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At least 649 records · Page 36Linked to original sources
PubMed2000

Corticotropin releasing hormone neurons in the paraventricular nucleus are direct targets for neuropeptide Y neurons in the arcuate nucleus: an anterograde tracing study.

In the present study, anterograde tracing combined with triple label immunofluorescent staining was conducted to examine the possible anatomical interactions between Neuropeptide Y (NPY) neurons in the arcuate nucleus of the hypothalamus (ARH) and the corticotropin releasing hormone (CRH) system in the paraventricular nucleus of the hypothalamus (PVH). The anterograde tracer, Phaseolus vulgaris leucoagglutinin (PHA-L), was iontophresed into the ARH of female rats and triple label immunofluorescence staining with three different fluorophores was performed to visualize PHA-L, NPY and CRH, with the aid of confocal microscopy. In PVH, NPY and PHA-L double-labeled fibers were found mainly in the parvocellular part of the PVH (PVHp). Confocal analysis demonstrated that NPY/PHA-L double-labeled fibers came in close apposition to CRH perikarya. In the median eminence, NPY/PHA-L double-labeled fibers were found both in the inner and the outer zones of the median eminence. However, very few double-labeled fibers were found in the proximity of CRH neuronal fibers in the median eminence. Double label staining was also performed to determine if NPY Y1 receptors were expressed in CRH neurons. Two different fluorophores were used to visualize CRH neurons and Y1 receptor. No convincing Y1-positive staining was found in CRH cell bodies in the PVH, even though Y1-positive staining in numerous fibers and cell bodies was observed throughout the region. However, Y1-positive fibers were shown to make close contact with CRH cell bodies in the PVH. In the ME, the majority of the Y1-positive fibers were located in the lateral portion of the ME, whereas the CRH fibers were found mainly in the medial portion of the external zone of the ME. The results of the present study suggest that ARH NPY neurons provide direct input into CRH cell bodies in the PVH region. However, the direct effects of NPY must be mediated by some receptor subtype other than Y1. Y1 receptor involvement in NPY modulation of CRH neuronal function in the PVH appears to be indirect through modulation of neuronal afferents making contact with CRH neurons.

Animals↗
PubMed2000

Neuronal nicotinic receptors in non-neuronal cells: new mediators of tobacco toxicity?

The nicotinic acetylcholine receptors are prototypic ionotropic receptors that mediate fast synaptic transmission. However, also non-excitable cells, and particularly the tegumental cells that line external and internal body surfaces, express acetylcholine receptors of neuronal type sensitive to nicotine. Bronchial epithelial cells, endothelial cells of blood vessels and skin keratinocytes express neuronal nicotinic receptors composed of alpha(3), alpha(5), beta(2) and beta(4) subunits, similar to those expressed in sympathetic ganglia, and neuronal nicotinic receptors composed of alpha(7) subunits. Neuronal nicotinic receptors in tegumental cells are involved in modulating cell shape and motility, and therefore in maintaining the integrity of the surfaces lined by those cells. Neuronal nicotinic receptors in non-neuronal tissues may modulate other functions, including cell proliferation and differentiation. Acetylcholine is synthesized, secreted and degraded by a variety of cells, including the tegumental cells that express neuronal nicotinic receptors. Thus, acetylcholine may function as a local "hormone" that is able to modulate cell functions that require fast adaptation to new conditions. The presence of neuronal nicotinic receptors sensitive to nicotine in tissues known to be involved in tobacco toxicity, like bronchi and blood vessels, raises the possibility that they mediate some of the toxic effects of smoking.

Bronchi↗
PubMed1998

Motor neuron-derived retinoid signaling specifies the subtype identity of spinal motor neurons.

The diversification of neuronal cell types in the vertebrate central nervous system depends on inductive signals provided by local organizing cell groups of both neural and nonneural origin. The influence of signals provided by postmitotic neurons on the fate of neurons born at subsequent development stages, however, remains unclear. We provide evidence that a retinoid-mediated signal provided by one subset of early-born spinal motor neurons imposes a local variation in the number of motor neurons generated at different axial levels and also specifies the identity of a later-born subset of motor neurons. Thus, in the vertebrate central nervous system the distinct fates of late-born neurons may be acquired in response to signals provided by early-born neurons.

Aldehyde Oxidoreductases↗
PubMed2001

In vitro clonal analysis of rat cerebral cortical neurons expressing latexin, a subtype-specific molecular marker of glutamatergic neurons.

