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PubMed2005

Structural and functional evidence supporting a role for leptin in central neural pathways influencing blood pressure in rats.

Leptin, a peptide hormone normally associated with body weight homeostasis, is implicated in the generation of obesity-induced hypertension. Administration of leptin increases sympathetic nerve activity and blood pressure; however, the neural circuity involved in this pressor effect is not clearly defined. In this review we describe experiments in which pseudorabies virus was injected into the heart, kidney and the vasculature within skeletal muscle to reveal the distribution of neurones in the hypothalamus that project to these cardiovascular tissues. This distribution is compared to the well-documented distribution of leptin receptors. Finally we discuss microinjection studies designed to examine the effect of leptin, in these regions, on sympathetic nerve discharge and arterial blood pressure. Leptin injected directly into the ventromedial hypothalamus, arcuate nucleus and lateral hypothalamic area (particularly the perifornical area) increased lumbar sympathetic nerve activity. In addition, microinjection into the ventromedial hypothalamus and parvocellular paraventricular nucleus increased blood pressure. Our results demonstrate a discrete set of hypothalamic pathways that may underlie the involvement of leptin in obesity-induced hypertension.

Animals↗
PubMed1998

Duodenal motility in fasting dogs: humoral and neural pathways mediating the colonic brake.

We have previously described a negative feedback loop that inhibits duodenal motility when nutrients are infused into the ileum and colon. In the present study, we examined the role of extrinsic innervation and plasma levels of peptide YY (PYY) in mediating this phenomenon. We perfused neurally intact (n = 5 dogs) or extrinsically denervated (n = 6 dogs) isolated loops of proximal colon with isomolar NaCl or a mixed-nutrient solution at 2 and 6 ml/min for 4 h during fasting or for 2 h beginning 15 min after a meal. Both rates of infusion with NaCl prolonged the cycle length of the duodenal migrating motor complex (MMC) in the group with neurally intact loops but not in the group with extrinsically denervated loops. Nutrient infusions increased the MMC cycle length in both groups. Integrated plasma concentrations of PYY were increased by nutrients but not by NaCl in both groups. These data suggest that increased volumes and unabsorbed nutrients in the proximal colon alter proximal small bowel motility. Volume-induced effects are mediated via extrinsic nerves, whereas nutrient-induced effects may be mediated by humoral factors, such as plasma PYY.

Animals↗
PubMed2002

Interhemispheric connection of auditory neural pathways assessed by auditory evoked magnetic fields in patients with fronto-temporal lobe infarction.

In auditory evoked magnetic fields (AEFs), the latency of temporal N100m response elicited by the ipsilateral ear stimulation (Ipsi-Stim) is generally longer than that of N100m response elicited by the contralateral ear stimulation (Cont-Stim). The reason for this difference remains unclear. We measured AEFs in patients with fronto-temporal or frontal lobe infarction to clarify this question. In the patients with fronto-temporal lobe infarction, the N100m peak latencies in the healthy hemisphere by Ipsi-Stim measurements were significantly longer than the corresponding normal values. Such a latency prolongation was not observed in the patients with frontal lobe infarction. The results suggest that auditory impulses originated from the ear may first arrive at the contralateral temporal cortex and then return to the ipsilateral temporal cortex mediating through the corpus callosum. The disturbance of interhemispheric conduction by ischemic temporal lesions likely delays the N100m latency at the contralateral temporal cortex. The mediation of interhemispheric route may, thus, make the ipsilateral N100m latency generally longer than the contralateral N100m latency.

Acoustic Stimulation↗
PubMed2003

Neural pathways between sacrocaudal afferents and lumbar pattern generators in neonatal rats.

Projections of sacrocaudal afferents (SCA) onto lumbar pattern generators were studied in isolated spinal cords of neonatal rats. A locomotor-like pattern could be produced by SCA stimulation in the majority of the preparations. The SCA-induced lumbar rhythm was abolished after blocking synaptic transmission in the sacrococcygeal (SC) cord by bathing its segments in a low-calcium, high-magnesium artificial cerebrospinal fluid and restored when the synaptic block was alleviated by local application of calcium onto specific SC segments prior to SCA stimulation. Thus the SCA evoked lumbar rhythm involves synaptic activation of relay neurons in the SC cord. Functional activation of these relays depends on non-N-methyl-D-aspartate (NMDA) receptors because the lumbar rhythm was abolished when the non-NMDA receptor antagonist CNQX was added to the SC cord. By contrast, pharmacological block of the rhythmicity in the SC cord by specific antagonists of NMDA receptors and alpha1 and alpha2 adrenoceptors did not impair the SCA-induced lumbar rhythm. Midsagittal splitting experiments of parts of the SC and lumbar cord revealed that crossed and uncrossed ascending/propriospinal pathways are coactivated by SCA stimulation. We suggest that these pathways ascend onto the thoracolumbar cord through the lateral, ventrolateral, and ventral funiculi, because a complete block of the lumbar rhythm could only be obtained with a bilateral interruption of all of these funiculi. The relevance of our findings to the neural control of the rhythmogenic networks in the spinal cord is discussed.

