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PubMed1968

Resting and action potentials recorded by the sucrose-gap method in the superior cervical ganglion of the rabbit.

1. Evoked ganglionic action potentials and drug-induced changes in resting potential were recorded by the sucrose-gap method. The height of the action potential was 10-20 mV.2. Since the amplitude of the P wave is inversely proportional to the external potassium concentration between 0.5 and 12 mM, the P wave is probably caused by a phase of increased permeability to K(+).3. In the absence of an anticholinesterase, the depolarizing actions of choline and acetylcholine on the ganglion are almost equal, whereas acetylcholine is 2-3 times more potent than choline on the fibres of the internal carotid nerve. In the presence of eserine, acetylcholine induces a depolarization of the ganglion of up to 14 mV, while increase in [K(+)](o) causes a depolarization of up to 55 mV.4. Although the post-ganglionic fibres in the distal pole of the ganglion are depolarized by drugs, for example, acetylcholine, they contribute little to drug-induced potential changes and probably little to evoked action potentials.5. The hyperpolarization which occurs after exposure of the ganglion to acetylcholine is not due to a phase of increased permeability to K(+).

Acetylcholine↗

PubMed1968

Intracellular recording from mammalian superior cervical ganglion in situ.

1. Recordings have been obtained by intracellularly placed microelectrodes from cells of the superior cervical ganglion of the rabbit. The ganglion was left in situ.2. In response to stimulation of the external carotid nerve, some cells responded with a single spike of short latency followed by a long-lasting hyperpolarization. These cells, presumably, were activated antidromically. The majority of cells, however, responded with an early spike followed by a long-lasting depolarization; superimposed on this depolarization were one or two spikes with latencies from 35 to 70 msec. Anatomical pathways responsible for this activation have been suggested.3. A variety of responses were recorded from different neurones when the preganglionic sympathetic trunk was stimulated. Many of the cells responded to maximal stimulation of the nerve with repetitive spikes. Stimuli of constant strength could elicit variable responses from a single neurone. This variability and the multiple spike response may be due to multiple pathways leading to the same cell and the possibility of the presence of internuncial neurones in the ganglion is suggested.4. Strong stimulation of the preganglionic sympathetic nerve trunk caused inhibitory effects at the ganglion cells.5. Direct stimulation of the ganglion cells through the recording microelectrode elicited only one spike even at high intensity. Thus the multiple spike response to orthodromic stimulation must have been due to a temporally dispersed afferent input.6. It is concluded that the organization of the rabbit superior cervical ganglion is more complex than has been suspected previously, and that integration as well as transmission takes place at the level of these neurones.

Animals↗

PubMed1969

Correlation between transmission and structure in avian ciliary ganglion synapses.

1. Extracellular responses from post-ganglionic axons of pigeon and chick isolated ciliary ganglia were elicited by stimulation of the presynaptic nerve. Intracellular recordings were also obtained from newly hatched pigeon and chick ganglion cells. The fine structure of ganglia from pigeons of various ages was examined with the electron microscope.2. In ganglia from chick embryos and pigeons up to 10 days old, the extracellular response was unimodal with a long latency and could be blocked by the addition of D-tubocurarine (D-TC) or hexamethonium to the bathing solution. A bimodal extracellular response appeared in pigeons about 10 days after hatching. Only the second peak of the response could be blocked by D-TC or hexamethonium. The response recorded from 22 to 26-day-old pigeons was similar to that seen in the adult.3. The intracellular recordings from ganglion cells of 2-week-old pigeons exhibit two post-synaptic potentials elicited by presynaptic stimulation. The first post-synaptic potential appears to be due to current flow through the ganglion cell during the presynaptic action potential. The second is chemically mediated. In pigeons from 1 to 6 days old, only the second post-synaptic potential is observed.4. The presynaptic terminals in the 4-day-old birds were in the form of calyces. In pigeons 7 days old or older, boutons appeared. The boutons were presumably formed as a result of cleavage of calyciform nerve terminals. Myelin was seen first in the 7-day-old pigeon, was well developed in the 16-day-old bird, and persisted in the adults.5. In adult ganglia, the first component of the extracellular response decreased and was finally abolished after 10-12 hr of superfusion with Tyrode solution. The second component of the response increased concomitantly. The only anatomical change noted in the ganglia after soaking was the disruption and separation of the myelin lamellae from each other and from around the ganglion and presynaptic terminals.6. It is concluded that the myelin is necessary for electrical transmission in the pigeon ciliary ganglion.