Latexin is expressed in a subset of glutamatergic projection neurons located in the lateral but not the dorsomedial neocortex in rat. In the present study, we performed clonal analysis of embryonic cortical neurons in vitro using latexin as a subtype-specific molecular marker of glutamatergic neurons to address whether certain precursors in early cortical anlage are already committed to a single molecular phenotype. Dissociated cells from lateral cortex at embryonic day 12 were labelled with a replication-deficient retroviral vector containing the bacterial lacZ gene, and cultured in a monolayer for 3 weeks. Double-immunofluorescence staining was used to simultaneously visualize latexin- and beta-galactosidase-immunopositive neurons. Out of 572 beta-galactosidase-immunopositive clones examined, 27 clones contained latexin-expressing neuron(s). Of these 27 clones, 25 clones that contained three or more neurons were mixed clones containing both latexin-immunopositive and -immunonegative neurons. These results suggest that committed precursors to producing solely latexin-expressing neurons are not exist in the early cerebral cortical anlage.

Animals↗
PubMed1997

Role of hippocampal serotonergic neurons in ischemic neuronal death.

To clarify the serotonergic mechanisms involved in the protection against ischemic neuronal damage, ZD-211 (citalopram HBr), a serotonin (5-hydroxytryptamine; 5-HT) re-uptake inhibitor, or buspirone, a 5-HT1A agonist, was locally administered into the hippocampus of gerbils. Additionally, to clarify the role of the 5-HT nervous system in the hippocampus during ischemic neuronal damage, animals were subjected to the local administration of 5,7-dihydroxytryptamine (5,7-DHT), a 5-HT neurotoxin, before ischemia challenge. Gerbils received intrahippocampal administration of ZD-211 (200 nmol/animal) or buspirone (20 nmol/animal) before 5-min ischemia. 5,7-DHT was intrahippocampally administered 7 days before a 2-min non-lethal ischemia challenge. In vehicle-treated animals subjected to 5 min of ischemia, almost all hippocampal CA1 pyramidal neurons were lost. The treatment with ZD-211 or buspirone showed a significant protective effect, and the number of neurons was significantly increased compared to vehicle-treated animals. Pretreatment with NAN-190, a 5-HT1A antagonist, completely abolished the protective effect of ZD-211 or buspirone. In the 5,7-DHT-treated animals, the number of neurons was significantly reduced following 2 min of ischemia compared to vehicle-treated animals in which this period of ischemia is non-lethal. Thus, intrahippocampal treatment with ZD-211 or buspirone can protect neuronal damage following transient ischemia in gerbils. These effects of ZD-211 and buspirone were mediated through the 5-HT1A receptor in the hippocampus. Furthermore, the destruction of the 5-HT nervous system in the hippocampus aggravated ischemic neuronal damage. Therefore, this study showed that the enhanced activity of the 5-HT nervous system in the hippocampus may protect against neuronal damage following cerebral ischemia.

5,7-Dihydroxytryptamine↗
PubMed2000

Somatostatin-IR neurons are a major subpopulation of the cuneothalamic neurons in the rat cuneate nucleus.

This study was aimed to localize and characterize the somatostatin-immunoreactive (SOM-IR) neurons in the rat cuneate nucleus (CN). By immuno-histochemistry, the SOM-IR neurons, which were widely distributed in the nucleus, were round, spindle or multiangular in shape (mean area = 226.1 +/ -3.1 microm(2), n = 1016). By electron microscopy, the neurons shared all the ultrastructural features of the cuneothalamic neurons (CTNs) which showed a slightly indented nucleus and a fairly rich cytoplasm containing well-developed Golgi apparatuses and rough endoplasmic reticulum (rER). The SOM immunoreaction product filled the cytoplasm of the neurons extending from the soma to the proximal and distal dendrites, which were postsynaptic to unlabeled boutons. In addition to soma and dendrites, SOM-IR boutons were also identified which made axodendritic synaptic contacts with SOM-IR dendrites. The SOM-IR neurons were characterized by using anti-SOM pre-embedding immunolabeling coupled with horseradish peroxidase (HRP) retrograde method, or SOM immunolabeling along with anti-glutamate, gamma-aminobutyric acid (GABA) or glycine post-embedding immunolabeling for identification of CTNs, glutamate-IR, GABA-IR and glycine-IR neurons, respectively. It was shown that more then 80% of the CTNs contained SOM and, furthermore, they contained glutamate but not GABA or glycine. On the basis of present findings, it is suggested the majority of the SOM-IR neurons in the rat CN are CTNs and that they may be involved in modulation of somatosensory synaptic transmission.

