Superior Cervical Ganglion Cells Research Articles

Sympathetic neurons outlive the original host after transplantation to the rat submandibular gland

Sympathetic ganglion tissue of aged (36 months) Wistar rats was allotransplanted into the submandibular gland (SMG) of young (3 months) animals to study whether sympathetic neurons can outlive the original host. The visbility of the transplants was evaluated one yeat postgrafting, using the formaldehyde-induced fluorescence technique (FIF) for histochemical demonstration of catecholamines, tyrosine hydroxylase (TH) immunohistochemistry, and morphometry. One year after transplantation, grafted superior cervical ganglion (SCG) cells demonstrated catecholamine fluorescence and tyrosine hydroxylase immunoreactivity. The transplants consisted of groups of sympathetic neurons dispersed in a fibrous matrix. After long postgrafting time, the sympathetic neurons of aged rats showed several signs of enhanced degeneration; increased autofluoroscent lipopigment, decreased neuronal density and reduced catecholamine fluorescence. The mean diameter of the transplanted aged neurons was significantly decreased. The histograms of grouped diameter values showed a shift to smaller cells in ganglion transplants. A subpopulation of small and medium-sized grafted neurons sent out fluorescent fibers, which were located in a fibrous scar area but did not extend into submandibular host tissue. The results indicate that a long postgrafting time induced degeneration which is comparable to normal aging changes in grafted very old neurons. Thus, aged sympathetic neurons maintain plasticity to survive as transplants, and under favourable conditions these neurons outlive the original host.

Cyclic AMP modulates but does not mediate the inhibition of [ 3H]norepinephrine release by activation of alpha-2 adrenergic receptors in cultured rat ganglion cells

The purpose of this study was to determine whether a decrease in cyclic AMP accumulation mediates the inhibition of norepinephrine release in response to alpha-2 adrenergic receptor activation in cultured rat superior cervical ganglion cells. Superior cervical ganglia from neonatal rats were dissociated and cultured on collagen-coated plastic strips. Neurotransmitter release was assessed by measuring the fractional overflow of tritium in superfused cells prelabeled with [ 3H]norepinephrine. Intracellular cyclic AMP accumulation was measured using radioimmunoassay. Electrical field stimulation at 1 Hz, 30 pulses, 1 ms duration at 20 min intervals produced an increase in the fractional overflow of tritium that was composed predominantly of intact [ 3H]norepinephrine. The alpha-2 adrenergic receptor agonist UK-14,304 dose-dependently attenuated the increase in fractional tritium overflow elicited by electrical field stimulation. The adenylyl cyclase activator, forskolin, increased cyclic AMP accumulation in superior cervical ganglion cells and UK-14,304 dose-dependently inhibited forskolin-stimulated cyclic AMP accumulation. UK-14,304 had no effect on basal cyclic AMP accumulation or cyclic AMP accumulation during electrical field stimulation. Forskolin (1–10 μM) or the non-hydrolysable cAMP analog, 8-(4-chlorophenylthio)adenosine 3′,5′-cyclic monophosphate (1–100 μM), slightly increased basal and dose-dependently potentiated the increase in fractional tritium overflow in response to electrical stimulation. Despite enhancement by forskolin and 8-(4-chlorophenylthio)adenosine 3′,5′-cyclic monophosphate of fractional tritium overflow caused by electrical field stimulation, UK-14304 (1–10 μM) reduced release to a similar degree as that observed in the absence of forskolin or 8-(4-chlorophenylthio)adenosine 3′,5′-cyclic monophosphate. These data suggest that in cultured rat superior cervical ganglion cells, stimulation of alpha-2 adrenergic receptors decreases cyclic AMP accumulation when adenyl cyclase is activated. A decrease in cyclic AMP does not mediate the inhibition of [ 3H]norepinephrine release in response to alpha-2 adrenergic receptor activation, although elevations in cyclic AMP can enhance electrically-stimulated release of [ 3H]norepinephrine.