2-Amino-5-phosphonovalerate↗
PubMed1996

Differential desensitization of mu- and delta- opioid receptors in selected neural pathways following chronic morphine treatment.

1. Morphine produces a plethora of pharmacological effects and its chronic administration induces several side-effects. The cellular mechanisms by which opiates induce these side-effects are not fully understood. Several studies suggest that regulation of adenylyl cyclase activity by opioids and other transmitters plays an important role in the control of neural function. 2. The aim of this study was to evaluate desensitization of mu- and delta- opioid receptors, defined as a reduced ability of opioid agonists to inhibit adenylyl cyclase activity, in four different brain structures known to be involved in opiate drug actions: caudate putamen, nucleus accumbens, thalamus and periaqueductal gray (PAG). Opiate regulation of adenylyl cyclase in these regions has been studied in control and morphine-dependent rats. 3. The chronic morphine treatment used in the present study (subcutaneous administration of 15.4 mg morphine/rat/day for 6 days via osmotic pump) induced significant physical dependence as indicated by naloxone-precipitated withdrawal symptoms. 4. Basal adenylyl cyclase in the four brain regions was not modified by this chronic morphine treatment. In the PAG and the thalamus, a desensitization of mu- and delta-opioid receptors was observed, characterized by a reduced ability of Tyr-D-Ala-Gly-(NMe)Phe-Gly-ol (DAMGO; mu), Tyr-D-Pen-Gly-Phe-D-Pen (DPDPE; delta) and [D-Ala2]-deltorphin-II (DT-II; delta) to inhibit adenylyl cyclase, activity following chronic morphine treatment. 5. The opioid receptor desensitization in PAG and thalamus appeared to be heterologous since the metabotropic glutamate receptor agonists, L-AP4 and glutamate, and the 5-hydroxytryptamine (5-HT)1A receptor agonist, R(+)-8-hydroxy-2-(di-n-propylamino)tetralin hydrobromide (8-OH-DPAT), also showed reduced inhibition of adenylyl cyclase activity following chronic morphine treatment. 6. In the nucleus accumbens and the caudate putamen, desensitization of delta-opioid receptor-mediated inhibition without modification of mu-opioid receptor-mediated inhibition was observed. An indirect mechanism probably involving dopaminergic systems is proposed to explain the desensitization of delta-mediated responses and the lack of mu-opioid receptor desensitization after chronic morphine treatment in caudate putamen and nucleus accumbens. 7. These results suggest that adaptive responses occurring during chronic morphine administration are not identical in all opiate-sensitive neural populations.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2006

Dorsal-ventral pattern of Delta trafficking is established by a Snail-Tom-Neuralized pathway.

The intracellular trafficking of the Notch ligand Delta plays an important role in the activation of the Notch pathway. We have addressed the snail-dependent regulation of Delta trafficking during the plasma membrane growth of the mesoderm in the Drosophila embryo. We show that Delta is retained in endocytic vesicles in the mesoderm but expressed on the surface of the adjacent ectoderm. This trafficking pattern requires Neuralized. We developed a protocol based on chromosomal deletion and microarray analysis that led to the identification of tom as the target of snail regulating Delta trafficking. Snail represses Tom expression in the mesoderm and thereby activates Delta trafficking. Overexpression of Tom abolishes Delta trafficking and signaling to the adjacent mesoectoderm. Loss of Tom produces mesoderm-type Delta trafficking in the entire blastoderm epithelium and an expansion of mesoectoderm gene expression. We propose that Tom antagonizes the activity of Neuralized and thus establishes a sharp mesoderm-mesoectoderm boundary of Notch signaling.

Animals↗
PubMed1990

Melatonin does not link the eyes to the rest of the circadian system in quail: a neural pathway is involved.

Blinding by enucleation has a dramatic effect on the circadian activity rhythm of Japanese quail. The activity patterns of enucleated birds held under 24-hr light-dark cycles are disrupted, although entrainment can persist in many birds. In constant darkness (DD), blinded birds are rendered arrhythmic. These results demonstrate that the eyes are a major component of the circadian system, and that insofar as enucleation produces arrhythmicity in DD, the eyes' role is not merely a photosensory one. The eyes of quail can synthesize and secrete the hormone melatonin, which has been implicated as a blood-borne messenger relaying timing information between elements of the circadian system in some avian species. However, the way in which the eyes communicate with the rest of the circadian system in quail appears to be neural, since (1) optic nerve section produces the same effects as blinding by enucleation on the circadian activity rhythm, and (2) eyes subjected to optic nerve section retain their ability to synthesize and secrete melatonin.