Age Factors↗

PubMed1976

Induction of cholinergic enzymes in chick ciliary ganglion and iris muscle cells during synapse formation.

1. In chick ciliary ganglia and irises, cholineacetyltransferase (ChAc) and acetylcholinesterase (AChE) activities were measured from the fifth day of incubation until 1 week after hatching. The changes in enzyme activity were correlated in time with previous electrophysiological and morphological findings of synapse formation in these tissues. 2. At Stage 26 (Hamburger & Hamilton, 1951; before synapse formation in the ganglia) low activities of ChAc (12 +/- 4 [mean +/- S.E.] p-mole of ACh synthesized/hr) were measured in the iris nerve terminals, indicating that ganglion cells are biochemically differentiated, immediately after cell migration is completed. The specific acitivities of ChAc and AChE rose during development and these increases were closely related to the onset and maturation of ganglionic and iris synaptic transmission. These increases in enzyme activities can be used in cholinergic synapses as an index of synapse formation. 3. The 200-fold specific increase of ChAc in iris nerve terminals which occurs at Stage 34 probably reflects an increase in synthesis of the enzyme in ganglion cells and suggests that the formation of the iris neuromuscular junction triggers the enzyme induction. It is implied that the cell responds to a signal ascending the axon from the terminal. 4. The initial increase of AChE specific activity in the ganglion occurs after transmission is established in all cells between Stage 30 and 34 and is mainly due to enzyme synthesis by the ganglion cells. In the iris there is a twofold increase in specific activity after the formation of neuromuscular junctions which probably reflects enzyme induction in the muscle subneural region. It is concluded that the specific induction of AChE in post-junctional cells is due to an influence of the prejunctional element. 5. During synaptic formation in the ciliary ganglion, reciprocal interactions between the neurones and their targets result in the induction of ChAc in the prejunctional elements and AChE in the post-junctional cells.

Acetylcholinesterase↗

PubMed1976

Physiological and morphological effects of post-ganglionic axotomy on presynaptic nerve terminals.

1. Electrophysiological and electron microscope studies were done on cells in the ciliary ganglion of chickens which had been axotomized on the day of hatching. 2. By the third day after post-ganglionic axotomy both electrical and chemical transmission through the ganglion were severely depressed; by the fifth day ganglionic transmission had disappeared. 3. Action potential initiation and conduction in axotomized cells and in their associated presynaptic nerve terminals were unimpaired 3-4 days after axotomy. 4. Depression of ganglionic transmission in 3-4 day axotomized preparations was due to a reduction in amplitude of both the excitatory post-synaptic potential (e.p.s.p.) and the electrical coupling potential in individual ganglion cells. 5. In addition to being reduced in amplitude, e.p.s.p.s in axotomized cells were more subject to fatigue during low frequency (1/sec) stimulation. 6. The reduction in e.p.s.p. amplitude was due to a reduction in both the mean quantal content of the e.p.s.p.s and the calculated depolarization produced by an individual quantum of transmitter. On the average the e.p.s.p. was reduced by a factor of about 4, the mean quantum content to about two thirds normal and the quantal size to about a third normal, compared with responses in unaxotomized cells of the same age. 7. Ultrastructural studies revealed a progressive maturation of pre-synaptic terminals in normal ganglia between 0 and 9 days after hatching. Over this period the content of synaptic vesicles and mitochondria in the terminals increased and the background matrix became more dense. 8. After axotomy these signs of maturation was abolished or reversed, particularly from the third day onward. In addition there was an increase in the number of cell sections in which no synaptic terminals were observed. 9. It was concluded that loss of synaptic transmission was due to at least three factors: a reduction in release of transmitter from presynaptic terminals, a reduction in quantal size, probably due to a loss of post-synaptic sensitivity, and a partial loss of presynaptic contact.

Action Potentials↗

PubMed1977

Specific innervation of guinea-pig superior cervical ganglion cells by preganglionic fibres arising from different levels of the spinal cord.

