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PubMed1987

Excitation of upper cervical inspiratory neurons by inspiratory neurons of the nucleus retroambigualis in the cat.

The experiments reported here examined inputs from inspiratory neurons of the nucleus retroambigualis to upper cervical inspiratory neurons. Antidromic mapping in contralateral C1 demonstrated the existence of axon collaterals for 9 of 19 nucleus retroambigualis axons tested (47%). Forty nucleus retroambigualis neurons were tested with antidromic mapping for a projection to the ipsilateral C1 segment; 9/40 (22%) had an ipsilateral axon (8 of these also projected contralaterally), and 2/40 (5%) had an axon collateral in ipsilateral C1. Cross-correlation histograms suggested monosynaptic excitation of an upper cervical inspiratory neuron by a contralateral nucleus retroambigualis neuron in 4/69 cases (6%) and common input to the pair in 2/69 cases (3%). Six of the 69 cross-correlograms were computed during antidromic activation of the nucleus retroambigualis neuron, and one of these six demonstrated direct excitation of the upper cervical inspiratory neuron by the retroambigualis neuron. We concluded that at least some upper cervical inspiratory neurons receive monosynaptic excitation from the contralateral, and possibly the ipsilateral, nucleus retroambigualis inspiratory neurons. These results, together with those published elsewhere for inputs from inspiratory neurons in the contralateral ventrolateral nucleus tractus solitarius, suggest that the rhythmic, inspiratory firing pattern of the upper cervical inspiratory neurons is due to excitatory inputs from these two inspiratory bulbospinal neuron populations.

Animals↗
PubMed1994

D1 dopamine receptor agonist-induced Fos-like immunoreactivity occurs in basal forebrain and mesopontine tegmentum cholinergic neurons and striatal neurons immunoreactive for neuropeptide Y.

The present study sought to determine whether the D1 dopamine receptor agonist CY 208-243 increases Fos-like immunoreactivity in neurochemically distinct populations of interneurons in the 6-hydroxydopamine-denervated striatum. In vivo microdialysis studies indicate that cholinergic interneurons in the striatum are excited by the administration of CY 208-243 and that this effect is potentiated by dopaminergic deafferentation. Since Fos is considered to be a marker of neuronal activity, we examined the overlap between CY-208-243-induced Fos-like immunoreactivity and striatal cholinergic interneurons labelled with the cholinergic marker enzyme choline acetyltransferase. Unexpectedly, cholinergic interneurons in the striatum were not found to express Fos-like immunoreactivity. However, D1 agonist-induced Fos-like immunoreactivity was found in neurons immunoreactive for neuropeptide Y. Consequently, the failure of cholinergic neurons in the striatum to express D1 agonist-induced Fos-like immunoreactivity does not appear to be a general property of striatal interneurons. Indeed, CY 208-243 increased Fos-like immunoreactivity in choline-acetyltransferase-positive neurons in the basal forebrain and lateral dorsal tegmental nucleus. In the case of cholinergic basal forebrain neurons, administration of CY 208-243 has been shown to enhance the release of acetylcholine from their terminals located in the frontal cortex. Thus, unlike cholinergic interneurons in the striatum, the expression of Fos-like immunoreactivity in cholinergic basal forebrain neurons is correlated with an increase in transmitter release. Choline acetyltransferase immunoreactivity was markedly reduced in cholinergic basal forebrain neurons ipsilateral to the 6-hydroxydopamine lesion. This decrease in choline acetyltransferase immunoreactivity was confined to a pocket of cortically projecting neurons located in the posterior part of the horizontal limb of the diagonal band which included the medial preoptic nucleus. Interestingly, D1 agonist-induced Fos-like immunoreactivity was located predominantly in those cholinergic neurons which displayed depressed choline acetyltransferase immunoreactivity. Since Fos is often induced as a consequence of increased activity, it is tempting to speculate that those neurons which stained weakly for choline acetyltransferase had been excited by the D1 agonist administration. Accordingly, the destruction of mesencephalic dopaminergic neurons with 6-hydroxydopamine may have deprived these cholinergic neurons of an excitatory D1 receptor-mediated drive, resulting in a reduction of choline acetyltransferase immunoreactivity. These results suggest that the degeneration of nigrostriatal dopamine neurons may contribute to the loss of cholinergic basal forebrain function in Parkinson's disease.