Animals↗
PubMed1985

Ovarian LHRH receptors increase following lesions of the major LHRH structures in the rat brain: involvement of a direct neural pathway.

Specific lesions of different brain structures known to contain or to be coursed by LHRH neurons have been carried out in intact cycling female rats in order to investigate the role played by central LHRH and neuronal systems in the regulation of ovarian and hypophyseal LHRH receptor (LHRH-R) levels, using the stable LHRH analog [D-Ser (TBU)6] Des-Gly10, LHRH ethylamide, buserelin. Radiofrequency lesions were placed bilaterally or unilaterally into female rats showing at least two consecutive estrous cycles, under pentobarbital anesthesia, while groups of animals were sham-operated. Bilateral lesions placed into the septal area and into the nucleus and tract of the diagonal band of Broca (DBB) resulted in a nearly 25-40% stimulation of LHRH binding activity within the ovaries and a 30% inhibition of LHRH analog binding to pituitary homogenate, while lesions placed into the medial preoptic area (MPO), where the majority of LHRH neurons are found, produced a doubling of ovarian LHRH-R accompanied by a 60% decrease of pituitary binding sites. Lesions involving the median eminence and arcuate hypothalamic nucleus, where the most conspicuous convergence of LHRH fibers occurs, produced a twofold increase in ovarian LHRH-R levels and an almost complete loss of pituitary LHRH-R binding capacity, with no change in affinity. In order to clarify the importance of direct neural signals modulating the ovarian LHRH-R concentration, lesions were placed in the right or left MPO and DBB, and the content of LHRH-R measured in right and left ovaries. Lesions placed unilaterally (right or left) produced a significant increase of LHRH-R binding activity within the ovary ipsilateral to the lesion, while a reduction or no effect was observed in the contralateral gland. Data show a marked stimulation of ovarian LHRH-R number following bilateral lesions placed in the major LHRH-containing structures, while pituitary LHRH binding sites are significantly inhibited, indicating impairment in the rate and/or amplitude of endogenous hypothalamic LHRH release. Furthermore results obtained following unilateral lesions indicate that a neural mechanism is involved in ovarian LHRH receptor induction and further reinforce our view that a direct neural connection links the brain and the ovaries.

Animals↗
PubMed2001

Traditional and new antipsychotic drugs differentially alter neurotransmission markers in basal ganglia-thalamocortical neural pathways.

The effects of three chronically administered antipsychotic drugs on selected neurochemical markers of dopaminergic and GABAergic transmission were compared within the cerebral regions making up the basal ganglia-thalamocortical parallel processing neuronal pathways. All three drugs reduce psychosis in humans, whereas only haloperidol, but not olanzapine or sertindole, induce purposeless oral chewing movements (CMs) in rats or cause high rates of parkinsonism or tardive dyskinesia in humans. Male Sprague Dawley rats were treated with haloperidol, sertindole, or olanzapine delivered in drinking water for 6 months at doses which produce drug plasma levels in rat in the human therapeutic range. Results show the expected dopamine D2 receptor upregulation in striatum predominantly with haloperidol, although mild D2 upregulation was apparent in striatum after olanzapine. GAD67 mRNA was increased in striatum and decreased in globus pallidus by haloperidol and sertindole, but not by olanzapine. In the substantia nigra pars reticulata (SNR), both olanzapine and sertindole failed to induce GABA(A) receptor upregulation or D1 receptor downregulation, but haloperidol did both, confirming a previous report. In thalamus, all three drugs increased GAD expression in the reticular nucleus, whereas only haloperidol decreased GABA(A) binding in the mediodorsal nucleus, actions consistent with a reduction in nigrothalamic, GABA-mediated neural transmission. These results are consistent with the idea that the two new antipsychotics tested have mild and regionally restricted actions within the basal ganglia nuclei and a common action on increasing GAD expression in the reticular nucleus of the thalamus (RtN). Haloperidol, in contrast, has a broad and potent action in basal ganglia, causing changes in SNR and in the mediodorsal nucleus, while also altering GAD mRNA in RtN, potentially reflective of its dyskinetic and antipsychotic actions.

Animals↗
PubMed1978

Differences in reaction times and average evoked potentials as a function of direct and indirect neural pathways.

Average evoked potentials and manula response latencies were collected during a simple detection task in which brief visual stimuli were presented to the left and right visual fields. Latencies generated by the ipsilateral stimulus-hand combinations were shorter than contralateral combinations only under certain conditions, impugning the hypothesis that the reaction time difference reflects interhemispheric transfer time. Certain evoked potential components recorded contralateral to the stimulus occurred earlier than their ipsilateral counterparts, but whether this difference can be interpreted as representing interhemispheric transfer time is also questioned.

