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PubMed1991

Calretinin immunoreactivity in cholinergic motor neurones, interneurones and vasomotor neurones in the guinea-pig small intestine.

Immunoreactivity for calretinin, a calcium-binding protein, was studied in neurones in the guinea-pig small intestine. 26 +/- 1% of myenteric neurones and 12 +/- 3% of submucous neurones were immunoreactive for calretinin. All calretinin-immunoreactive neurones were also immunoreactive for choline acetyltransferase and hence are likely to be cholinergic. In the myenteric plexus, two subtypes of Dogiel type-I calretinin-immunoreactive neurones could be distinguished from their projections and neurochemical coding. Some calretinin-immunoreactive myenteric neurones had short projections to the tertiary plexus, and hence are likely to be cholinergic motor neurones to the longitudinal muscle. Some of these cells were also immunoreactive for substance P. The remaining myenteric neurones, immunoreactive for calretinin, enkephalin, neurofilament protein triplet and substance P, are likely to be orad-projecting, cholinergic interneurones. Calretinin immunoreactivity was also found in cholinergic neurones in the submucosa, which project to the submucosal vasculature and mucosal glands, and which are likely to mediate vasodilation. Thus, calretinin immunoreactivity in the guinea-pig small intestine is confined to three functional classes of cholinergic neurones. It is possible, for the first time, to distinguish these classes of cells from other enteric neurones.

Animals↗
PubMed1982

Quantitative immunocytochemistry of tyrosine hydroxylase in rat brain. II. Variations in the amount of tyrosine hydroxylase among individual neurons of the locus coeruleus in relationship to neuronal morphology and topography.

We sought to determine by a computer assisted quantitative immunocytochemical method using the peroxidase-antiperoxidase (PAP) technique if individual neurons of the nucleus locus coeruleus (LC) varied with respect to the amount of tyrosine hydroxylase (TH) within each cell and, if so, whether the amount of TH is related to morphometric characteristics and/or location of the neuron within the LC. Appropriate immunohistochemical reaction conditions were used so that the intensity of DAB reaction product formed in the PAP reaction was directly and linearly related to the amount of TH enzyme protein present in the tissue. The distribution of the average optical density of 1425 individual LC neurons obtained from 5 animals and standardized to an overall mean density varies unimodally over a 3-fold range. The relationship between staining intensity and morphological and topographic characteristics of individual neurons was examined. There was no correlation between staining intensity and morphological features of individual neurons, including cytoplasmic area. However, differences in the amount of TH in individual neurons correlated significantly (P less than 0.01) with the location of the cell in LC: the lightest staining neurons were located in the central core of the LC. The density of staining did not differ significantly in the other 4 traditionally defined regions of LC (the anterior, posterior, and ventral poles of the LC and the nucleus subcoeruleus) which form a rim around the central core. Similarly, cells which are closest to the center of mass of the LC showed a lighter staining intensity than cells located progressively further from the center. These lighter staining cells in the center were also packed more closely together (P less than 0.01). Therefore dense packing of neurons correlates with light staining intensity (P less than 0.01). We conclude that neurons of the LC vary with respect to the amount of TH, which in turn relates to the location of the cell in the LC and possibly its packing density, but not its morphometric characteristics. Since in noradrenergic neurons, the amount of TH is directly influenced by firing rate, the results suggest that the biochemical heterogeneity of LC neurons reflects differences in their functional activities. In turn, this may relate to heterogeneity of LC with respect to projection fields.

Animals↗
PubMed1992

Acute alcohol alters the excitability of cerebellar Purkinje neurons and hippocampal neurons in culture.