Caffeine promotes survival of cultured sympathetic neurons deprived of nerve growth factor through a cAMP-dependent mechanism

The effects of caffeine on neuronal survival independent of trophic factor support were examined in developing superior cervical ganglion in vitro. We found that caffeine promoted neuronal survival in the absence of nerve growth-factor (NGF) in a dose-dependent manner ( EC 50 = 6 mM ). Pulse treatment with caffeine or high K + (40 mM), which caused only a transient increase in intracellular free Ca 2+ levels ([Ca 2+] i), did not promote survival. In contrast, caffeine potentiated the saving effect of various phosphodiesterase inhibitors including theophylline ( EC 50 = 3 mM ) and 3-isobutyl-1-metylxanthine ( EC 50 = 0.4 mM ). Non-xanthine phosphodiesterase inhibitor Ro 20–1724 potentiated the survival promoting effect of caffeine or IBMX. Indeed, administration of 20 mM caffeine rapidly restored the cAMP level of NGF-deprived neurons to normal (0.34 pmol/well) within 10 min; the level reached a plateau level (0.69 pmol/well) at 10 h. Even after 1 day, the sustained level was maintained in the presence of caffeine. In contrast, noradrenaline and isoproterenol, which cause only a transient increase in cAMP levels, did not support survival. These data, in conjunction with others, suggest that sustained levels of second messengers, including not only the [Ca 2+] i but also the cAMP level, would support the survival of superior cervical ganglion cells independent of trophic factor support.

A monoclonal anti-glycoconjugate antibody defines a stage and position-dependent gradient in the developing sympathoadrenal system

The expression of complex carbohydrate antigens was analysed in developing sympathoadrenal cells of the rat using monoclonal antibodies that react with unique carbohydrate structures. CC1 and CC4 are monoclonal antibodies that react specifically with beta-N-acetylgalactosamine and alpha-galactose/alpha-fucose moieties, respectively. CC1-reactive glycoconjugates are expressed in embryonic superior cervical ganglion (SCG) cells as early as embryonic day 15 (E15). CC4 is expressed in the SCG only for a brief period starting at E18 and then disappearing at P5. During their transient period of expression, CC1 antigens are expressed uniformly throughout the SCG at E15-17, but are then restricted to the rostral portion of the SCG from E18 to P4. CC4 is also concentrated in the rostral portion of the SCG between E21 and P4. In the adrenal medulla, CC1 and CC4 antigens display a post-natal onset of expression commencing approximately at P14 and continue to be expressed on a subset of cells which contain tyrosine hydroxylase (TH). The expression of CC1, however, is restricted to phenylethanolamine-N-methyltransferase-(PNMT)-negative chromaffin cells, whereas CC4 is not. CC1 and CC4-expressing cells appear to be scattered throughout the adrenal medulla without any particular topographic orientation. These findings suggest that the CC1 monoclonal antibody defines a stage-specific differentiation antigen in the sympathoadrenal lineage. Additionally, the CC1 antigen may confer important positional information in the embryonic SCG by distinguishing rostral from caudal neuronal cell bodies.

Effect of neurotransmitters on axoplasmic transport: acetylcholine effect on superior cervical ganglion cells

The effect of acetylcholine (ACh) on particle movements along axons of cultured superior cervical ganglion cells was analyzed with a computer-assisted video-enhanced differential interference contrast microscope system. ACh suppressed the axoplasmic transport reversibly in both anterograde and retrograde directions. A muscarinic agonist, arecoline, mimicked the ACh effect, but nicotine did not. An experiment with the Ca 2+-indicator dye, fura-2, revealed that ACh suppressed the transport without any change of intracellular Ca 2+ concentration. ACh also suppressed the axoplasmic transport in Ca 2+-free medium. Islet-activating protein (IAP), pertussis toxin, blocked the ACh effect. These results indicate that ACh activates muscarinic receptors and suppresses fast axoplasmic transport through the activation of IAP-sensitive GTP-binding protein, irrespective of Ca 2+ ions.