1. The synaptic contribution of preganglionic nerve fibres arising from the last cervical (C8) and the first seven thoracic spinal cord segments (T1-T7) to neurones of the guinea-pig superior cervical ganglion has been studied by means of intracellular recording during ventral root stimulation in vitro. 2. The majority of neurones received innervation from the middle segments (T2 and T3) of the length of spinal cord from which preganglionic fibres derive; an intermediate number of ganglion cells were innervated by fibres from the segments adjacent to these (T1, T4, and T5), and relatively few neurones by fibres from the most rostral and caudal segments supplying innervation to the ganglion (C8, T6 and T7). 3. Each neurone received preganglionic terminals from multiple thoracic segments (range 1-7, mean = 4-0). The estimated minimum number of preganglionic fibres contacting each neurone was 10, on average. 4. As a rule, the spinal segments innervating a neurone were contiguous. Thus we rarely encountered neurones innervated by segments located both rostrally and caudally to a segment which failed to provide innervation. 5. Neurones tended to be innervated predominantly by axons arising from a single spinal segment, with adjacent segments contributing a synaptic influence that diminished as a function of their distance from the dominant segment. All segments provided dominant innervation to at least some neurones. 6. Stimulating the ventral roots of C8-T7 in vivo showed that the axons arising from each segment produced a characteristic pattern of peripheral effects. Thus different populations of neurones in the superior cervical ganglion of the guinea-pig are innervated by preganglionic axons from different levels of the spinal cord, as originally suggested by Langley (1892) for the cat, dog, and rabbit. 7. On the basis of our in vitro studies we conclude that underlying the specificity of innervation of neurones of the superior cervical ganglion that can be inferred from in vivo experiments is a tendency for individual neurones to be innervated in a systematically graded fashion by a contiguous subset of the eight spinal segments which provide innervation to the ganglion.

Action Potentials↗

PubMed1977

Regenerative amacrine cell depolarization and formation of on-off ganglion cell response.

1. Recordings from amacrine and ganglion cells in the mudpuppy retina suggest mechanisms whereby the relatively slow, sustained light responses measured in bipolar cells are converted to rapid, brief, transient activity in the on-off ganglion cells. 2. Double-barrel electrodes were used to control the membrane potential under voltage clamp. The clamp revealed synaptic currents, but eliminated the otherwise obvious spike activity elicited by steps of illumination in both amacrine and ganglion cells, suggesting that the spikes are initiated near the somata. 3. The synaptic current in the on-off ganglion cells was biphasic: a brief inward (depolarizing) membrane current preceded a transient outward (hyperpolarizing) membrane current by about 20 msec. Each component could be isolated by polarizing the membrane to a level near the reversal potential for the other. Each was apparently due to a transient conductance increase of sawtooth shape with a 40 msec time to peak and a decay longer than 400 msec. 4. Synaptic membrane current in amacrine cells was monophasic and inward (depolarizing) of similar sawtooth shape at all potential levels. It was apparently mediated by a conductance increase to ions with a reversal potential more positive than the dark level. 5. When amacrine cells were depolarized in the dark under voltage clamp, a large transient inward membrane current with threshold within 4 mV of the dark level was generated. This regenerative event is capable of boosting a small, 4 mV e.p.s.p. to more than 30 mV in a few milliseconds, thereby generating the leading edge of a rapid sawtooth response. 6. The results suggest that the rapid transient on-off activity in ganglion cells is mediated by opposing sawtooth shaped synaptic currents with different latencies. It is inferred that each of these antagonistic imputs is generated by a regenerative depolarization in amacrine cells which then form synaptic inputs to the ganglion cells.

Action Potentials↗

PubMed1977

Self-facilitation of ganglion cells in the retina of the turtle.

1. Ganglion cells responses to illumination and to optic nerve stimulation were recorded intracellularly from the retina of the turtle. All ganglion cells were identified by their antidromic responses to optic nerve stimulation.2. When solitary spikes are produced following antidromic, orthodromic or intracellular stimulation, about 20% of the recorded ganglion cells show an additional depolarization along the falling phase of the action potential (post-spike depolarization, PSD).3. The PSD following the antidromic action potential disappears upon collision with a direct spike or when the antidromic spike is prevented from invading the cell soma.4. By pairing two optic nerve stimuli the PSD is depressed with brief interstimulus intervals, but gradually recovers to the control amplitude 600-800 msec after the conditioning shock.5. The PSD is tentatively interpreted as an e.p.s.p. transmitted by ganglion cell collaterals originating at the level of the soma dendritic complex of the recorded cell.6. The interspike interval histogram of ganglion cells showing PSD is characterized by a peak at about 10 msec, as opposed to a peak between 12 and 100 msec observed in cells without PSD. It is suggested that the occurrence of PSD facilitate the onset of additional action potentials at brief interspikes intervals, thus potentiating ganglion cell discharges.