Animals↗
PubMed2003

A neuron-specific EGF family protein, NELL2, promotes survival of neurons through mitogen-activated protein kinases.

NELL2 is a neuron-specific thrombospondin-1-like extracellular protein containing six epidermal growth factor-like domains. NELL2 is highly expressed in the hippocampus and cerebral cortex. Although the involvement of NELL2 in neural functions has been inferred from its expression and biochemical profiles, biological roles of NELL2 remain uncertain. We evaluated the survival effect of NELL2 using primary cultured neurons from fetal rat brain following treatment with a recombinant NELL2 protein. NELL2 increased survival of neurons from the hippocampus and cerebral cortex. We further examined the protective effect of NELL2 from oxygen-glucose deprivation- and beta-amyloid-induced neuronal death, and found that NELL2 did not protect neurons from these insults. To understand signaling properties underlying the survival effect, we studied activation of mitogen-activated protein kinases (MAPKs) by NELL2. Treatment of primary cultured cells from the hippocampus with NELL2 enhanced phosphorylation of c-jun N-terminal kinase (JNK), whereas phosphorylation of extracellular signal-regulated kinase (ERK) was decreased by NELL2 treatment. NELL2-enhanced survival of hippocampal neurons was completely blocked by SP600125, an anthrapyrazolone inhibitor of JNK, while treatment of MEK (MAPK/ERK kinase) inhibitors per se enhanced survival of neurons similar to NELL2 treatment. These results suggest that NELL2 promotes survival of neurons by modulating MAPK activities.

Amyloid beta-Peptides↗
PubMed1997

Consequences of hypoxia on the cell size of neuropeptide-Y neurons and the role of ascorbate in cultured neurons from chick embryo.

The effect of ascorbate on the cell size of neuropeptide-Y neurons (NPY) and ascorbate uptake was studied in hypoxic neuronal cultures from chick embryo. Primary neuronal cultures plated on coverslips or on plastic dishes were switched to the serum free or serum supplemented medium and exposed to the normoxia or hypoxia for 8 h. Vehicle (homocysteine) or L-ascorbic acid was added to the incubation medium at 0 h. Cell size and relative optical density of NPY positive neurons on coverslips were measured by image analysis and ascorbate content in the cell culture on dishes was determined by HPLC. Hypoxia increased the size of NPY neurons in vehicle treated cultures but not in ascorbate supplemented cultures containing serum free or serum supplemented medium. Contrastingly, normoxic NPY neurons were damaged by ascorbate in serum free medium and not by incubation with ascorbate in serum supplemented medium. These results indicate that the inhibition of hypoxic induced neuronal swelling by ascorbate is consistent with its antioxidant properties and presence of ascorbate in serum free medium under normoxic conditions may act as a proxidant for cultured neurons.

Animals↗
PubMed1997

Epileptic neurons induce augmenting synaptic depolarizations in non-epileptic neurons (buccal ganglia, Helix pomatia).

Spread of epileptic activity was studied by inducing epileptiform activity (pentylenetetrazol, PTZ) in one part of a nervous system and by analyzing responses of neurons in a non-PTZ-treated part (identified neurons, paired buccal ganglia, Helix pomatia). Paroxysmal depolarization shifts (PDS) induced time-locked depolarizations in non-epileptic neurons (latency ca. 5 s, duration ca. 1 min, amplitude < or =20 mV). Amplitudes were augmenting during several hours of epileptic activity. Depolarizations were accompanied by an increase in membrane resistance and they were blocked in 'high Mg-low Ca' solutions. It is assumed that the potentials represent a typical widespread response of non-epileptic neurons to PDS of other neurons. This response may be induced via non-specific releases of substances of the epileptically active neurons thereby activating neighboring neurons which in turn activate neurons in control ganglion.

Animals↗
PubMed2000

Nitrergic neurons make synapses on dual-input dendritic spines of neurons in the cerebral cortex and the striatum of the rat: implication for a postsynaptic action of nitric oxide.