Regulation of tyrosine hydroxylase gene expression in the rat carotid body by hypoxia.

The activity (Vmax) of tyrosine hydroxylase (TH; EC 1.14.16.2), the rate limiting enzyme in the synthesis of catecholamines, is increased in carotid body, superior cervical ganglion, and the adrenal medulla during hypoxia (i.e., reduced PaO2). The present study was undertaken to determine if the increase in TH activity in these tissues during hypoxia is regulated at the level of TH mRNA. Adult rats were exposed to hypoxia (10% O2) or room air for periods lasting from 1 to 48 h. The carotid bodies, superior cervical ganglia, and adrenals were removed and processed for in situ hybridization using 35S-labeled oligonucleotide probes. The concentration of TH mRNA was increased by hypoxia at all time points in carotid body type I cells, but not in cells of either superior cervical ganglion or adrenal medulla. The increase in TH mRNA in carotid body during hypoxia did not require innervation of the carotid body or intact adrenal glands. In addition, hypercapnia, another physiological stimulus of carotid body activity, failed to induce an increase in TH mRNA in type I cells. Our findings suggest that hypoxia stimulates TH gene expression in the carotid body by a mechanism that is intrinsic to type I cells.

Mechanism of Neurotransmitter Release Elicited by the Preferential ?1-Adrenergic Receptor Agonist Phenylephrine in Superfused Superior Cervical Ganglion Cells in Culture

Phenylephrine increased [3H]norepinephrine efflux and accumulation of cyclic AMP in cultured rat superior cervical ganglion cells superfused with Tyrode's solution. The purpose of this study was to determine the mechanism and relationship between these two events. Electrical stimulation (1-2 Hz), potassium chloride (50 mM), and the preferential alpha 1-adrenergic receptor agonist phenylephrine (1-100 microM) increased fractional tritium efflux, whereas methoxamine, cirazoline, and amidephrine were relatively ineffective. Phenylephrine, but not methoxamine and cirazoline, also increased cyclic AMP accumulation. Phenylephrine-induced tritium efflux was not altered by alpha- and beta-adrenergic receptor antagonists or by removal of extracellular calcium. Phenylephrine-induced cyclic AMP accumulation was blocked by the beta-adrenergic receptor antagonists propranolol and atenolol. Forskolin (10 microM) and the nonhydrolyzable cyclic AMP analogue 8-(4-chlorophenylthio)cyclic AMP (100 microM) had minimal effect on tritium efflux. However, phenylephrine-evoked increase in tritium efflux was dose dependently attenuated by the neuronal uptake blocker cocaine, and phenylephrine dose-dependently inhibited the incorporation of [3H]norepinephrine into neuronal stores. We conclude that the increase in tritium efflux induced by phenylephrine is independent of cyclic AMP accumulation and appears to be mediated by uptake of phenylephrine via the neuronal carrier-mediated amine transport process, which in turn promotes efflux of the adrenergic transmitter from its storage sites.

Regeneration of acetylcholinesterase in clonal neuroblastoma-glioma hybrid NG108-15 cells after soman inhibition: effect of glycyl-l-glutamine