Action Potentials↗

PubMed1980

Effects of synaptic and antidromic stimulation on tyrosine hydroxylase activity in the rat superior cervical ganglion.

1. The effects of orthodromic and antidromic stimulation of the rat superior cervical ganglion on the specific activity of the enzyme tyrosine hydroxylase have been studied. 2. Orthodromic stimulation of the ganglion via the sympathetic trunk produced an increase in the activity of tyrosine hydroxylase when measured 3 days later while causing no change in the protein content of the ganglion. This increase in the specific activity of tyrosine hydroxylase was blocked by administration of the nicotinic antagonist, hexamethonium. 3. Antidromic stimulation of the superior cervical ganglion by stimulating the internal carotid nerve, the external carotid nerve or both nerves simultaneously produced no change in the specific activity of tyrosine hydroxylase. 4. Parallel increases in tyrosine hydroxylase activity and protein content per ganglion were seen when the internal carotid nerve was stimulated but similar changes were seen in "sham-stimulated" animals. These "non-specific" changes were apparently produced by the trauma involved in the extensive dissection necessary to position electrodes on this nerve trunk. 5. We conclude that an increase frequency of firing in post-ganglionic neurones is not a sufficient stimulus to elevate the specific activity of tyrosine hydroxylase. Rather some other aspect of nicotinic receptor stimulation seems to be required.

Animals↗

PubMed1984

On the two subdivisions and intrinsic synaptic connexions in the submandibular ganglion of the rat.

Parasympathetic neurones in the submandibular ganglion of the rat innervate the submandibular and sublingual salivary glands. Neurones which innervate the submandibular gland (s.m. neurones) are usually located along the salivary ducts which drain both glands. Neurones which innervate the sublingual gland (s.l. neurones) are located in the thin sheet of tissue which lies between the salivary ducts and the lingual nerve. The existence and characteristics of intrinsic synaptic connexions were studied electrophysiologically in these two divisions of the submandibular ganglion. Three days or more after denervating the ganglion two types of excitatory intrinsic synaptic potentials--chemical and electrical--were recorded in ganglion cells. Chemical synaptic responses were reversibly blocked by nicotinic antagonists such as hexamethonium (10 microM) and D-tubocurarine (100 microM). Intrinsic chemical synapses were common among s.m. neurones (present in 72% of neurones) but only 12% of s.l. neurones were coupled with chemical synapses. Electrical coupling was found among 31% of s.m. neurones but was not observed between s.l. neurones. Electrotonic coupling in s.m. neurones in denervated and intact ganglia was directly demonstrated by impaling adjacent neurones with separate micro-electrodes. The average coupling ratio for current pulses injected into one cell and recorded in the adjacent cell was 0.06. During the first 30 days after birth, the number of synaptic inputs from preganglionic (chorda tympani) axons was markedly reduced in both s.m. and s.l. neurones, whereas the incidence of electrical synaptic connexions remained unchanged. The effect of long-term denervation (up to 4 months) on intrinsic synapses was examined. The membrane properties of the parasympathetic neurones and the intrinsic synaptic connexions were maintained without marked changes. It is concluded that the submandibular ganglion in the rat consists of two distinct populations of parasympathetic neurones. The two classes of neurones differ in (1) their location within the ganglion, (2) their target organs and (3) the incidence of intrinsic synapses. Possible mechanisms for the development, maintenance and function of these intrinsic synapses are discussed.

Action Potentials↗

PubMed1992

The role of acetylcholinesterase in denervation supersensitivity in the frog cardiac ganglion.