Acute exposure to ethanol at 22 and 44 mM concentrations altered several features of the current-evoked voltage responses of cerebellar Purkinje neurons and hippocampal neurons studied in culture model systems. Whole cell current clamp techniques were used. At 22 mM, ethanol depressed current-evoked spiking in the hippocampal neurons but enhanced the current-evoked spiking in the Purkinje neurons. In both neuronal types, 44 mM ethanol depressed spiking, the amplitude of the afterhyperpolarization generated at the termination of a current pulse and the amplitude of the off-response generated at the termination of a hyperpolarizing pulse. Ethanol had little or no effect on resting membrane potential or the passive membrane properties measured near resting level in either neuronal type. Some changes in the current-voltage curves were observed at more depolarized or hyperpolarized potentials in both neuronal types. In the Purkinje neurons, where spontaneous activity was a prominent feature of some recordings, exposure to ethanol reduced the frequency of the spontaneous events. These results indicate that acute exposure to ethanol at intoxicating doses alters the membrane excitability of these two CNS neuronal types. The ethanol induced changes in neuronal excitability presumably contribute to the changes in firing properties observed in extracellular recordings from these neuronal types in vivo and the behavioral effects observed during alcohol intoxication in animal models.

Animals↗
PubMed1994

Use of Fos-related antigens (FRAs) as markers of neuronal activity: FRA changes in dopamine neurons during proestrus, pregnancy and lactation.

This manuscript describes the use of staining of Fos-related antigens (FRAs) as markers for changes in neuronal activity. The model system consisted of the tuberoinfundibular dopamine (TIDA) neurons located in the arcuate nucleus of the hypothalamus. Under normal conditions, these neurons are devoid of c-Fos staining even though the neurons are tonically active and can express FRAs. During specific neuroendocrine states the neurons undergo changes in activity, as described by other studies. At times when the activity is relatively high as in pregnancy and during proestrus, approximately 50%-60% of the TIDA neurons expressed FRA immunoreactivity. Moreover changes over the course of proestrus paralleled known shifts in TIDA activity (declining as the day progressed). At times when TIDA activity is suppressed, such as during lactation, FRA staining in TIDA neurons was markedly reduced or absent. Upon removal of the suckling stimulus, FRA staining rose to reach peak expression 12-24 h after pup removal (without coordinate induction of c-Fos). These data suggest that FRA staining can serve as a useful marker of activity in the TIDA neurons which permits not only assessment of stimulated activity but also suppressed function in the neurons. A cautionary note in using this approach along with acquisition of serial blood samples for hormone measurement is that surgical procedures for monitoring plasma hormone levels are associated with strong long-lived induction of FRAs (and c-Fos) in many neurons (including the TIDA neurons) that can confound interpretation of FRA staining.

Analysis of Variance↗
PubMed1996

Local injection of kainic acid causes widespread degeneration of NADPH-d neurons and induction of NADPH-d in neurons, endothelial cells and reactive astrocytes.

Nitric oxide (NO), a diffusible gas, is a messenger molecule that mediates vascular dilatation and neural transmission. The enzyme nitric oxide synthase (NOS) present in neurons is activated by Ca2+ influx associated with activation of glutamate receptors. Cultured cortical neurons containing NOS are selectively vulnerable to injury by kainic acid (KA). However, the relationship between NOS neurons and excitotoxicity under in vivo conditions is not entirely clear. In the present study, we examined the time course and spatial distribution of changes in NOS neurons caused by an intracortical microinjection of KA in adult rats. NADPH-diaphorase (NADPH-d) histochemistry was used as a marker for NOS and the neuronal changes were correlated with changes in glial cells and endothelial cells. We demonstrated a rapid loss of NADPH-d neurons in the lesion center and degeneration of NADPH-d neurons and nerve terminals throughout ipsilateral cortex and hippocampus; the striatal neurons appeared to be unaffected. Subsequent to cortical neuronal degeneration, new NADPH-d activity appeared in proliferative reactive astrocytes and in endothelial cells at lesion periphery, and in neuronal groups at lesion periphery, in ipsilateral entorhinal cortex and bilateral hippocampus. These findings indicate that neurons expressing NADPH-d in cerebral cortex and hippocampus are selectively vulnerable to KA toxicity in vivo. The subsequent induction of NOS in neural and non-neural cells may be regarded as an adaptive response to the kainate-induced brain lesion.

Animals↗
PubMed1992

Persistent innervation of the rat neocortex by basal forebrain cholinergic neurons despite the massive reduction of cortical target neurons. I. Morphometric analysis.