Acetylcholinesterase (AChE) in the clonal NG108-15 cell line has been previously characterized. This cell line represents an in vitro system to study AChE regulation and effects of chemical compounds that may alter AChE activity. Recently, glycyl-L-glutamine (GLG) was demonstrated to function as a neurotrophic factor for maintenance of AChE content in cat denervated superior cervical ganglion cells. In the present study, regeneration of AChE activity in cultures of undifferentiated NG108-15 cells after soman inhibition was investigated in the presence and absence of GLG. Cells were treated with soman (5.5 x 10(-6) M) for 15 min and then washed to remove excess soman. Culture medium containing either GLG (10(-6), 10(-5), or 10(-4) M) or glycyl-L-glutamic acid (10(-6) M) was added to cultures after soman treatment and remained in the medium until cell harvest. Cells were physically detached at various times after soman treatment and specific AChE activity was determined. After soman, AChE activity dramatically decreased to less than 1% of untreated cellular activity at 1 hr. AChE activity gradually increased after 5 hr, while untreated cell AChE activity was regained 20 hr after soman. The t1/2 for AChE regeneration was approximately 10 hr. GLG did not increase the rate of AChE regeneration after soman inhibition. These results indicate that GLG is not a directly acting neurotrophic factor for AChE synthesis in NG108-15 cells after chemical AChE inactivation.

The responsiveness of SIF cells in the rat superior cervical ganglion to prolonged hypoxia

The responsiveness of SIF cells in the rat superior cervical ganglion to prolonged hypoxia

Early commitment of precursor cells from the rat superior cervical ganglion to neuronal or nonneuronal fates

To determine whether postmigratory neural crest cells retain the capacity to give rise to multiple cell types, the clonal progeny of embryonic rat superior cervical ganglion (SCG) cells were examined in culture. Double labeling with BrdU and neurofilament antibodies demonstrated that neuron precursors from the E14.5 SCG continued to proliferate for several days in culture. Using the BAG retrovirus to examine the progeny of single cells, we obtained several kinds of distinct clones from SCG cultures after 3 days. At E14.5, during peak neuro-genesis in vivo, neuron-containing clones composed of one to seven cells were common. At El 7.5, after neurons have been born in vivo, most clones in vitro contained flat cells, primarily reflecting glial cell division. Even in cultures from E13.5 ganglia, mixed clones containing neurons and flat cells were rarely observed. These observations suggest that neuronal and nonneuronal cell precursors are specified during or before early gangliogenesis.

Principal neurons and small intensely fluorescent (SIF) cells in the rat superior cervical ganglion have distinct developmental histories

Sympathetic ganglia contain 2 adrenergic derivatives of the neural crest: principal neurons and small, intensely fluorescent (SIF) cells. The developmental mechanisms responsible for the generation of these 2 cell classes in vivo are not well understood. To examine the possible developmental and lineage relationships between differentiating principal neurons and SIF cells, a fluorescence microscopic study utilizing antibodies against tyrosine hydroxylase (TH) and catecholamine histofluorescence has been combined with the ultrastructural examination of embryonic and postnatal rat superior cervical ganglia (SCG). On embryonic day 12.5, before neuroblasts had become postmitotic, the cells in the SCG possessed intense TH immunoreactivity and had weak to bright catecholamine histofluorescence, but no cells displayed the fine structure of mature SIF cells or neurons. At embryonic days 16.5 and 18.5, postmitotic principal neurons expressed more moderate levels of TH and catecholamines characteristic of the late embryonic and postnatal SCG. By contrast, a small number of cells containing intense TH or catecholamine fluorescence were present in embryonic day 16.5 and older ganglia. Almost all of the intensely fluorescent cells observed were found apposed to capillaries within the ganglion. These embryonic intensely fluorescent cells were larger than SIF cells seen postnatally. Ultrastructural examination of developing ganglia confirmed that cells containing numerous large, dense-cored vesicles (LDCVs) were a prominent feature of ganglia that also contained intensely fluorescent cells. In addition, some embryonic cells containing LDCVs were mitotic. From these and other studies, it seems likely that during development, neuron precursors, in response to differentiation factors such as fibroblast growth factor (FGF) and/or NGF, acquire overt neuronal traits and become postmitotic. Subsequently, cells resembling mature SIF cells appear next to blood vessels, where they may have received other instructional signals such as glucocorticoids. This developmental scheme suggests that the differentiation of principal neurons and SIF cells is independently regulated, and that the ability of SIF cells to convert into principal neurons observed in vitro cannot account for the generation of neurons in vivo.

