of the amygdala block the expression of fear-potentiated startle. These latter amygdaloid nuclei may actually be the site of plasticity for fear conditioning, because local infusion of the NMDA antagonist AP5 blocks the acquisition but not the expression of fear-potentiated startle. 4. Finally, we have begun to investigate brain systems that might be involved in the inhibition of fear. Local infusion of AP5 into the amygdala was found to block the acquisition of experimental extinction, a prototypical method for reducing fear. We have also established a reliable procedure for producing conditioned inhibition of fear-potentiated startle and hope to eventually understand the neural systems involved in this phenomenon.

Acoustic Stimulation↗

PubMed2006

Calcium transients and calcium signalling during early neurogenesis in the amphibian embryo Xenopus laevis.

Development of the vertebrate embryonic nervous system is characterized by a cascade of signalling events. In Xenopus, the initial step in this cascade results from signals emanating from the dorsal mesoderm that divert the fate of the ectoderm from an epidermal to a neural lineage. These signals include extracellular antagonists of the bone morphogenetic protein (BMP). Experiments performed with isolated ectoderm suggest that epidermis is induced by BMP, whereas neural fates arise by default following BMP inhibition; however, we show that this mechanism is not sufficient for neural determination. Ca2+ imaging of intact Xenopus embryos reveals patterns of Ca2+ transients in the dorsal ectoderm but not in the ventral ectoderm. These increases in intracellular calcium concentration ([Ca2+](i)), which occur via the activation of dihydropyridine (DHP)-sensitive Ca2+ channels, are necessary and sufficient to orientate the ectodermal cells toward a neural fate. On the one hand, the treatments that antagonize the increase in [Ca2+](i), inhibit neuralization, while on the other hand, an artificial increase in [Ca2+](i), whatever its origin, neuralizes the ectoderm. Using these properties, we have constructed a subtractive cDNA library between untreated ectoderm and caffeine-treated ectoderm. The caffeine stimulates an increase in [Ca2+](i) and thus orientates the cells towards the neural pathway. We have identified early Ca2+ target genes expressed in neural territories. One of these genes, an arginine methyl transferase, controls the expression of the early proneural gene, Zic3. Here, we discuss an alternative model where Ca2+ plays a central regulatory role in early neurogenesis. This model integrates the activation of a Ca2+ -dependent signalling pathway due to an influx of Ca2+ through DHP-Ca2+ channels. While Ca2+ is required for neural determination, epidermal determination occurs when Ca2+ -dependent signalling pathways are inactive.

Animals↗

PubMed2002

VGF is required for obesity induced by diet, gold thioglucose treatment, and agouti and is differentially regulated in pro-opiomelanocortin- and neuropeptide Y-containing arcuate neurons in response to fasting.

Targeted deletion of the gene encoding the neuronal and neuroendocrine secreted polypeptide VGF (nonacronymic) produces a lean, hypermetabolic mouse. Consistent with this phenotype, VGF mRNA levels are regulated in the hypothalamic arcuate nucleus in response to fasting. To gain insight into the site(s) and mechanism(s) of action of VGF, we further characterized VGF expression in the hypothalamus. Double-label studies indicated that VGF and pro-opiomelanocortin were coexpressed in lateral arcuate neurons in the fed state, and that VGF expression was induced after fasting in medial arcuate neurons that synthesize neuropeptide Y (NPY). Like NPY, VGF mRNA induction in this region of the hypothalamus in fasted mice was inhibited by exogenous leptin. In leptin-deficient ob/ob and receptor-mutant db/db mice, VGF mRNA levels in the medial arcuate were elevated. To identify neural pathways that are functionally compromised by Vgf ablation, VGF mutant mice were crossed with obese A(y)/a (agouti) and ob/ob mice. VGF deficiency completely blocked the development of obesity in A(y)/a mice, whereas deletion of Vgf in ob/ob mice attenuated weight gain but had no impact on adiposity. Hypothalamic levels of NPY and agouti-related polypeptide mRNAs in both double-mutant lines were dramatically elevated 10- to 15-fold above those of wild-type mice. VGF-deficient mice were also found to resist diet- and gold thioglucose-induced obesity. These data and the susceptibility of VGF mutant mice to monosodium glutamate-induced obesity are consistent with a role for VGF in outflow pathways, downstream of hypothalamic and/or brainstem melanocortin 4 receptors, that project via the autonomic nervous system to peripheral metabolic tissues and regulate energy homeostasis.

Agouti Signaling Protein↗

PubMed1985

Effects of varicocele after unilateral orchiectomy and sympathectomy.