Acetylcholine↗
PubMed2003

Enkephalinergic striatal projection neurons become less affected by quinolinic acid than substance P-containing striatal projection neurons as rats age.

While the excitotoxic vulnerability of striatal neurons is known to be greater in juvenile than adult animals, it is uncertain if striatal neuron types decline differentially in their vulnerability with age. To examine this issue, we unilaterally injected quinolinic acid (QA), an N-methyl-d-aspartate (NMDA) receptor agonist, into the striatum of juvenile and adult rats, and used in situ hybridization histochemistry with oligonucleotide probes for preproenkephalin and preprotachykinin mRNA to label surviving enkephalinergic (ENK) and substance P-containing (SP) neurons in adjacent sections through the injection center. The results confirmed that the region of severe damage is greater in young than adult animals, but revealed that at the very center of the QA injection, labeled neuron abundance was lower in adult than juvenile striatum. In juvenile rats, the vulnerability of the ENK neurons at all distances from the injection center was the same as that of the SP neurons. By contrast, in adult rats, the ENK neuron survival was greater than the SP neuron survival at all distances beyond the lesion center. The SP neuron survival outside the injection center in the adult rats was similar to that in juvenile rats, while the ENK neuron survival beyond the injection center was better in adult than juvenile rats. These data indicate that there is an age-dependent decrease in the vulnerability of ENK but not SP striatal projection neurons to QA-mediated injury in rats. The results also raise the possibility that, if an excitotoxic process is involved in HD pathogenesis, a differential age-related decline in the sensitivity of striatal projection neuron types to this process may contribute to the more uniform striatal neuron loss in juvenile-onset Huntington's disease (HD) and the more differential loss in adult-onset HD.

Aging↗
PubMed2005

Degeneration of dopaminergic neurons triggers an expression of individual enzymes of dopamine synthesis in non-dopaminergic neurons of the arcuate nucleus in adult rats.

Non-dopaminergic neurons expressing individual complementary enzymes dopamine (DA) synthesis were shown to produce DA in cooperation [Ugrumov, M., Melnikova, V., Ershov, P., Balan, I., Calas A., 2002. Tyrosine hydroxylase- and/or aromatic L-amino acid decarboxylase-expressing neurons in the rat arcuate nucleus: ontogenesis and functional significance. Psychoneuroendocrinology 27, 533-548; Ugrumov, M.V., Melnikova, V.I., Lavrentyeva, A.V., Kudrin, V.S., Rayevsky, K.S., 2004. Dopamine synthesis by non-dopaminergic neurons expressing individual complementary enzymes of the dopamine synthetic pathway in the arcuate nucleus of fetal rats. Neuroscience 124, 629-635]. This study was aimed at testing our hypothesis that the cooperative synthesis of DA in non-dopaminergic neurons is an adaptive reaction under functional insufficiency of the dopaminergic system. Functional insufficiency of the tuberoinfundibular dopaminergic system was provoked by 6-OHDA-induced degeneration of dopaminergic neurons in the arcuate nucleus in adult rats. Bienzymatic (dopaminergic) neurons and monoenzymatic neurons expressing tyrosine hydroxylase (TH) or aromatic L-amino acid decarboxylase (AADC) were detected with a double-immunofluorescent technique on cryostat sections. The 6-OHDA-induced degeneration of dopaminergic neurons was accompanied by a significant increase of the number of monoenzymatic TH neurons and AADC neurons that appears to support our hypothesis. The reaction of bienzymatic and monoenzymatic neuron populations to the 6-OHDA administration occurred to be region-specific. The former disappeared in the dorsomedial region of the arcuate nucleus while the latter increased in the ventrolateral region. Thus, degeneration of dopaminergic neurons in the arcuate nucleus of adult rats is accompanied by the expression of individual enzymes of DA synthesis in non-dopaminergic neurons that may be an adaptive reaction.