In Alzheimer's disease, a characteristic neurochemical abnormality is the loss of cholinergic enzymes in the neocortex, reflecting the degeneration of basal forebrain neurons responsible for cholinergic innervation of the neocortex. It is hypothesized that basal forebrain neuronal degeneration results from a reduction in the level of trophic factors synthesized by neurons in the target regions of cholinergic projections. Data from a large number of animal lesioning studies tend to support this theory; however, most of these lesions also induce widespread, nonspecific injury responses in the CNS. To directly test the dependence of basal forebrain cholinergic neurons on target-derived neurotrophic support, pregnant Sprague-Dawley rats were injected with moderate doses of methylazoxymethanol acetate (MAM) on Gestational Days 14 and 15. Extensive morphometric analysis of offspring reveals that the prenatal administration of MAM during this period of neurogenesis results in the ablation of 40-70% of cortical neurons, without significant effects on the hippocampus or the genesis of basal forebrain cholinergic neurons. Examination of MAM-treated animals at several ages reveals no significant differences in neuronal density of cholinergic neurons as compared to controls. Extensive analysis of animal brains at several time points has failed to reveal any evidence of classical injury responses which might be responsible for preservation of basal forebrain neurons. These results contradict the theory that mature basal forebrain cholinergic neurons are critically dependent on the availability of target-derived neurotrophic factors and are therefore unlikely to be the major etiological factor in basal forebrain neuronal degeneration characteristic of Alzheimer's disease.

Acetylcholine↗
PubMed1992

Stimulation of neuron survival by basic FGF and CNTF is a direct effect and not mediated by non-neuronal cells: evidence from single cell cultures.

The multifunctional proteins, basic fibroblast growth factor (bFGF) and ciliary neurotrophic factor (CNTF), share a capacity to promote in vitro and in vivo survival of several, partly overlapping neuron populations. Whether they can affect neurons directly or whether their supportive effects are mediated by non-neuronal cells and their growth factor products has been addressed in this study by establishing single neuron cultures from embryonic chick ciliary ganglia. Cultures with one or two neurons and without any non-neuronal cells were obtained by limiting dilution of ganglionic cell suspensions on 96-well microtiter plates. In the presence of bFGF about 80% of the wells that contained 1 or 2 neurons at the time of seeding, had this (these) neuron(s) maintained after 1 and 5 days. Absence of bFGF resulted in the death of neurons in over 80% of the wells screened. Identical results were obtained with CNTF. These data demonstrate the effectiveness of bFGF and CNTF at the single neuron level, but do not rule out that the factors may act indirectly on neurons, particularly in complex in vitro and in vivo situations.

Animals↗
PubMed2004

Medullary adrenergic neurons contribute to the cocaine- and amphetamine-regulated transcript-immunoreactive innervation of thyrotropin-releasing hormone synthesizing neurons in the hypothalamic paraventricular nucleus.

Cocaine- and amphetamine-regulated transcript (CART)-IR axons densely innervate the thyrotropin-releasing hormone (TRH) neurons in the hypothalamic paraventricular nucleus (PVN), partly arising from neuronal perikarya in the hypothalamic arcuate nucleus. The source of the remaining CART innervation, however, is unknown. We have recently demonstrated that neurons co-containing adrenaline and CART in the C1-3 areas of the medulla project to the PVN. Since adrenergic neurons densely innervate the hypophysiotropic TRH neurons, we raised the possibility that adrenergic neurons contribute to the CART-IR innervation of hypophysiotropic TRH neurons. Combined in situ hybridization and immunocytochemistry was performed to study the colocalization of CART and phenylethanolamine N-methyltransferase (PNMT), the synthesizing enzyme of adrenaline, in axons innervating the hypophysiotropic TRH neurons. PNMT was observed in 44% of CART-IR axons in juxtaposition to the hypophysiotropic TRH neurons and CART-IR was observed in approximately 50% of all PNMT axons in contact with proTRH perikarya in the PVN. We conclude that adrenergic neurons of the medulla give rise to approximately half of the CART-IR axons innervating hypophysiotropic TRH neurons in the PVN, and propose that CART may play important role in the modulation of adrenergic input to the hypothalamic-pituitary-thyroid axis.