An experimental varicocele was created in the adult rat by partial ligation of the left renal vein. There was a significant bilateral elevation of both testicular blood flow and temperature in the varicocele animals (p less than 0.01). Mean testicular blood flow for control and varicocele animals was 29.6 +/- 1.0 and 39.8 +/- 2.0 ml./min./100 gm. tissue, while mean testicular temperature was 34.4 +/- 0.1 and 35.3 +/- 0.2C, respectively. A left orchiectomy was combined with a left varicocele to determine if the left testis is essential for the right testicular response to a varicocele. Elevation of right testicular blood flow was not altered by left orchiectomy (p less than 0.05); however, right testicular temperature was no longer significantly increased. Mean right testicular blood flow and temperature for this group was 39.0 +/- 1.5 ml./min./100 gm. tissue and 34.2 +/- 0.15C, respectively. A left sympathectomy was combined with a left varicocele to ascertain if the right testicular response to the left varicocele was mediated through a neural pathway. A significant bilateral increase in testicular blood flow was noted with a left sympathectomy alone, and thereby masked the ability to evaluate the right testicular response to the simultaneous left sympathectomy and varicocele. Elevation of right testicular blood flow in response to the left varicocele is independent of the presence of a left testis and any immune response it may stimulate. The role of the sympathetic nervous system as a mediator of the bilateral varicocele effect remains undetermined.

Animals↗

PubMed2006

Anatomy of the avian hippocampal formation.

Increasing knowledge of the avian hippocampal formation (hippocampus and parahippocampal area) suggests that it plays a role in a variety of behaviors, such as homing, cache retrieving, visual discrimination, imprinting, and sexual behavior. Knowledge of the neural circuits in the hippocampal formation and its related areas or nuclei is important for the understanding of these functions. This review therefore describes the functional neuroanatomy of the avian hippocampal formations, i.e., its subdivisions, cytoarchitecture, and afferent and efferent connections. Evidence obtained by a combination of Nissl staining and tract-tracing shows that the pigeon hippocampal formation can be divided into seven subdivisions: dorsolateral (DL), dorsomedial (DM), triangular (Tr), V-shaped (V), magnocellular (Ma), parvocellular, and cell-poor regions. DL and DM can be further divided into dorsal and ventral, and lateral and medial portions, respectively. In the hippocampal formation, reciprocal connections are found between DL-DM, DL-Tr, DL-Ma, DM-Ma, DM-V, and Tr-V. Neurons in the V-shaped layer appear to be intrinsic neurons. Sensory inputs from higher order visual and olfactory stations enter DL and DM, are modified or integrated by intrinsic hippocampal circuitry, and the outputs are sent, via DL and DM, to various telencephalic nuclei, septum, and hypothalamus. The neural pathways indicate that the hippocampal formation plays a central role in the limbic system, which also includes the dorsolateral corticoid area, nucleus taeniae of the amygdala, posterior pallial amygdala, septum, medial part of the anterior dorsolateral nucleus of the thalamus, and the lateral mammillary nucleus. Connectional and comparative studies, including the use of kainic acid excitotoxicity, suggest that the V-shaped layer is comparable to the dentate gyrus of the mammalian hippocampal formation and DM to Ammon's horn and subiculum.

Animals↗

PubMedDate not supplied

Ethanol affects hypothalamic neurons projecting to the hippocampus and inhibits dentate granule cell LTP.

In previous studies we demonstrated that ethanol inhibition of hippocampal granule cell long-term potentiation (LTP) is mediated by angiotensin II (AII), and the inhibition can be blocked by losartan, a specific AII receptor antagonist. The purpose of the present study was to demonstrate that this low-dose ethanol inhibition of dentate granule cell LTP induction is mediated by lateral hypothalamic (LH) afferents that project to the granule cells. In urethane anesthetized rats, we compared the effects of ethanol infusion, 6.0 microliter/30 min, by means of an open-ended push-pull type cannula, in both the LH and the dentate gyrus, on dentate granule cell LTP. Results demonstrate a dose-dependent inhibition of LTP induction when the LH is perfused that can be blocked by losartan, 10 mg/kg i.p.. Four doses of ethanol were used: 5, 10, 20, and 30 mM. There was no effect when the dentate gyrus was infused with 30 mM ethanol and normal granule cell LTP was observed. Also, these results demonstrate for the first time a low-dose ethanol effect on a physiological function, LTP in a specific neural pathway, directly related to the anterograde amnesia produced by ethanol on short-term memory. Therefore, these data support our hypothesis that ethanol inhibition of LTP induction at the medial perforant path-granule cell synapse can be attributed to a presynaptic release of AII and cannot be explained in terms of a direct postsynaptic effect on the granule cells.