Pre-embedding electron microscopic immunocytochemistry was used to examine the ultrastructure of neurons containing nitric oxide synthase and to evaluate their synaptic relationships with target neurons in the striatum and sensorimotor cerebral cortex. Intense nitric oxide synthase immunoreactivity was found by light and electron microscopy in a type of aspiny neuron scattered in these two regions. The intensity of the labeling was uniform in the soma, dendrites and axon terminals of these neurons. In both forebrain regions, nitric oxide synthase-immunoreactive neurons received synaptic contacts from unlabeled terminals, which were mostly apposed to small-caliber dendrites. The unlabeled symmetric contacts were generally about four times as abundant as the unlabeled asymmetric contacts on the nitric oxide synthase-immunoreactive neurons. Terminals labeled for nitric oxide synthase were filled with synaptic vesicles and were observed to contact unlabeled neurons. Only 54% (in the cerebral cortex) and 44.3% (in the striatum) of the nitric oxide synthase-immunoreactive terminals making apposition with the target structures were observed to form synaptic membrane specializations within the plane of the randomly sampled sections. The most common targets of nitric oxide synthase-immunoreactive terminals were thin dendritic shafts (54% of the immunoreactive terminals in the cortex and 75.7% of the immunoreactive terminals in the striatum), while dendritic spines were a common secondary target (42% of the immunoreactive terminals in the cortex and 20.6% of the immunoreactive terminals in the striatum). The spines contacted by nitric oxide synthase-immunoreactive terminals typically also received an asymmetric synaptic contact from an unlabeled axon terminal. These findings suggest that: (i) nitric oxide synthase-immunoreactive neurons in the cortex and striatum preponderantly receive inhibitory input; (ii) nitric oxide synthase-containing terminals commonly make synaptic contact with target structures in the cortex and striatum; (iii) spines targeted by nitric oxide synthase-containing terminals in the cortex and striatum commonly receive an asymmetric contact as well, which may provide a basis for a synaptic interaction of nitric oxide with excitatory input to individual spines.

Animals↗
PubMed1998

Rostroventrolateral medulla neurons preferentially project to target-specified sympathetic preganglionic neurons.

The rostroventrolateral medulla is a key site for the regulation of vasomotor tone. Sympatho-excitatory neurons project from this region to contact sympathetic preganglionic neurons located in the intermediolateral nucleus of the thoracic and lumbat spinal cord. Functional studies show that stimulation of specific sites in the ventral medulla lead to selective activation of different vascular effectors. The present study was designed to determine the anatomical basis for this selectivity in vasomotor control. Anterograde and retrograde tracing methods were utilized to determine if the descending rostral ventrolateral projection is topographically organized such that neurons in particular locations within the nucleus project preferentially and contact a specific group of sympathetic preganglionic neurons. For this purpose spinally-projecting neurons at 15 sites from three separate rostrocaudal locations within the rostroventrolateral medulla in nine rats were anterogradely labelled with biotin dextran amine. The spinal cord was examined for axon terminals having close apposition to two groups of sympathetic preganglionic neurons, those projecting to the superior cervical ganglion and those to the adrenal medulla which were retrogradely labelled with cholera B chain-conjugated horseradish peroxidase. Areas of close apposition between retrogradely-labelled dendrites, cell bodies and anterogradely-labelled axons were found. Axons descending from the more rostral part of the rostroventrolateral medulla produced the highest density of close appositions to sympathetic preganglionic neurons in both target-specific populations. Caudal rostroventrolateral medulla injection sites gave rise to a less dense distribution of axons and terminals around the spinal sympathetic nuclei. This study has demonstrated that spinally-projecting neurons in the rostroventrolateral medulla are both topographically and viscerotopically organized. It is suggested that such an arrangement provides the means for selective and differential control of autonomic effectors and in particular those involved in cardiovascular regulation.

Animals↗
PubMed1998

Insulin-like growth factor-I analogue prevents apoptosis mediated through an interleukin-1 beta converting enzyme (caspase-1)-like protease of cerebellar external granular layer neurons: developmental stage-specific mechanisms of neuronal cell death.