Afferent Pathways↗
PubMed2005

Pontine reticular formation neurons are implicated in the neuronal network for generalized clonic seizures which is intensified by audiogenic kindling.

The caudal pontine reticular formation nucleus (cPRF) is implicated in seizure propagation to the spinal cord in several forms of generalized convulsive seizures, including audiogenic seizures (AGS). Focal microinjection studies implicate cPRF as a requisite neuronal network site subserving generalized AGS in the moderate severity substrain of genetically epilepsy-prone rats (GEPR-3s). AGS in GEPR-3s culminate in generalized clonus, but daily repetition of AGS (AGS kindling) results in an additional seizure behavior, facial and forelimb (F and F) clonus, not seen prior to kindling. This study examined cPRF neuronal firing changes and seizure behaviors during AGS in GEPR-3s. We examined extracellular cPRF neuronal responses to acoustic stimuli (12 kHz) and observed neuronal firing during AGS. cPRF neurons exhibited onset responses to acoustic stimuli before and after AGS kindling. After AGS kindling, increased neuronal firing occurred, and response latencies were prolonged. Tonic neuronal firing occurred during generalized clonus, which changed to burst firing after AGS kindling. Burst firing also occurred during F and F clonus. Increased neuronal firing and the change from tonic to burst firing suggest that AGS kindling involves increased cPRF excitability. These data support an important role for cPRF neurons in generation of generalized clonus in unkindled GEPR-3s, which is increased by AGS kindling. The increased cPRF response latency might reflect a greater role of rostral components of the AGS neuronal network in transmission of acoustic responses to cPRF. This study also suggests that cPRF neurons may be involved in F and F clonus, which was unexpected since F and F clonus is thought to originate primarily in forebrain structures.

Acoustic Stimulation↗
PubMed2005

Central vagal stimulation activates enteric cholinergic neurons in the stomach and VIP neurons in the duodenum in conscious rats.

The influence of central vagal stimulation induced by 2h cold exposure or intracisternal injection of thyrotropin-releasing hormone (TRH) analog, RX-77368, on gastro-duodenal enteric cholinergic neuronal activity was assessed in conscious rats with Fos and peripheral choline acetyltransferase (pChAT) immunoreactivity (IR). pChAT-IR was detected in 68%, 70% and 73% of corpus, antrum and duodenum submucosal neurons, respectively, and in 65% of gastric and 46% of duodenal myenteric neurons. Cold and RX-77368 induced Fos-IR in over 90% of gastric submucosal and myenteric neurons, while in duodenum only 25-27% of submucosal and 50-51% myenteric duodenal neurons were Fos positive. In the stomach, cold induced Fos-IR in 93% of submucosal and 97% of myenteric pChAT-IR neurons, while in the duodenum only 7% submucosal and 5% myenteric pChAT-IR neurons were Fos positive. In the duodenum, cold induced Fos in 91% of submucosal and 99% of myenteric VIP-IR neurons. RX-77368 induces similar percentages of Fos/pChAT-IR and Fos/VIP-IR neurons. These results indicate that increased central vagal outflow activates cholinergic neurons in the stomach while in the duodenum, VIP neurons are preferentially stimulated.

Animals↗
PubMed2000

Brainstem catecholaminergic neurons activated by hypoxemia express GR and are coordinately activated with fetal sheep hypothalamic paraventricular CRH neurons.

In late gestation, challenges to fetal homeostasis are accompanied by increases in adrenocorticotropin (ACTH) concentrations in fetal peripheral plasma and Fos (c-fos protein) activation in corticotropin-releasing hormone (CRH) neurons of the fetal hypothalamic paraventricular nucleus (PVN). In adults, ventrolateral brainstem catecholaminergic (CA) neurons (A1/C1, A2/C2) project to the parvocellular neurons of the PVN, possess glucocorticoid receptors (GR) and are Fos activated in parallel with CRH neurons of the PVN during hypoxia. Such observations suggest a role for the aforementioned medullary neurons in the function of the hypothalamo-pituitary-adrenal axis. The present study utilized late gestation fetal sheep, stereotaxic methodology and retrograde axon tracing and immunocytochemical techniques to investigate the relationship between activation of fetal brainstem CA neurons and activation of fetal PVN CRH immunopositive neurons in response to hypoxemia. Results indicated that: (1) the largest brainstem CA projection to PVN CRH neurons is from A1/C1 neurons, (2) brainstem neurons exhibit GR immunostaining and (3) brainstem CA neurons show a strong correlation (A1/C1 - r(2)=0.894, P<0.005; A2/C2 - r(2)=0. 848; P<0.002) of Fos activation with Fos activation in PVN CRH cells. We conclude that in late gestation the brainstem A1/C1 and A2/C2 areas are in position to influence the function of the hypothalamo-pituitary-adrenal axis during hypoxemic challenges to homeostasis in a fashion similar to that which has been demonstrated in the adult rat.