Adrenergic Agents↗
PubMed2004

Astrocytes repress the neuronal expression of GLAST and GLT glutamate transporters in cultured hippocampal neurons from embryonic rats.

Glutamate extracellular levels are regulated by specific transporters. Five subtypes have been identified. The two major ones, GLAST and GLT (glutamate transporters 1 and 2, respectively), are localized in astroglia in normal mature brain. However, in neuron-enriched hippocampal cultures, these proteins are expressed in neurons during the early in vitro development (Plachez et al., 2000). Here, we show that, in these cultures, GLAST and GLT neuronal expression is transient and no longer observed after 7 days in vitro, a stage at which the few astrocytes present in the culture are maturing. Moreover, we demonstrate that these few astrocytes are responsible for the repression of this neuronal expression. Indeed, addition of conditioned medium prepared from primary cultures of hippocampal astrocytes, to cultured hippocampal neurons, rapidly leads to the suppression of neuronal GLAST expression, without affecting neuronal GLT expression. However, when neurons are seeded and co-cultured on a layer of hippocampal astrocytes, they do not develop any immunoreactivity towards GLAST or GLT antibodies. Altogether, these results indicate that glia modulate the expression of GLAST and GLT glutamate transporters in neurons, via at least two distinct mechanisms. Neuronal GLAST expression is likely repressed via the release or the uptake of soluble factors by glia. The repression of neuronal GLT expression probably results from glia-neuron interactions. This further reinforces the fundamental role of direct or indirect neuron-glia interactions in the development of the central nervous system.

Amino Acid Transport System X-AG↗
PubMed1998

Nerve growth factor maintains regulation of intracellular calcium in neonatal sympathetic neurons but not in mature or aged neurons.

We examined the effects of nerve growth factor on the regulation of intracellular calcium levels of superior cervical ganglion neurons in terms of postnatal maturation and ageing. Rat superior cervical ganglion neurons from three age groups (neonatal: 0 to one-day-old, young adult: three to six-month-old, and aged: more than 24-month-old) were dissociated and cultured in the presence or absence of 100 ng/ml of nerve growth factor. Intracellular free calcium levels ([Ca2+]i) were measured using the fura-2 microfluorometry. Nerve growth factor treatment increased the resting [Ca2+]i of neonatal neurons, although it had no effect on those of mature and aged neurons. We further examined the effects of nerve growth factor on the transient increase of [Ca2+]i induced by methacholine (0.1 mM), caffeine (20 mM) or high-potassium medium (40 mM K+). Nerve growth factor pre-treatment significantly increased the population of neonatal superior cervical ganglion neurons which responded to methacholine, whereas almost all young adult and aged neurons responded to methacholine regardless of pre-treatment of nerve growth factor. Caffeine induced a cyclic alteration of [Ca2+]i (oscillation) in 45% of the neonatal superior cervical ganglion neurons when they were maintained without nerve growth factor, but nerve growth factor treatment suppressed the oscillation to 10% of neurons. In contrast to neonatal neurons, all of the young adult and aged neurons showed only a transient increase of [Ca2+]i in response to caffeine independent of nerve growth factor treatment. There was no significant effect of nerve growth factor on K+ depolarization-induced [Ca2+]i elevations at any of the ages studied. Nerve growth factor did not substantially alter the pattern of the transients induced by these three agents. Our results indicate that exogenous nerve growth factor is necessary to maintain normal acetylcholine receptor-mediated [Ca2+]i responses as well as Ca(2+)-induced Ca2+ release from intracellular calcium storage in neonatal superior cervical ganglion neurons. In mature superior cervical ganglion neurons, Ca2+ homeostasis becomes independent of exogenous nerve growth factor, and Ca2+ homeostasis and its independency are well preserved in aged neurons.

Aging↗
PubMed2002

Rhythmic activities of the sympatho-excitatory neurons in the medulla of rabbits: neurons controlling cutaneous vasomotion.