1. The sensitivity of normal and denervated cardiac ganglion cells to the cholinergic agonists acetylcholine and carbamylcholine (carbachol) were compared in the frog, Rana pipiens. Acetylcholine and carbachol bind to the same acetylcholine receptors, but, unlike acetylcholine, carbachol is resistant to hydrolysis by acetylcholinesterase. 2. Sensitivity was assessed by the peak depolarization elicited in response to a sustained pulse of ligand emitted from a pipette positioned 10 microns from the ganglion cell surface. This technique allows the sensitivity of the entire cell to be recorded with a single measurement. 3. The acetylcholine sensitivity of normal cardiac ganglion cells was increased by inhibiting extracellular acetylcholinesterase with echothiophate. 4. Denervation increased the sensitivity of cardiac ganglion cells to acetylcholine but not to carbachol. 5. Following the inhibition of extracellular acetylcholinesterase with echothiophate, sensitivity to acetylcholine was similar in normal and in denervated ganglion cells. 6. The increased sensitivity to acetylcholine of cardiac ganglion cells following denervation is caused by a reduction in the hydrolysis of the transmitter by acetylcholinesterase rather than by changes in the number and/or properties of acetylcholine receptors.

Acetylcholine↗

PubMed1993

Enteric GABA-containing nerves projecting to the guinea-pig inferior mesenteric ganglion modulate acetylcholine release.

1. The effect of GABA and GABA receptor-modulating drugs on release of [3H]acetylcholine was studied in the guinea-pig inferior mesenteric ganglion. 2. GABA caused a dose-dependent increase in [3H]acetylcholine release during stimulation of the lumbar colonic nerves. Muscimol (10 microM) and diazepam (5 microM) also increased [3H]acetylcholine release during stimulation of the lumbar colonic nerves whereas baclofen (10 microM) had no effect. 3. Bicuculline (20-100 microM) and picrotoxin (50 microM) alone reduced [3H]acetylcholine release during electrical stimulation of the lumbar colonic nerves whereas phaclofen (300 microM) had no effect. 4. Bicuculline (100 microM) significantly decreased whereas diazepam (5 microM) significantly increased distension-induced [3H]acetylcholine release. 5. Colonic distension significantly increased [3H]GABA release in the inferior mesenteric ganglion compared to basal periods when the colon was not distended. Distension-induced release of [3H]GABA resulted from active neuronal transmission from the colon to the inferior mesenteric ganglion, since perfusion of the inferior mesenteric ganglion with tetrodotoxin (1 microM) reduced basal release of [3H]GABA and abolished distension-evoked increases in the release of [3H]GABA. 6. In contrast to its excitatory effects on peripheral colonic afferent cholinergic nerves, exogenous GABA caused a dose-dependent decrease in [3H]acetylcholine release during electrical stimulation of the central lumbar splanchnic nerves. Baclofen (10 microM) also inhibited [3H]acetylcholine release whereas muscimol (10 microM) or diazepam (5 microM) had no effect. Phaclofen (300 microM) antagonized the inhibitory effects of exogenous GABA (10 microM) and of baclofen (10 microM). Bicuculline (100 microM), picrotoxin (50 microM) and phaclofen (300 microM) alone had no effect on [3H]acetylcholine release during splanchnic nerve stimulation. 7. Phaclofen (300 microM) increased [3H]acetylcholine release during simultaneous electrical stimulation of the lumbar colonic nerves and splanchnic nerves and when GABAA receptors were blocked by bicuculline (20 microM). 8. The data suggest that GABAA receptors facilitate release of acetylcholine from peripheral cholinergic mechanosensory nerves projecting from the colon to the inferior mesenteric ganglion and that GABAB receptors inhibit release of acetylcholine from central cholinergic nerves. Enteric GABA-containing nerves projecting to the inferior mesenteric ganglion are mechanosensory. Endogenous release of GABA may act on GABAA receptors to facilitate peripheral cholinergic mechanosensory transmission and/or on GABAB receptors to inhibit central cholinergic transmission.

Acetylcholine↗

PubMed1996

Modulation by opioid peptides of mechanosensory pathways supplying the guinea-pig inferior mesenteric ganglion.