Adrenocorticotropic Hormone↗
PubMed1989

Adrenergic neurons in the rostral ventrolateral medulla: ultrastructure and synaptic relations with other transmitter-identified neurons.

The first part of this chapter demonstrates that the C1 adrenergic neurons have high mitochondrial content and a close proximity to capillaries and glia suggestive of a high metabolic activity and a possible chemosensory function. Adrenergic terminals arising primarily from these neurons (1) can influence sympathetic nerve discharge through direct contacts on sympathetic preganglionic neurons in the IML of the spinal cord; and (2) are one of the more prevalent synaptic inputs to the principally noradrenergic neurons in the locus coeruleus. In both the IML and locus coeruleus, adrenergic terminals may be either excitatory (asymmetric synapses) or inhibitory (symmetric synapses) depending on their distribution on the post-synaptic target. The second part of this chapter shows that C1 adrenergic neurons in the RVL are modulated by synaptic associations with a variety of transmitter systems (see schematic Fig. 8). Specifically, C1 adrenergic neurons receive (1) major inhibitory input (symmetric synapses) from GABA-ergic and opioid terminals as well as from unidentified (unlabelled) transmitter-containing terminals; (2) major excitatory input (asymmetric synapses) from terminals containing substance P as well as other unidentified terminals and (3) minor inputs from cholinergic, adrenergic and noradrenergic pathways. Moreover, cholinergic terminals in the RVL form symmetric synapses mainly on unidentified transmitter-containing neurons rather than the C1 neurons suggesting that the reported cardiovascular effects of cholinergic agents in the RVL are most likely mediated via inhibitory interneurons. Within the RVL, adrenergic and noradrenergic terminals innervate cholinergic and opioid neurons. Thus, these results not only provide direct evidence that a number of transmitters modulate the activity of C1 adrenergic neurons, but also suggest new directions for studies of functional interactions involving catecholaminergic regulation of other transmitter-containing neurons within the RVL.

Animals↗
PubMed2001

Inhibition of neuronal nitric oxide synthase results in neurodegenerative changes in the axotomised dorsal root ganglion neurons: evidence for a neuroprotective role of nitric oxide in vivo.

In axotomised adult rat dorsal root ganglion (DRG), many neurons show a marked increase in expression of neuronal nitric oxide synthase (nNOS). It has been established that NO functions as a neuron-glial signalling molecule by generating cGMP in glia cells that surround the neuron in DRG. Furthermore, in cultures of dissociated DRG deprived of nerve growth factor, many neurons expressed nNOS and cGMP and subsequently died if either enzyme's activity was inhibited suggesting that NO-cGMP pathway could be neuroprotective in stressed DRG neurons. This has now been tested in vivo. It was found, 10 days after sciatic axotomy that nNOS was expressed in 36% of DRG neurons in the L5 and L6 ganglia giving rise to the damaged nerve, compared with 6% in contralateral ganglia. Almost all nNOS neurons and 24% of non-nNOS neurons expressed c-Jun in their nuclei. Ten days following axotomy, treatment with the relatively selective nNOS-blocker, 1-(2-trifluoromethylphenyl) imidazole (TRIM), caused morphology changes in approximately 50% of neurons that consisted of vacuolations, blebbing and highly irregular cell boundaries. Sham operated, TRIM treated, nerve-sectioned, vehicle treated, and controls did not show these changes. These observations further support the view that NO could be neuroprotective in some injured/stressed primary sensory neurons.