Spontaneous activities of the reticulospinal neurons in the reticular formation of the rostroventral medulla, of the ear sympathetic nerve (ESNA) and of the renal sympathetic nerve (RSNA) were analyzed with regard to cardiac cycle- and respiration-related rhythm in the anesthetized, vagotomized and immobilized rabbits. A reticulospinal neuron that was concurrently excited with increase in the ESNA and/or reduction of the blood flow of the ear skin by electrical stimulation of the dorsomedial hypothalamus was tentatively named as a cutaneous sympatho-excitatory neuron (Cu neuron). More than half of the Cu neurons (13/22) had a respiration-related rhythmic activity as well as the ESNA. Activity of most of the Cu neurons (19/22) was not modulated with the frequency of the heartbeat and the ESNA had little or no cardiac cycle-related activity. Simultaneous recording shows that the degree of modulation (relative power of the power spectrum of the post event time histogram at the frequency of the respiration) of activity of the Cu neurons correlated with that of the ESNA. On the other hand, most (13/18) of the barosensitive sympatho-excitatory reticulospinal neurons in the rostral ventrolateral medulla (RVLM neurons) had both cardiac cycle- and respiration-related activity as well as the RSNA had. The Cu neurons were located at the medial sites to the location of the RVLM neurons. These results further showed that the Cu neurons controlled the cutaneous vasoconstrictor fibers and that the sympatho-excitatory neurons were located at the different sites in the ventral medulla according to their function.

Adrenergic Fibers↗
PubMed1982

Lateral hypothalamic neurones: osmosensitivity and the influence of activating magnocellular neurosecretory neurones.

1. The activity of single cells in the supraoptic nucleus and the lateral hypothalamus of urethane-anaesthetized rats was studied during electrical stimulation of the neural stalk.2. Neurones activated antidromically from the neural stalk were either unaffected or, rarely, slightly affected by single shocks or by brief trains of shocks presented at an intensity just below that necessary for antidromic invasion. Thus there does not appear to be a strong synaptic coupling between rat supraoptic neurones.3. In contrast, many lateral hypothalamic neurones, and particularly those in the perinuclear zone, were strongly affected by neural stalk stimulation, being either orthodromically excited or inhibited. Thus, rat magnocellular neurosecretory neurones appear to project, directly or indirectly, to the lateral hypothalamus.4. Thirty-one lateral hypothalamic neurones were studied following an I.P. injection of 1 ml. 1.5 M-NaCl. Eighteen neurones responded to this osmotic stimulus with a change of at least 1 spike/sec in mean firing rate.5. Fifteen of the thirty-one neurones were strongly affected by neural stalk stimulation (eight inhibited, seven excited). Ten of these fifteen neurones were affected in the same way by osmotic stimulation. The remaining sixteen out of thirty-one neurones were unresponsive to neural stalk stimulation, and of these, ten were also unresponsive to osmotic stimulation. Thus most lateral hypothalamic neurones responded in a similar way to neural stalk stimulation and to systemic osmotic stimulation.6. Thus the osmosensitivity of some neurones in the lateral hypothalamus may be mediated by synaptic input arising from the magnocellular neurosecretory neurones. However, the osmosensitivity of some lateral hypothalamic neurones cannot be explained in this way, and probably derives from osmoreceptors other than the magnocellular neurones.

Animals↗
PubMed1995

Neuronal discharge of preoptic/anterior hypothalamic thermosensitive neurons: relation to NREM sleep.