1. Radioimmunological techniques were used in isolated guinea-pig inferior mesenteric ganglion (IMG)-colon preparations to determine whether opioid peptides and neurotensin8-13 (NT8-13), the C-terminal region of NT1-13 recognized by neurotensin receptors, modulate distension-induced release of substance P (SP)- and vasoactive intestinal polypeptide (VIP)-like immunoreactive (LI) material. 2. Colonic distension significantly increased the amount of SP- and VIP-LI material released in the ganglionic superfusate. A low-Ca2+ (0.1 mM), high-Mg2+ (15 mM) solution blocked their release. 3. In vivo capsaicin pretreatment abolished release of SP-LI material during colonic distension but had no significant effect on distension-induced release of VIP-LI material. 4. The addition of [Leu5]enkephalin, [Met5]enkephalin, PL017 (a mu-receptor agonist) and DPDPE (a delta-receptor agonist) to the ganglion side of a two-compartment chamber blocked distension-induced release of SP-LI material. The addition of naloxone and ICI-174,864 (a delta-receptor antagonist) to the ganglion compartment reversed the inhibitory effect of the mu- and delta-receptor agonists. 5. Addition of [Leu5]enkephalin and [Met5]enkephalin to the ganglion compartment had no significant effect on release of VIP-LI material during colonic distension. 6. Addition of NT8-13 to the ganglion compartment significantly increased in the amount of SP-LI material released during colonic distension but had no affect on distension-induced release of VIP-LI material. 7. The results suggest the hypothesis that under in vivo conditions, enkephalinergic nerves decrease and neurotensinergic nerves increase the release of SP from peripheral branches of primary afferent sensory nerves.

Animals↗

PubMed1997

Pituitary adenylate cyclase activating polypeptide and nitric oxide synthase are expressed in the rat ciliary ganglion.

AIMS: To study the distribution in the rat ciliary ganglion of neurons synthesising and storing the recently discovered neuropeptide pituitary adenylate cyclase activating polypeptide (PACAP) and neuronal nitric oxide synthase (NOS), the neuronal marker of the novel gaseous transmitter nitric oxide. METHODS: Neurons expressing PACAP and neuronal NOS mRNA were identified in the rat ciliary ganglion by in situ hybridisation with radiolabelled oligonucleotide probes. Immunocytochemistry was used to demonstrate immunoreactive neuropeptides and NOS. RESULTS: Immunocytochemistry demonstrated immunoreactivity for PACAP and NOS in a small number of neuronal cell bodies. In situ hybridisation revealed that NOS and PACAP were expressed in numerous ganglion cell somata. The well established ciliary messengers vasoactive intestinal peptide and neuropeptide Y were found in a large number of neuronal cell bodies. CONCLUSION: These results demonstrate that PACAP and NOS are synthesised and stored in the ciliary ganglion. These findings further illustrate the mixed nature of the ciliary ganglion and may provide a basis for the understanding of the diverse physiological functions of this ganglion.

Animals↗

PubMed1984

Evidence for noncholinergic ganglionic neural stimulation of B cell secretion.

Insulin levels increase after 2-deoxyglucose (2DG) administration in dogs. This observation is in contrast to the decrease in insulin level post-2DG in baboons and rabbits. To evaluate a possible neural mechanism mediating this increase in insulin level, we studied normal mongrel dogs with 2DG alone, 2DG during ganglionic blockade, beta-adrenergic blockade, and postganglionic parasympathetic blockade. There was an increase in plasma epinephrine, norepinephrine, pancreatic polypeptide, insulin, and glucose post-2DG alone. During ganglionic blockade, the increase in epinephrine, norepinephrine, and pancreatic polypeptide post-2DG was completely abolished, verifying ganglionic blockade of sympathetic and parasympathetic pathways, respectively. Despite this, ganglionic blockade failed to abolish the insulin rise after 2DG. Postganglionic parasympathetic blockade did not change the insulin rise after 2DG. However, beta-adrenergic blockade completely abolished the insulin rise after 2DG. The above data suggests that 1) the insulin rise post-2DG is beta-adrenergic but 2) the ganglionic neurotransmitter mediating the 2DG-induced insulin rise during ganglionic blockade is noncholinergic (possibly peptidergic).

Animals↗

PubMed1990

Presynaptic modulation of ganglionic ACh release by muscarinic and nicotinic receptors.

The present experiments were undertaken to investigate the effects of atropine and d-tubocurarine on acetylcholine (ACh) release and ganglionic synaptic transmission in the isolated cat stellate ganglion. Ganglionic release of picomole amounts of ACh was measured by radioenzymatic assay, and ganglionic transmission was estimated on the basis of the compound action potential recorded from the postganglionic stellate cardiac nerve. Atropine (5 microM) produced a significant increase in both spontaneous and evoked ACh release from the ganglion while depressing synaptic transmission. d-Tubocurarine (20 microM) also caused a significant, though smaller, increase in spontaneous release of ACh but had little effect on evoked release of ACh. These results suggest that ACh release and synaptic transmission in the cat stellate ganglion are subject to cholinergic feedback regulation, which appears to be mediated predominantly via muscarinic presynaptic receptors.