Angiotensin II↗

PubMed2003

Proteolipid protein gene mutation induces altered ventilatory response to hypoxia in the myelin-deficient rat.

Pelizaeus Merzbacher disease is an X-linked dysmyelinating disorder of the CNS, resulting from mutations in the proteolipid protein (PLP) gene. An animal model for this disorder, the myelin-deficient (MD) rat, carries a point mutation in the PLP gene and exhibits a phenotype similar to the fatal, connatal disease, including extensive dysmyelination, tremors, ataxia, and death at approximately postnatal day 21 (P21). We postulated that early death might result from disruption of myelinated neural pathways in the caudal brainstem and altered ventilatory response to oxygen deprivation or hypercapnic stimulus. Using barometric plethysmography to measure respiratory function, we found that the MD rat develops lethal hypoxic depression of breathing at P21, but hypercapnic ventilatory response is normal. Histologic examination of the caudal brainstem in the MD rat at this age showed extensive dysmyelination and downregulation of NMDA and to a lesser extent GABA(A) receptors on neurons in the nucleus tractus solitarius, hypoglossal nucleus, and dorsal motor nucleus of the vagus. Unexpectedly, immunoreactive PLP/DM20 was detected in neurons in the caudal brainstem. Not all biosynthetic functions and structural elements were altered in these neurons, because phosphorylated and nonphosphorylated neurofilament and choline acetyltransferase expression were comparable between MD and wild-type rats. These findings suggest that PLP is expressed in neurons in the developing brainstem and that PLP gene mutation can selectively disrupt central processing of afferent neural input from peripheral chemoreceptors, leaving the central chemosensory system for hypercapnia intact.

Animals↗

PubMed2005

Anatomy and neurochemistry of the pair bond.

Studies in monogamous rodents have begun to elucidate the neural circuitry underlying the formation and maintenance of selective pair bonds between mates. This research suggests that at least three distinct, yet interconnected, neural pathways interact in the establishment of the pair bond. These include circuits involved in conveying somatosensory information from the genitalia to the brain during sexual activity, the mesolimbic dopamine circuits of reward and reinforcement, and neuropeptidergic circuits involved specifically in the processing of socially salient cues. Here we present an integrated description of the interaction of these circuits in a model of pair bond formation in rodents with a discussion of the implications of these findings for evolution, individual variation, and human bonding.

Animals↗

PubMed1999

Gastric mucosal erosion produced by NMDA microinfusions in the lateral hypothalamus: effect of selective knife cuts.

Bilateral infusions of N-methyl-D-aspartate (NMDA) into the lateral hypothalamus (LH) produce gastric erosions in rats. The present study attempted to determine the neural pathways that mediate this effect. In order to interrupt axonal transmission, knife cuts (KC) were made in different planes adjacent to the LH. In separate groups of rats, KC were made anterior, posterior or lateral to the LH just prior to bilateral NMDA infusions (20 micrograms/microliter). The incidence of gastric erosions was measured 24 h after NMDA infusions. Animals receiving sham KC and infused with NMDA exhibited significantly more gastric erosions than those infused with vehicle. Lateral parasagittal KC blocked the occurrence of gastric erosions produced by NMDA, whereas anterior coronal KC significantly increased the incidence of erosions produced by NMDA. Posterior coronal KC did not alter the incidence of gastric erosions produced by NMDA infusions into the LH. These results suggest that intrinsic LH neurons with gastric function project axons laterally and probably descend through the internal capsule to brainstem medullary nuclei. The results of the anterior KC suggest that the LH sends and/or receives inhibitory projections from neural structures (possibly the amygdaloid complex) anterior to the plane of the KC.

Animals↗

PubMed2000

Neural structures that mediate sympathoexcitation during hypoxia.

The sympathetic adjustments triggered by acute mild hypoxia (sympathetic chemoreflex) are initiated by activation of peripheral chemoreceptors whereas more severe hypoxia activates the sympathetic outflow via direct effects on the brainstem. In both cases the rostral ventrolateral medulla (RVLM) plays a critical role in these responses. The first part of this review briefly describes the general input-output properties of the presympathetic neurons of RVLM before focusing on the neural pathways leading to their excitation in response to peripheral chemoreceptor stimulation. The extent to which the central respiratory network contributes to the sympathetic chemoreflex is then discussed before briefly alluding to its role in obstructive sleep apnea and other pathologies. The second half of the review examines the direct effects of hypoxia on RVLM neurons and whether this region and the presympathetic neurons in particular qualify as a physiological central oxygen sensor. The literature is also examined in the context of cerebral ischemia, the Cushing response and the genesis of certain forms of hypertension.

Animals↗