Thermosensitive neurons of the preoptic/anterior hypothalamic area (POAH) have been implicated in the regulation of non-rapid eye movement (NREM) sleep. We attempted to identify those medial POAH thermosensitive neurons that may be involved in NREM sleep regulation. The thermosensitivity of medial POAH neurons was studied in five freely moving adult cats by local cooling or warming of the medial POAH with a water-perfused thermode. Of 308 neurons, 65 (21%) were classified as thermosensitive, including 31 (10%) warm-sensitive and 34 (11%) cold-sensitive neurons. The spontaneous discharge rates of 28 warm-sensitive, 34 cold-sensitive, and 115 randomly selected thermoinsensitive neurons were recorded through one to three sleep-waking cycles. Patterns of spontaneous activity for warm- and cold-sensitive neurons were different. Of 28 warm-sensitive neurons, 18 (64%) exhibited increased discharge rate during NREM sleep compared with waking (NREM/wake, > or = 1.2). This subpopulation of warm-sensitive neurons also exhibited significantly increased thermosensitivity when tested during NREM sleep. Of 34 cold-sensitive neurons, 25 (74%) discharged more slowly during NREM sleep compared with waking (NREM/wake, < or = 0.8). This subpopulation of cold-sensitive neurons exhibited decreased thermosensitivity during NREM sleep. These results are consistent with a hypothesis that the activation of sleep-related warm-sensitive neurons and the deactivation of wake-related cold-sensitive neurons may play a key role in the onset and regulation of NREM sleep.

Animals↗
PubMed1987

Functional associations among simultaneously monitored lateral medullary respiratory neurons in the cat. II. Evidence for inhibitory actions of expiratory neurons.

Arrays of extracellular electrodes were used to monitor simultaneously several (2-8) respiratory neurons in the lateral medulla of anesthetized, paralyzed, bilaterally vagotomized, artificially ventilated cats. Efferent phrenic nerve activity was also recorded. The average discharge rate as a function of time in the respiratory cycle was determined for each neuron. Most cells were tested for spinal or vagal axonal projections using antidromic stimulation methods. Cross-correlational methods were used to analyze spike trains of 480 cell pairs. Each pair included at least one neuron most active during the expiratory phase. All simultaneously recorded neurons were located in the same side of the brain stem. Twenty-six percent (33/129) of the expiratory (E) neuron pairs exhibited short time scale correlations indicative of paucisynaptic interactions or shared inputs, whereas 8% (27/351) of the pairs consisting of an E neuron and an inspiratory (I) cell were similarly correlated. Evidence for several inhibitory actions of E neurons was found: 1) inhibition of I neurons by E neurons with both decrementing (DEC) and augmenting (AUG) firing patterns; 2) inhibition of E-DEC and E-AUG neurons by E-DEC cells; 3) inhibition of E-DEC and E-AUG neurons by E-AUG neurons; and 4) inhibition of E-DEC neurons by tonic I-E phase-spanning cells. Because several cells were recorded simultaneously, direct evidence for concurrent parallel and serial inhibitory processes was also obtained. The results suggest and support several hypotheses for mechanisms that may help to generate and control the pattern and coordination of respiratory motoneuron activities.

Animals↗
PubMed1996

Anatomy and physiology of saccadic long-lead burst neurons recorded in the alert squirrel monkey. II. Pontine neurons.

1. The discharge patterns and axonal projections of saccadic long-lead burst neurons (LLBNs) with somata in the pontine reticular formation were studied in alert squirrel monkeys with the use of the method of intraaxonal recording and horseradish peroxidase injection. 2. The largest population of stained neurons were afferents to the cerebellum. They originated in the dorsomedial nucleus reticularis tegmenti pontis (NRTP) including its dorsal cell group (N = 5), the preabducens intrafascicular nucleus (N = 5), and the raphe pontis (N = 1). Axons of all neurons coursed under NRTP and entered brachium pontis without having synapsed in the brain stem. Three axons sent collaterals to the floccular lobe, but other more distant targets of these and the other cerebellar afferents could not be determined. Movement fields of these neurons were intermediate between vectorial and directional types. 3. Four neurons had their somata in nucleus reticularis pontis oralis and terminations in the brain stem reticular formation. Each neuron was different, but all terminated in the region containing excitatory burst neurons, and most terminated in the region containing inhibitory burst neurons. Other targets include nucleus reticularis pontis oralis and caudalis, NRTP, raphe interpositus, and the spinal cord. Discharge patterns included both vectorial and directional types. 4. Two reticulospinal neurons had large multipolar somata either just rostral or ventral to the abducens nucleus. These neurons also projected to the medullary reticular formation, caudal nucleus prepositus hypoglossi, and dorsal and ventral paramedian reticular nucleus. 5. The functional implications of the connections of these LLBNs and those reported in the companion paper are extensively discussed. The fact that the efferents of the superior colliculus target the regions containing medium-lead saccadic burst neurons confirms the role of the colliculus in saccade generation. However, the finding that many other neurons project to these regions and the finding that superior colliculus efferents project more heavily to areas containing reticulospinal neurons argue for a diminished role of the superior colliculus in saccade generation but an augmented role in head movement control.