Using an organotypic slice culture system of neonatal rat cerebellum, we examined developmental stage-specific mechanisms of cell death of granule neurons. This culture system allows a serial process of granule neuron development including their proliferation during the early culture period and the proceeding migration from the external granular layer to the internal granular layer in the presence of a supraphysiological concentration (5 micrograms/ml) of insulin. Insulin deprivation induced apoptosis of granule neurons in external granular layer but not in internal granular layer. A truncated analogue of insulin-like growth factor-I (des (1-3) insulin-like growth factor-I) prevented this apoptosis at a concentration of 65-650 ng/ml. Some apoptotic granule neurons expressed proliferating cell nuclear antigen but not TAG-1, a marker protein of the postmitotic and premigratory granule neurons. Thus, this apoptosis occurred at a specific stage in granule neuron development: at the stage before TAG-1 expression and at least partly at the proliferative state. Ac-YVAD-CHO, an inhibitor of interleukin-1 beta converting enzyme (caspase-1)-like proteases, had a protective effect on this apoptosis. Interleukin-1 beta converting enzyme (caspase-1)-like protease activity increased under the apoptosis-induced condition. High concentration of K+, which is known to prevent granule neuron apoptosis in dissociated cultures, had a partial protective effect on this apoptosis. These findings suggest that (i) cerebellar granule neurons fall into apoptosis at the specific developmental stage unless stimulated by insulin-like growth factor-I (analogue), (ii) this apoptosis is mediated through an interleukin-1 beta converting enzyme-like protease, and (iii) this apoptosis consists of K(+)-sensitive and K(+)-insensitive components.

Animals↗
PubMed1999

Single-unit activity of dorsomedial arcuate neurons and diurnal changes of tuberoinfundibular dopaminergic neuron activity in female rats with neonatal monosodium glutamate treatment.

Neonatal monosodium glutamate (MSG)-treated rats were used in this study to answer two questions: (1) whether or not the dopamine-responsive dorsomedial arcuate (dm-ARN) neurons are tuberoinfundibular dopaminergic (TIDA) neurons, and (2) whether or not the remaining TIDA neurons in MSG-treated rats are functioning normally. MSG (4 mg/g b. wt., subcutaneously [s.c.]) or saline was given to neonatal Sprague-Dawley rats on days 1, 3, 5, 7, and 9 after birth. The female rats were ovariectomized at 50 days of age and treated with estrogen for 1 week before they were used between 65-90 days of age. The tyrosine hydroxylase-immunoreactive (TH-ir) neurons located in the dm and ventrolateral (vl) parts of the ARN were significantly reduced in MSG-treated rats, as determined by immunohistochemical method. Some TH-ir cells, however, were visible along the border of the third ventricle. Using single-unit recording in brain slices, we found that dopamine inhibited significantly fewer percentage of dm-ARN neurons in MSG-treated (28.2%, n = 39) than in saline-treated rats (73.3%, n = 15). In contrast, bombesin exhibited similar effects (over 70% excitation) in both groups. Using neurochemical means, neonatal MSG treatment produced significant decreases of both 3,4-dihydroxyphenylacetic acid and dopamine levels, but not their ratios, in the median eminence. Moreover, the diurnal change of TIDA neuronal activity persisted in the MSG-treated rats; so did the estrogen-induced afternoon prolactin surge. All these results indicate that neonatal MSG-treatment reduced the number and altered the location of TIDA and dopamine-responsive dm-ARN neurons. The remaining TIDA neurons seemed to be able to maintain their basal activities and diurnal rhythm.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2001

Coordinate regulation of motor neuron subtype identity and pan-neuronal properties by the bHLH repressor Olig2.

Within the developing vertebrate nervous system, the mechanisms that coordinate neuronal subtype identity with generic features of neuronal differentiation are poorly defined. We show here that a bHLH protein, Olig2, is expressed selectively by motor neuron progenitors and has a key role in specifying the subtype identity and pan-neuronal properties of developing motor neurons. The role of Olig2 in the specification of motor neuron subtype identity depends on regulatory interactions with progenitor homeodomain proteins, whereas its role in promoting pan-neuronal properties is associated with expression of another bHLH protein, Ngn2. Both aspects of Olig2 function appear to depend on its activity as a transcriptional repressor. Together, these studies show that Olig2 has a critical role in integrating diverse features of motor neuron differentiation in the developing spinal cord.

Animals↗
PubMed2004

Disabled-1-regulated adhesion of migrating neurons to radial glial fiber contributes to neuronal positioning during early corticogenesis.

Disabled-1 regulates laminar organization in the developing mammalian brain. Although mutation of the disabled-1 gene in scrambler mice results in abnormalities in neuronal positioning, migratory behavior linked to Disabled-1 signaling is not completely understood. Here we show that newborn neurons in the scrambler cortex remain attached to the process of their parental radial glia during the entire course of radial migration, whereas wild-type neurons detach from the glial fiber in the later stage of migration. This abnormal neuronal-glial adhesion is highly linked to the positional abnormality of scrambler neurons and depends intrinsically on Disabled-1 Tyr220 and Tyr232, potential phosphorylation sites during corticogenesis. Importantly, phosphorylation at those sites regulates alpha3 integrin levels, which is critical for the timely detachment of migrating neurons from radial glia. Altogether, these results outline the molecular mechanism by which Disabled-1 signaling controls the adhesive property of neurons to radial glia, thereby maintaining proper neuronal positioning during corticogenesis.