Animals↗
PubMed1999

Transgenic expression of B-50/GAP-43 in mature olfactory neurons triggers downregulation of native B-50/GAP-43 expression in immature olfactory neurons.

The adult mammalian olfactory neuroepithelium is an unusual neural tissue, since it maintains its capacity to form new neurons throughout life. Newly formed neurons differentiate in the basal layers of the olfactory neuroepithelium and express B-50/GAP-43, a protein implicated in neurite outgrowth. During maturation these neurons migrate into the upper portion of the epithelium, upregulate expression of olfactory marker protein (OMP) and concomitantly downregulate the expression of B-50/GAP-43. Transgenic mice that exhibit OMP-promoter directed expression of B-50/GAP-43 in mature olfactory neurons display an unexpected decrease in the complement of B-50/GAP-43-positive cells in the lower region of the olfactory epithelium [A.J.G.D. Holtmaat, P.A. Dijkhuizen, A.B. Oestreicher, H. J. Romijn, N.M.T. Van der Lugt, A. Berns, F.L. Margolis, W.H. Gispen, J. Verhaagen, Directed expression of the growth-associated protein B-50/GAP-43 to olfactory neurons in transgenic mice results in changes in axon morphology and extraglomerular growth, J. Neurosci. 15 (1995) 7953-7965]. We have investigated whether the decrement in B-50/GAP-43-positive cells in this region was due to a dislocation of the immature neurons to other regions of the olfactory epithelium or to a downregulation of B-50/GAP-43 synthesis in these immature neurons. In eight of nine independent transgenic mouse lines that express the transgene in different numbers of olfactory neurons, a decline in the number of B-50/GAP-43-expressing neurons in the basal portion of the olfactory neuroepithelium was observed, both at the protein level and the mRNA level. An alternative marker for immature cells, a juvenile form of tubulin, was normally expressed in this location, indicating that the olfactory epithelium of OMP-B-50/GAP-43 transgenic mice contains a normal complement of immature olfactory neurons and that most of these neurons display a downregulation of B-50/GAP-43 expression.

Animals↗
PubMed2002

Medullary adrenergic neurons contribute to the neuropeptide Y-ergic innervation of hypophysiotropic thyrotropin-releasing hormone-synthesizing neurons in the rat.

The arcuate nucleus gives rise to approximately 80% of the neuropeptide Y (NPY)-immunoreactive (IR) innervation to thyrotropin-releasing hormone (TRH) neurons in the hypothalamic paraventricular nucleus (PVN). However, the source of the remaining 20% is unknown. Since medullary adrenergic neurons synthesize NPY and also innervate the hypophysiotropic TRH neurons, we raised the possibility that adrenergic neurons contribute to the NPY-ergic innervation of TRH neurons in the PVN. Triple-labeling immunofluorescence was performed to study the colocalization of NPY and phenylethanolamine N-methyltransferase (PNMT)--the key enzyme of adrenaline synthesis--in axons in association with hypophysiotropic TRH neurons. NPY-immunoreactivity was observed in 74% of PNMT-IR axon varicosities apposed to proTRH-IR neurons, comprising 26% of all NPY-IR axons in contact with proTRH perikarya and dendrites in the PVN. We conclude that at least two distinct populations of NPY neurons innervate hypophysiotropic TRH neurons, the NPY neurons of the hypothalamic arcuate nucleus and the medullary adrenergic neurons that co-contain NPY.

Animals↗
PubMed1997

Functional characterization of caudal hypoglossal neurons by spectral patterns of neuronal discharges in the rat.