Animals↗
PubMed1981

Effect of non-neuronal cells on peptide content of cultured sensory neurones.

The peptide substances P (SP) and somatostatin (SOM) are present in small-diameter neurones of dorsal root ganglia (DRG) and in small-diameter fibres that project to the spinal cord dorsal horn. It is not known whether SP or SOM coexist with other transmitter molecules but, since both peptides can be released from sensory neurones and both can alter neuronal firing rates in the dorsal horn, it seems likely that they are involved in some way in synaptic transmission in the spinal cord. SP has generally excitatory effects in the spinal cord whereas SOM exerts inhibitory effects, and it is not at all clear which subclass of nociceptive afferents contain SP or SOM. Mudge, Leeman & Fischbach (1979) have studied sensory neurones derived from chick DRG grown in dissociated cell culture. When the neurones are grown in the absence of non-neuronal cells, they contain SP but relatively little SOM. The amount of SOM produced by these neurones is greatly increased (c. 50-fold) when the neurones are grown together with ganglionic non-neuronal cells or with medium 'conditioned' by incubation with such cells. The increase in SOM content is not accompanied by an increase in SP content or a detectable change in neuronal survival. The DRG non-neuronal cells consist of two major cell types--glial cells and fibroblasts. Indirect evidence suggests that glial cells rather then fibroblasts are responsible for the increased production of SOM by the neurones. Raff and his colleagues (Brockes, Fields & Raff, 1979) have used immunological techniques to obtain purified cultures of these two cell types. Work currently in progress is aimed at extending the above observations to the rat and firmly establishing whether glial cells can indeed influence SOM production in sensory neurones.

Animals↗
PubMed2006

Histaminergic neurons protect the developing hippocampus from kainic acid-induced neuronal damage in an organotypic coculture system.

The central histaminergic neuron system inhibits epileptic seizures, which is suggested to occur mainly through histamine 1 (H1) and histamine 3 (H3) receptors. However, the importance of histaminergic neurons in seizure-induced cell damage is poorly known. In this study, we used an organotypic coculture system and confocal microscopy to examine whether histaminergic neurons, which were verified by immunohistochemistry, have any protective effect on kainic acid (KA)-induced neuronal damage in the developing hippocampus. Fluoro-Jade B, a specific marker for degenerating neurons, indicated that, after the 12 h KA (5 microM) treatment, neuronal damage was significantly attenuated in the hippocampus cultured together with the posterior hypothalamic slice containing histaminergic neurons [HI plus HY (POST)] when compared with the hippocampus cultured alone (HI) or with the anterior hypothalamus devoid of histaminergic neurons. Moreover, alpha-fluoromethylhistidine, an inhibitor of histamine synthesis, eliminated the neuroprotective effect in KA-treated HI plus HY (POST), and extracellularly applied histamine (1 nM to 100 microM) significantly attenuated neuronal damage only at 1 nM concentration in HI. After the 6 h KA treatment, spontaneous electrical activity registered in the CA1 subregion contained significantly less burst activity in HI plus HY (POST) than in HI. Finally, in KA-treated slices, the H3 receptor antagonist thioperamide enhanced the neuroprotective effect of histaminergic neurons, whereas the H1 receptor antagonists triprolidine and mepyramine dose-dependently decreased the neuroprotection in HI plus HY (POST). Our results suggest that histaminergic neurons protect the developing hippocampus from KA-induced neuronal damage, with regulation of neuronal survival being at least partly mediated through H1 and H3 receptors.

Animals↗
PubMed1991

Properties of "possibly" cholinergic neurons ascending from the rat ponto-mesencephalic area: comparison with noradrenergic and serotonergic neurons.