Detection of sialic acid residues in the axonal reticulum of rat superior cervical ganglion cells by lectin-gold cytochemistry.

Highly glycosylated compounds have been demonstrated in the axonal reticulum elements of the superior cervical ganglion cells of the rat, and this is considered to suggest a connection of the reticulum with the trans Golgi side. In the present study, the axonal reticulum and the Golgi elements were further characterized by post-embedding methods of lectin-gold cytochemistry to determine their carbohydrate residues and to see, more specifically, if sialic acid residues could be detected in the axonal reticulum elements. Therefore, the affinity of neuronal cell structures for Limax flavus agglutinin (LFA), wheat germ agglutinin (WGA), and Ricinus communis agglutinin I (RCA-I) was tested in ultra-thin sections of glycolmethacrylate-embedded material, counterstained with phosphotungstic acid (PTA) at low pH. The trans Golgi network, the Golgi-associated axonal reticulum, the reticulum within axons, the large dense-cored vesicles, and the plasma membranes were reactive for all three lectins used. We conclude that the axonal reticulum elements carry sialic acid residues, relating them to the trans Golgi network. The present results support the concept that the axonal reticulum is an extension of the trans network of the Golgi apparatus specialized for neurosecretion.

Paraganglionic cell response to chronic imipramine and handling stress: an ultrastructural study

The ultrastructure and connectivity of monoamine-storing paraganglionic cells in the rat superior cervical ganglion were investigated following chronic treatment with imipramine (Tofranil, Ciba-Geigy) and compared with uninjected unhandled controls and saline injected animals. The study reveals a significant decrease in the number of dense core vesicles in the drug-treated group (P less than 0.001) which is regarded as a specific effect due to receptor blocking actions of imipramine. A significant reduction in the maximum diameter of the external rim and internal cores of the vesicles (P less than 0.05) in the drug-treated group is mimicked to a certain extent by saline injections, indicating a mixed effect of stress handling and specific alteration. Although the paraganglionic cell morphology is unaltered in the group comparisons, the interrelationship of the paraganglionic cells to surrounding neural processes is significantly altered in both the control versus saline and the control versus drug group comparisons (P less than 0.05). The drug- and saline-induced alterations of neural connectivity may reflect stress-induced general changes demonstrating the plasticity of the paraganglionic cell population.

Decentralization induces long-term c-fos protein-like immunoreactivity in non-neuronal cells in the rat superior cervical ganglion

The expression of c-fos protein(s) was studied immunohistochemically in the intact and decentralized superior cervical ganglia (SCG) of adult rats. C-fos protein(s)-like immunoreactivity (c-fos-LI) was detected in 1–2% of the principal ganglion cells but not in the satellite or Schwann cells of the intact SCG. After transection of the cervical sympathetic trunk, satellite and Schwann cells in the ganglion expressed c-fos-LI from one hour through 8 days following the operation. The maximal staining was seen 1 day postransection (d.p.t.), when the c-fos-LI was intense throughout the ganglion. No change was observed in the c-fos-LI of the principal neurons. At 8 d.p.t. the number of immunoreactive cells and their staining intensity had decreased, and at 14 d.p.t. they were back to the control level. These results suggest that a long-term expression of c-fos protein(s) is induced in the SCG satellite and Schwann cells after preganglionic denervation possibly related to their activation during nerve degeneration and regeneration.