This study evaluated the spectral characteristics of neuronal discharges in the caudal hypoglossal nucleus and their physiological relevance in adult, male Sprague Dawley rats which were anaesthetized and maintained with pentobarbital sodium. Based on auto-spectral analysis of extracellular single-neuron activity, three spectral patterns were identified in the spontaneous discharges of hypoglossal neurons. Neurons that exhibited a rhythmic pattern manifested a concentrated peak in the auto-spectrogram that corresponded to the mean discharge rate. A majority of hypoglossal neurons displayed the modulated pattern, which was manifested either as scattered power densities (wide-band modulated pattern) or with a peak frequency component that was different from the mean discharge rate (narrow-band modulated pattern). Neurons that exhibited a mixed pattern displayed both rhythmic and modulated spectral patterns. Cross-spectral analysis further revealed that respiratory modulation constituted a major physiological influence on caudal hypoglossal neurons. The respiratory modulated pattern, however, could be converted to a mixed pattern in the presence of a central dipsogen, angiotensin III. The results suggest that the spectral patterns of neuronal discharges in caudal hypoglossal neurons represent manifestations of multiple physiological information, including that regarding respiration and dipsogenesis, which is encoded in these neurons. It was also shown that this information may only be revealed by auto-spectral and cross-spectral analysis of neuronal discharge signals.

Angiotensin III↗
PubMed1999

Vasoactive intestinal peptide neurons as synaptic targets for vasopressin neurons in the suprachiasmatic nucleus. Double-label immunocytochemical demonstration in the rat.

Cellular relationships between neurons producing vasopressin or vasoactive intestinal peptide in the suprachiasmatic nucleus of the hypothalamus, the main component of the central circadian timing system in mammals, were investigated in the rat using double immunocytochemistry. Analysis of serial confocal images revealed that the vasopressin-synthesizing neurons not only are important targets for the vasoactive intestinal peptide-synthesizing neurons, as previously demonstrated, but also establish reciprocal axosomatic contacts with these neurons, which have never been reported. On average, 5.4 vasoactive intestinal peptide contacts per vasopressin perikaryon and 1.7 vasopressin contacts per vasoactive intestinal peptide perikaryon were counted. That both types of neurons are linked by reciprocal synapses was confirmed at the electron microscopic level using a combination of immunoperoxidase and immunogold-silver labeling. Existence of an anatomical substrate for a vasopressinergic control of the vasoactive intestinal peptide neurons may have important functional consequences. In view (i) of the presumed, direct or indirect, involvement of the vasopressin neurons in relaying pacemaker information within and outside the suprachiasmatic nucleus, and (ii) of the established role of the vasoactive intestinal peptide neurons as the main light-sensitive cells, it provides support for a neuronal mechanism through which the circadian clock may regulate inputs related to environmental messages. Our electron-microscopic data also extended earlier observations, pointing to the involvement of vasopressin and vasoactive intestinal peptide terminals in so-called double synapses that, conceivably, could regulate neuronal synchronization in the suprachiasmatic nucleus. A morphological basis for non-synaptic interactions that could be involved in ephaptic and/or paracrine communication between both types of peptidergic neurons is also reported.

Animals↗
PubMed1999

Activity of voltage-operated calcium channels in rat cerebellar granule neurons and neuronal survival.

Neuronal activity and Ca2+ channel activation play important roles in neuronal survival and development. In cerebellar granule neurons, the culture conditions can induce differential expression of various membrane receptor proteins. To test the hypothesis that culture conditions might affect the activity of voltage-operated Ca2+ channels, the present study analysed the differences in Ca2+ signalling between granule neurons grown in the presence of normal (5 mM) or high (25 mM) KCl. The Ca2+ transients evoked by 50 mM KCl developed similarly in both cultures, as a function of age. In contrast, when compared with neurons grown in 25 mM KCl, a proportion of the neurons grown in normal KCl showed, between days in vitro 4 and 6, a higher Ca2+ transient in response to 12.5 mM KCl. These neurons were less sensitive to the effect of 10 microM nifedipine and, conversely, more sensitive to the effects of 10 microM omega-conotoxin MVIIC when stimulated with 50 mM KCl, indicating that they express preferentially, at this stage, the N- and/or Q-type Ca2+ channels. This period of maximal activity of the N/Q-type Ca2+ channels was associated with a significant increase in the rate of neuronal apoptosis. The present study also shows, by comparing the rates of neuronal apoptosis, that the long-term maintenance in 25 mM KCl appears to "synchronize" and sensitize the neuronal population to the apoptotic process. These results illustrate the differential effect the culture conditions can have on the expression and activity of Ca2+ channels, which, in turn, can modulate neuronal survival.

Animals↗