In urethane-anesthetized rats single neuronal activity was recorded in the laterodorsal tegmental nucleus, which has a dense complement of cholinergic neurons. In many experiments neuronal activity was recorded also in the dorsal raphe and locus coeruleus for comparison. In each experiment two to five active sites were marked with pontamine sky blue, deposited from the recording electrode ionophoretically and located histologically. Most neurons of the laterodorsal tegmental nucleus responded antidromically to stimulation of either one or more of the following sites: medial frontal cortex, medial septal nucleus, lateral geniculate nucleus or superior colliculus. Conduction velocities of their axons, estimated from latencies of antidromic responses, were within the range of unmyelinated fibers. Most of them gave rise to broad spikes (positive stroke, greater than 1.0 msec; negative stroke, greater than 3.0 msec), resembling monoaminergic neurons. Others generated brief spikes (positive and negative strokes, less than 0.8 and less than 2.2 msec). The former are probably cholinergic. Some neurons in the laterodorsal tegmental nucleus had rather regular spontaneous firing at a low rate (0.2-5 Hz), while others were not spontaneously active. Their response to noxious stimulation (tail pinch) was different from neuron to neuron, but that most frequently encountered was limited to phasic excitation, in contrast to locus coeruleus neurons which showed phasic excitation followed by mild tonic excitation; and to dorsal raphe neurons likely to be suppressed. Upon repetition of tail pinch the response of laterodorsal tegmental nucleus neurons tended to become weak or disappear while a desynchronized pattern continued to appear in the EEG in each occasion. Thus, putative cholinergic neurons, which constitute a major group in the laterodorsal tegmental nucleus, have properties similar to those of monoaminergic neurons, except for the phasic and decrementing nature of their response to tail pinch. The cholinergic, noradrenergic, and serotonergic ascending projections seem likely to subserve different roles in regulating activity of the forebrain.

Action Potentials↗
PubMed1988

Neurite outgrowth in individual neurons of a neuronal population is differentially regulated by calcium and cyclic AMP.

In identified Helisoma neurons, intracellular calcium can regulate neurite elongation and growth cone motility. Neurotransmitters such as 5-HT suppress both neurite elongation and the filopodial and lamellipodial movements of growth cones by causing increases in intracellular calcium (Haydon et al., 1984; Cohan et al., 1987; Mattson and Kater, 1987). Since an additional second messenger, cyclic AMP (cAMP), is known to mediate many physiological effects of neurotransmitters, we tested (1) the possible involvement of cAMP in the regulation of neurite outgrowth from Helisoma buccal neurons and (2) calcium-cAMP interrelationships in the regulation of outgrowth. The cAMP-elevating agents forskolin (5 x 10(-6)-10(-4) M) and dibutyryl cAMP (dbcAMP; 5 x 10(-3)-10(-2) M) suppressed neurite elongation and growth cone movements in identified neurons B19 (5-HT sensitive) and B5 (5-HT insensitive); the suppression was reversible. Exposure of these particular identified neurons to the calcium channel blocker La3+ (10(-5) M) or a culture medium with reduced calcium prevented and reversed the suppressive effects of forskolin and dbcAMP. In order to determine if the results on neurons B5 and B19 were representative of all neurons or only a subset, we examined a larger population of neurons. Calcium ionophore A23187 suppressed outgrowth from all neurons in mass dissociate cultures of buccal neurons, while forskolin or dbcAMP plus IBMX suppressed outgrowth from only one-half of buccal neurons. Finally, we found that 2 subpopulations exist among the neurons whose outgrowth is suppressed by cAMP: One subpopulation requires calcium influx for cAMP to act, while the other does not. Thus, even within the relatively small population of neuronal types comprising the buccal ganglion of Helisoma, second messengers within different neurons can act and interact in different ways to regulate outgrowth.

Animals↗
PubMed1986

Differential survival of fetal and adult neurons and non-neuronal cells exposed chronically to ethanol in cell culture.