Pseudorabies virus: a highly specific transneuronal cell body marker in the sympathetic nervous system

The present report presents a series of experiments using Bartha's K strain of pseudorabies virus (PRV) designed to test the specificity of this virus as a retrograde transneuronal marker in the sympathetic nervous system of rats. Three experiments were performed. First, an injection of PRV was made in the anterior chamber of the eye, followed 24 hr later by an injection of WGA-HRP. PRV infected neurons in the superior cervical ganglion (SCG) always contained WGA-HRP. This dual labeling of SCG neurons suggests that the PRV cell body labeling does not nonspecifically infect nearby neurons. Second, after PRV injections into the pinna or eye, a specific segmental distribution of the transneuronal cell body labeling occurred in the intermediolateral cell column and related spinal areas. After eye injections, the majority of transneuronally labeled neurons were in the T1-T3 segments. After pinna injections, the majority of labeled cells were in the T2-T5 segments. Since the SCG cells innervating these 2 end organs lie in close proximity to each other within the ganglion, these results suggest that a specific transfer of the virus to the preganglionic neurons occurred, possibly via a transsynaptic mechanism. Third, virally infected glial cells were rarely found in the SCG or spinal cord. In summary, Bartha's K strain of PRV is a specific transneuronal retrograde grader marker in the sympathetic nervous system.

Sympathetic sprouting into neonatally denervated contralateral target: superior cervical ganglion neuronal numbers and sizes

Unilateral superior cervical ganglionectomy results in establishment of an atypical functional projection from the contralateral ganglion to the denervated superior tarsal muscle in neonatal but not in juvenile or adult rats. Previous studies of peripheral nervous system development have attributed enhanced neuroplasticity to either formation of pathways by surplus cells rescued from cell death (hypothanasia-induced hyperplasia), or more vigorous terminal arborization of neurons innervating adjacent target zones (collateral sprouting with associated somatic hypertrophy). In the present study, experiments were performed to determine if neonatal sympathetic sprouting to contralaterally denervated target is associated with superior cervical ganglion neuronal hyperplasia or hypertrophy. Fluoro-Gold injections of right superior tarsal muscle in adult rats following neonatal ganglionectomies labelled cells in the contralateral superior cervical ganglion, whereas cells were labelled strictly ipsilaterally in sham operates. Profile areas of contralaterally projecting neuronal somata were twice as large as those providing ipsilateral innervation. Ganglion volumes, neuronal nuclear diameters and packing densities, and total neuronal numbers in left superior cervical ganglia of animals receiving neonatal right superior cervical ganglionectomy were comparable to those of both right and left ganglia of sham-operated controls. It is concluded that establishment of a contralateral projection does not rescue significant numbers of neurons from naturally occurring cell death. Rather, contralateral sprouting derives from neurons showing pronounced somatic hypertrophy.

Mast cells in the guinea pig superior cervical ganglion: a functional and histological assessment

We have previously found that antigenic stimulation of mast cells in the guinea pig superior cervical ganglion leads to membrane depolarization of principal neurons and a long-term increase in the efficacy of ganglionic transmission. In this study experiments were conducted to discern the histological, immunological and pharmacological characteristics of the mast cells within the superior cervical ganglion. Mast cells within the superior cervical ganglion could be stained with toluidine blue or berberine sulfate, the latter indicating that heparin-like molecules were present in the granules. Stainable mast cells were distributed throughout the ganglion with no gross evidence of regional localization. The number of mast cells stained with toluidine blue was reduced significantly ( P < 0.01) in contralateral ganglia that had been exposed to the sensitizing antigen (ovalbumin), indicating antigen-induced degranulation. The superior cervical ganglion contained 208 ± 6 picomole of histamine (mean ± SEM, n = 66). Ovalbumin evoked the release of histamine from the superior cervical ganglion in a concentration-dependent fashion. At maximally effective concentrations, ovalbumin released 33 ± 2% of the total histamine stores (mean ± SEM, n = 61). Similar values were obtained with antigen-challenged stellate ganglia. A temperature of 37°C and an extracellular calcium concentration of 1 mM was required to elicit optimal antigen-induced responses. In addition to releasing histamine, antigenic stimulation of the ganglion resulted in a 3- to 5-fold increase in the synthesis and release of arachidonic acid metabolites including peptidoleukotriene, thromboxane B 2, prostaglandins (PG) E 2, F 2 α, D 2, the PGD 2 metabolite 9α 11β-PGF 2, and the prostacyclin metabolite 6-keto PGF 1 α. Various putative mast cell secretagogues were examined for their ability to activate the superior cervical ganglion mast cell, as indicated by evoked histamine release. In contrast to rat peritoneal mast cells, high concentrations of substance P, compound 48/80, and nerve growth factor failed to stimulate the ganglion mast cells. Preganglionic nerve stimulation, electrical field stimulation of axons and cell bodies, or depolarizing concentrations of potassium chloride also failed to activate the superior cervical ganglion mast cells. These results suggest that substances released by membrane depolarization do not influence the function of the resident mast cells. The results demonstrate that the mast cells within sympathetic ganglia can be actively sensitized to respond to specific antigen. These mast cells are similar to lung parenchymal mast cells with respect to histological, immunological and pharmacological characteristics. Finally, the data are consistent with a hypothesis that the antigen-induced effects on superior cervical ganglion neurons occur secondary to the synthesis and release of a variety of bioactive substances, including biogenic amines, heparin-like molecules, and cyclooxygenase and lipoxygenase products of arachidonic acid.