Acetylcholine↗

PubMed2004

Parasympathetic control of the heart. I. An interventriculo-septal ganglion is the major source of the vagal intracardiac innervation of the ventricles.

The locations, projections, and functions of the intracardiac ganglia are incompletely understood. Immunocytochemical labeling with the general neuronal marker protein gene product 9.5 (PGP 9.5) was used to determine the distribution of intracardiac neurons throughout the cat atria and ventricles. Fluorescence microscopy was used to determine the number of neurons within these ganglia. There are eight regions of the cat heart that contain intracardiac ganglia. The numbers of neurons found within these intracardiac ganglia vary dramatically. The total number of neurons found in the heart (6,274 +/- 1,061) is almost evenly divided between the atria and the ventricles. The largest ganglion is found in the interventricular septum (IVS). Retrogradely labeled fluorescent tracer studies indicated that the vagal intracardiac innervation of the anterior surface of the right ventricle originates predominantly in the IVS ganglion. A cranioventricular (CV) ganglion was retrogradely labeled from the anterior surface of the left ventricle but not from the anterior surface of the right ventricle. These new neuroanatomic data support the prior physiological hypothesis that the CV ganglion in the cat exerts a negative inotropic effect on the left ventricle. A total of three separate intracardiac ganglia innervate the left ventricle, i.e., the CV, IVS, and a second left ventricular (LV2) ganglion. However, the IVS ganglion provides the major source of innervation to both the left and right ventricles. This dual innervation pattern may help to coordinate or segregate vagal effects on left and right ventricular performance.

Animals↗

PubMed1976

Responses to acetylcholine of ganglion cells in an isolated mammalian retina.

1. Rabbit retinas were isolated and superfused with a physiological medium. Ganglion cell activity was recorded during stimulation with focused light, and receptive fields were mapped. Receptive fields were identical to those found in vivo and did not change during a 6-h incubation. After the receptive field of a ganglion cell had been identified, acetylcholine or related agents were introduced singly or in combination into the medium, and their effect on the cell's spontaneous and light-evoked activity was observed. 2. Ganglion cells with on-center or directionally selective receptive fields were excited when ACh was added to the medium. The response to exogenous ACh was prevented by cholinergic antagonists. 3. These cells' spontaneous activity and response to light were enhanced by anticholinesterase and depressed by cholinergic antagonists. Antagonists varied in their ability to block the light-evoked response, with dihydro-beta-erythroidine the most effective. 4. Thresholds for ACh or the related agents were low, ranging from 1 to 40 muM; their effects were rapidly and completely reversed when the retina was returned to control medium. 5. In retinas incubated in medium containing 20 mM Mg2+ and 0.2 mM Ca2+, ganglion cells lost completely both their spontaneous and light-evoked activity, but retained their ability to generate action potentials in response to elevated K+. Ganglion cell activity rapidly returned to normal when the retina was returned to medium containing normal electrolytes. On-center and directionally selective cells were excited by ACh in retinas where synaptic transmission had been inhibited by 20 mM Mg2+ and 0.2 mM Ca2+. 6. The responses of on-center and directionally selective cells to ACh, to anticholinesterase, and to cholinergic antagonists in control medium indicate that the retina contains one or more synapses using ACh as a neurotransmitter. The response to ACh in retinas exposed to 20 mM Mg2+ and 0.2 mM Ca2+ suggests that at least one such synapse in on the ganglion cell itself. 7. Off-center cells were inhomogenous in their response to ACh. Although some responded just as the other classes of cell, the majority responded quite weakly and a subgroup was encountered which was entirely unaffected by even 1 mM ACh, by levels of physostigmine which inactivate virtually all retinal acetyl-cholinesterase, or by high concentrations of cholinergic antagonists. Only 2 of 20 off-cells tested in the presence of 20 mM Mg2+ and 0.2 mM Ca2+ were excited by ACh. Apparently ACh is not a primary transmitter for most off-cells.

Acetylcholine↗