Animals↗
PubMed2001

Nicotine stimulation of dorsal raphe neurons: effects on laterodorsal and pedunculopontine neurons.

Previous studies showed that nicotine suppresses the ponto-geniculo-occipital (PGO) spikes of rapid eye movement (REM) sleep in cats. This effect may depend on stimulation of dorsal raphe nucleus (DRN) serotoninergic neurons that inhibit the pedunculopontine (PPT) and laterodorsal tegmental (LDT) cholinergic neurons, generators of PGO spikes. For testing this hypothesis 37 experiments were performed in rat midbrain slices. Nicotine (2 mM), administered locally into DRN, significantly increased the firing rate of 81.1% DRN neurons and serotonin release while simultaneously and significantly decreasing the firing rate of 80.8% LDT neurons and of 81.8% PPT neurons. The inhibition of LDT neurons by nicotine administered into DRN was blocked by the 5-HT1A receptor antagonist WAY-100635 (140 nM) administered into LDT. These results indicate that nicotine inhibits the activity of LDT and PPT neurons and consequently the generation of PGO spikes through stimulation of DRN serotoninergic neurons.

Action Potentials↗
PubMed1997

Neuronal-enriched cultures from embryonic rat ventral mesencephalon for pharmacological studies of dopamine neurons.

The method described herein provides a convenient and rapid procedure to obtain enriched neuronal cultures containing reproducible numbers of dopamine (DA) cells. These cultures allow experimental paradigms designed to study the effect of drugs on DA neurons without astroglial mediation. Neuronal-enriched cultures are prepared from the mesencephalon of rat embryos at the 14th day of gestation (E14). At that moment, DA cells of the developing substantia nigra are located ventrally at the level of the mesencephalic flexure. Because the neurons of the pars compacta are mostly born between E12 and E15, E14 corresponds to an optimal stage for obtaining a high survival of DA cells. A defined medium (EF12) allows the maturation of DA neurons and reduces drastically the number of astrocytes. After 7 days in vitro (DIV) in EF12, the cultures contain 2-5% astrocytes (GFAP+ cells) and DA neurons represent 0.5-2% of the cells, as assessed by immunostaining to tyrosine hydroxylase (TH). The function of DA neurons is assessed by [3H]DA uptake and of those non-DA neurons by the high affinity [3H]GABA uptake. Cell survival is assessed by Trypan blue dye exclusion.

Animals↗
PubMed2002

Functional connectivity between neurons generating resting discharge in renal sympathetic neurons in the rabbit.

In anaesthetised rabbits, we analysed the cross-correlations of resting discharges in pairs of simultaneously recorded renal neurons. The study of 428 significant cross-correlations showed three pure types of neuronal co-ordination and two combined effects. Pure shared input was observed in 202 pairs of neurons (47.2%). The width of cross-correlogram peak was 222.9 +/- 7.2 ms. The peak height of shared input was 4.8 +/- 0.2 spikes s(-1) and was significantly related with correlogram width. Pure excitatory connection was found in 24 neuronal pairs (5.6%). Its peak width was 7.9 +/- 1.9 ms and it was shifted from time zero by 13.3 +/- 3.4 ms. The amplitude of the peak was 19.6 +/- 4.6 spikes s(-1). In 165 pairs of neurons (38.6%), excitatory connection was combined with shared input component. Pure reciprocal activation was seen in only 5 pairs of neurons (1.1%) while in 32 pairs (7.5%) it was accompanied by shared input co-ordination. The distance between narrow peaks measured in the combined type of co-ordination was 32.5 +/- 3.5 ms and the mean peak height was 4.1 +/- 0.7 spikes s(-1). Shared input in pure form and that accompanying both excitatory connection and reciprocal activation were significantly related to the frequency of discharge of neurons contributing to the cross-correlogram. The incidence and basic properties of the encountered types of neural coordination may indicate a pattern of interconnections between cells generating vasomotor tone in renal sympathetic neurons.

Action Potentials↗