Adult↗
PubMed2001

Neural pathways connecting the deutocerebrum and lateral protocerebrum in the brains of decapod crustaceans.

The olfactory and accessory lobes of eureptantian decapod crustaceans are bilateral brain neuropil regions located within the deutocerebrum. Although the olfactory lobe seems to receive only primary olfactory inputs, the accessory lobe receives higher-order multimodal (including olfactory) inputs. The output pathways from both the olfactory and accessory lobes are provided by the axons of a large population of projection neurons, whose somata lie adjacent to the lobes. The axons of these neurons form a large tract that projects bilaterally to the medulla terminalis and hemiellipsoid body in the lateral protocerebrum. To gain insights into the ways in which olfactory information is processed on leaving the deutocerebrum, we examined the neuroanatomy of the projection neuron pathways of three species of eureptantian decapod crustaceans: the freshwater crayfish, Procambarus clarkii and Orconectes rusticus, and the clawed lobster, Homarus americanus. Projection neurons were labeled by focal injections of the lipophilic tracers DiI and DiA into the olfactory and accessory lobes. In all three species, projection neurons innervating the accessory lobe were found to exclusively innervate the neuropils of the hemiellipsoid body. In contrast, projection neurons innervating the olfactory lobes primarily target neuropil regions of the medulla terminalis. The results of this study indicate, therefore, that the projection neuron pathways from the olfactory and accessory lobes project to separate, largely nonoverlapping regions of the lateral protocerebrum. The implications of these findings for our understanding of the processing of olfactory information in the brains of decapod crustaceans are discussed.

Animals↗
PubMed1975

Neural pathways from the vestibular labyrinths to the flocculus in the cat.

In decerebrate, unanesthetized cats, responses in the flocculus were evoked by electric stimulation of the vestibular nerves and by natural stimulation of horizontal head angular acceleration. Field potentials in the flocculus and intracellular recording from Purkinje cells following vestibular nerve stimulation indicated that the responses were produced by mossy fiber inputs. Field potentials evoked from the contralateral labyrinth were as large as those from the ipsilateral one. There was considerable convergence of bilateral labyrinthine mossy fiber inputs to a Purkinje cell. In view of the effects of incision at the midline of the cerebellum and the brain stem, inputs from the contralateral labyrinth were mainly conveyed through the midline of the brain stem and partly through the midline of the cerebellum. Primary vestibular afferents were involved in the transcerebellar crossed pathway. Fibers of the secondary vestibular neurons projecting to the contralateral flocculus were implicated in the brain stem-mediated pathway and, in part, presumably in the transcerebellar crossed pathway. About one-third of the axon spikes examined in the flocculus responded to horizontal head angular acceleration. Commissural inhibition was observed in more than half of the axon spikes in the flocculus which were presumed to be mono- or polysynaptically activated from the vestibular nerve.

Animals↗
PubMed1985

Retrograde tracing of neural pathways with a protein-gold complex. I. Light microscopic detection after silver intensification.

In this study I have used a tracer complex made of wheat germ agglutinin horseradish peroxidase conjugate (WGA*HRP) coupled to colloidal gold for retrograde tracing of neuronal pathways at the light microscopic level. Visualization of the gold was achieved by silver precipitation (the gold silver intensification method) with gold particles acting as specific cores of nucleation. The presence of horseradish peroxidase in the protein conjugate allowed this method to be compared with classical histochemistry using tetramethylbenzidine as a chromogen. The gold silver intensification method proved to be reliable, specific and sensitive. It has been demonstrated to be useful with fixatives containing a high percentage of paraformaldehyde and compatible with histochemical procedures to show projections of transmitter specific pathways.

Animals↗
PubMed1988

Olfactory neural pathway in mouse hepatitis virus nasoencephalitis.

The mechanism of brain infection with mouse hepatitis virus-JHM was studied in BALB/cByJ mice following intranasal inoculation, and found to be a consequence of direct viral spread along olfactory nerves into olfactory bulbs of the brain. Infection was followed sequentially from nose to brain, using microscopy, immunohistochemistry and virus quantification. Lesions, antigen and virus were observed in the olfactory bulb and anterior brain as early as 2 days and posterior brain by 4 days after inoculation. Viral antigen extended through nasal mucosa into submucosa, then coursed along the olfactory nerve perineurium and fibers, through the cribriform plate into the olfactory bulbs. On days 4 and 7, viral antigen was found in the antero-ventral brain, along ventral meninges, olfactory tracts and anterior ramifications of the lateral ventricles. Virus was cleared from nose by 10 days and anterior brain by 20 days, but persisted in posterior brain for 20 days after inoculation. Mice also developed disseminated infection, with viremia and hepatitis. Infection of brain did not correlate with presence of viremia. In contrast to intranasally inoculated mice, orally-inoculated mice did not develop encephalitis, despite evidence of disseminated infection.

Animals↗