Purification of the growth-associated protein GAP-43 by reversed phase chromatography: amino acid sequence analysis and cDNA identification

GAP-43 is a neuronal phosphoprotein. Increased synthesis and axonal transport of GAP-43 has been associated with axon growth, and altered phosphorylation of GAP-43 has been associated with changes in synaptic efficacy. Here we report a rapid and effective procedure employing reverse-phase HPLC for the purification of GAP-43 from rat brain. To characterize the protein purified by this procedure, we generated proteolytic fragments and determined their amino acid sequences. These directly determined sequences, corresponding to 56% of the GAP-43 amino acids, confirm recently reported sequences deduced from the nucleotide sequences of cDNAs. Using oligonucleotide probes constructed according to these amino acid sequences, we identified GAP-43 cDNAs in a library prepared from neonatal rat superior cervical ganglion cells. One of these cDNAs was 1.1 kB in size; it hybridized specifically with a 1.5 kB RNA from brain, but not from liver, and contained the entire coding sequence for GAP-43. This cDNA differed from recently reported cDNAs in its 3′ untranslated region.

Heat generation associated with synaptic transmission in the mammalian superior cervical ganglion

By use of a thermal detector constructed with a thin polyvinylidene fluoride film (PVDF), heat production in the superior cervical ganglion (SCG) of the guinea pig was examined. A single electric shock applied to the preganglionic nerve evokes a temperature rise of approximately 1.5 x 10(-6) deg. The thermal responses summate when the preganglionic nerve is stimulated repetitively. The amplitude of the thermal response is increased when the preparation is treated with a high Ca2+ medium. Treatment with agents that block ganglionic transmission (high Mg2+, d-tubocurarine, hexamethonium, TTX) reversibly suppresses thermal response. It is thus concluded that the thermal responses described in this paper are generated by the physico-chemical events underlying postsynaptic electrogenesis in the SCG cells.

Dynorphin-containing pilomotor neurons in the superior cervical ganglion of guinea pigs

Retrograde axonal tracing and double-labelling immunofluorescence have been combined to determine the neuropeptide content of identified pilomotor neurons in the superior cervical ganglion of guinea pigs. These neurons lacked immunoreactivity to neuropeptide Y (NPY) but they generally contained low levels of immunoreactivity to prodynorphin-derived peptides, including dynorphin A(1–8), dynorphin A(1–17), and α-neo-endorphin. Thus pilomotor neurons are neurochemically distinct from superior cervical ganglion cells which contain immunoreactivity to NPY and prodynorphin-derived peptides and which innervate the iris and most of the vasculature in the head of guinea pigs. They are also distinct from sympathetic secretomotor neurons which lack both NPY and prodynorphin-derived peptides.