Neural cell cultures of dissociated dorsal root ganglia (DRG) were used to investigate the effect of chronic ethanol exposure on the differential survival of fetal and adult neurons and non-neuronal cells. After 12 days of culture in ethanol (20 DIV), counts were made of both neurons and non-neural cells. Unexpectedly, the adult neurons showed a slightly greater degeneration with increasing ethanol than fetal neurons; the adult and the fetal neurons had LD50s of 1.78 and 2.08 gm% respectively. In contrast, for the non-neuronal cells the differential response was reversed; the fetal non neuronal cells were more affected than the adult non neuronal cells with LD50s of 0.7 gm% and 0.94 gm% for fetal and adult non-neuronal cells respectively. Also independent of developmental stage, the non-neuronal cells were 2 to 3 times more sensitive (in terms of survival) to increasing ethanol than the neurons. Electron microscopic examination suggested an increased amount of lipofuscin and dilated endoplasmic reticulum in the adult neurons exposed to ethanol. The possible significance of the results to fetal alcohol syndrome (FAS) is discussed.

Age Factors↗
PubMed1986

Mauthner neurons survive metamorphosis in anurans: a comparative HRP study on the cytoarchitecture of Mauthner neurons in amphibians.

Giant medullary neurons were revealed in adult Xenopus laevis and Rana esculenta following HRP injections to the spinal cord. These neurons were identified as Mauthner neurons because (1) they have the same position and orientation as the larval Mauthner neurons, i.e., they lie at the level of the VIIIth nerve root. (2) they have two large dendritic trees that for each species are similar to those of the larval Mauthner neurons, (3) they are clearly distinguishable from other large reticular neurons, (4) they have close connections with the VIIIth nerve afferents, (5) they have a decussating descending axon, the largest of the adult brainstem, and (6) they have a reduced axon cap, i.e., a dense neuropil without cap dendrites. Mauthner neurons were also identified in adult Xenopus muelleri, Hymenochirus curtipes, Hyla cinerea, Rhacophorus leucomystax, and Kalula pulchra. No Mauthner neuron was identified in larval or adult Bombina bombina or Bufo bufo or in adult Bufo terrestris, Bombina orientalis, or Scaphiopus holbrookii. Cytoarchitecture and the elaborate dendritic trees were also revealed in urodeles. Mauthner neurons of terrestrial forms (Ambystoma tigrinum, Paramesotriton chinensis) exhibit a less-extensive branching of the "lateral line" dendrite but otherwise show no signs of involution or regression compared to aquatic forms (Siredon mexicanum, Cynops pyrrhogaster). No Mauthner neuron was identified in larval or adult Ichthyophis kohtaoensis. Besides the topographical relations between Mauthner neurons and afferent fibers from the lateral line and the VIIIth nerve we could demonstrate a projection of trigeminal and mesencephalic neurons onto the soma of the amphibian Mauthner neuron.

Ambystoma↗
PubMed1989

Brainstem projecting neurons in the rat basal forebrain: neurochemical, topographical, and physiological distinctions from cortically projecting cholinergic neurons.

Magnocellular regions of the basal forebrain contain cholinergic neurons that project to the cerebral cortex. Neurons in the same basal forebrain regions innervate the brainstem. The present study investigated whether these brainstem projecting neurons are cholinergic, project also to the cortex, and share similar physiological properties as cortically projecting neurons. Data with retrograde tracing from various regions of the pons, medulla, and cortex combined with choline acetyltransferase immunofluorescence indicated that: 1) brainstem projecting neurons are usually segregated from cortically projecting and/or cholinergic neurons in the basal forebrain, 2) virtually no brainstem projecting neurons in the basal forebrain are cholinergic, and 3) only rarely do basal forebrain neurons have axon collaterals that project to both cortex and brainstem. Extracellular recordings from basal forebrain neurons confirmed the paucity of axonal collateralization and the topographic segregation between cortically and brainstem projecting basal forebrain neurons, and, in addition, showed that brainstem projecting neurons have a slower mean conduction velocity than cortically projecting neurons. These observations suggest that basal forebrain neurons projecting to the brainstem (pons, medulla) and the cortex represent separate cell populations in terms of projections, neurotransmitter content, distribution, and physiological properties.

Action Potentials↗