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Acetylcholine receptors of thoracic dorsal midline neurones in the cockroach Periplaneta americana.

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Archives of Insect Biochemistry and Physiology 21 :289-301 (1992)
Acetylcholine Receptors of Thoracic Dorsal
Midline Neurones in the Cockroach,
Periplaneta americana
Donglin Bai, Heinrich Erdbrugger, Heinz Breer, and David B. Sattelle
AFRC Laboratory of Molecular Signalling, Department of Zoology, University of Cambridge,
Cambridge, United Kingdom (0.B., D. B.S.); lnstitute of Zoophysiology, University of
Stuttgart-Hohenheim, Stuttgart, Germany (H.E., H . B . )
The actions of acetylcholine and cholinergic ligands have been studied using dorsal
midline neuron= from the rnetathoracic ganglion of the cockroachPeriplaneta americana.
Both nicotine and oxotremorine depolarized dorsal midline neuronal cell bodies.
Doseresponse curves for nicotine and oxotremorine saturated at different levels.
Nicotine-induced depolarizations were completely or partially blocked by mecamylamine, d-tubocurarine, strychnine, and bicuculline, but were insensitive to a-bungarotoxin (100 nM), atropine (100 fl),
scopolamine (10 pM), and pirenzepine (50 pM).
Following pretreatment with collagenase, the dorsal midline neurones were sensitive to
high doses of a-bungarotoxin (3 @). Oxotremorine-induced depolarizations were
blocked by scopolamine (1 0 fl),
atropine (100 pM), and pirenzepine (50 $4) and were
insensitive to mecamylamine (10 pM) and d-tubocurarine(100 pM). The results indicate
the coexistence of at least two distinct acetylcholine receptors on dorsal midline neuronal
cell bodies in the cockroach metathoracic ganglion. o 1992 WiIey-Liss, Inc.
Key words: a-bungarotoxin, nicotinic acetylcholine receptor, muscarinic acetylcholine
receptor, mecamylamine, pirenzepine
Insect nAChRs", in contrast to vertebrates and some invertebrates, appear
to be confined to the nervous system and are present at relatively high
Acknowledgments: The authors are indebted to Drs. Colin A. Leech and Nicola M. Anthony for
helpful advice and discussion during the course of this work.
Received March 23, 1992; accepted July 21, 1992.
Address reprint requests to David B. Sattelle, AFRC Laboratory of Molecular Signalling, Department
of Zoology, University of Cambridge, Downing Street, Cambridge CB2 3EJ, U.K.
*Abbreviations used: ACh = acetylcholine; CNS = central nervous system; Q = fast coxal depressor
motor neurone; DM = dorsal midline neurone; DUM = dorsal unpaired median neurone; DUMETi =
dorsal unpaired median neurone innervating the extensor tibiae muscle; EC50 = concentration required
to produce 50% of maximum response; lCS0 = concentration requiredto inhibit response by 50%; mAChR
= muscarinic acetylcholine receptor; nAChR = nicotinic acetylcholine receptor; R = resistance.
0 1992 Wiley-Liss, Inc.
Bai et al.
concentrations [l].Many insect nicotinic receptors are sensitive to a-bungarotoxin [2]. For example, this snake toxin blocks functional nicotinic receptors on identifiable interneurones [3-51 and motor neurones in the cockroach
Peripluneta americana [4,6,7]. However, dorsal unpaired median neurone
(DUMETi) of the locust Schistocerca nitens and unidentified DUM neurones in
the third thoracic ganglion of cockroach respond to nicotine, but are less
sensitive to a-bungarotoxin [8,9], Also, a depolarizing response to nicotine
that is insensitive to a-bungarotoxin is present in the larval nervous system
of Drosophila melanogaster [ 101. Insect muscarinic receptors, though less abundant overall, are also widely distributed in the nervous system of the locust
Locusta migratoria [ll],cockroach [12-141, and Drosophila [10,15,16].
Dorsal unpaired median neurones have been characterized in several insect
orders, such as cockroach [17], firefly [18], moth [19], and cricket [20]. Located
on the dorsal midline of the ganglion, they send axons symmetrically to both
sides of peripheral nerve roots of the ganglion.
The DUM neurones in the metathoracic ganglion of the cockroach have
been classified into 6 different types on the basis of the branching of their
axons 1171.
A differential sensitivity to a-bungarotoxin between the identifiable fast
coxal depressor motor neurone Df and dorsal midline neurones of the cockroach metathoracic ganglion has been detected [9]. Recently, using dissociated, cultured, dorsal midline neurones from the cockroach terminal
abdominal ganglion, Lapied et al. [21] detected more than one type of
cholinergic receptor, including one that is a-bungarotoxin-insensitive. Although a detailed pharmacological profile has been determined for the nicotinic type of receptors on motor neurone Df in situ [7], little is known of the
cholinergic pharmacology of in situ dorsal midline neurones.
Neuronal nicotinic receptors that exhibit differences in sensitivity to a-bungarotoxin and K-bungarotoxin are present in the nervous systems of vertebrates [22,23], but less is known of the diversity of nicotinic receptors in
insects. Recently, cloning and sequencing of putative insect nicotinic receptor
subunits have revealed both d i k e and non-a-like polypeptides 126273.
Subtypes of muscarinic receptors, which share some pharmacological properties with the Mi and M2 receptors of vertebrates, have been detected in the
insect nervous system [ZS]. Also, two putative muscarinic receptors have been
cloned and sequenced from Drosophila 129,301. In the present study, pharmacological data suggest the coexistence of nicotinic receptors and pirenzepinesensitive muscarinic receptors on cell bodies of thoracic dorsal midline
neurones of the cockroach (Periplanefa a7sericana).
Experiments were performed at room temperature (21-24°C) on adult male
cockroaches. The methathoracic ganglion was removed from the animal,
desheathed, and then transferred to a Perspex experimental chamber, perfused continuously with cockroach saline at a rate of 1ml/min. Drug applica-
nAChRs of Dorsal Midline Neurones
tion was via this bath perfusion system, either using a pipette to inject 100 pl
agonist directly into the chamber, or using a syringe pump (Raze1A-99; Raze11
Scientific Instruments, Inc., Stanford, CT) to inject agonists into the experimental chamber. Cells were located using a binocular microscope. Intracellular recordings were made from neuronal cell bodies located in the dorsal
midline region of the ganglion, using glass microelectrodes (R = 20-50M a)
filled with 2 M potassium acetate solution and connected to a high-impedance
DC amplifier. Cockroach saline consisted of 214 mM NaC1,3.1 mM KCl, 9 mM
CaClz, 50 mM sucrose, 10 mM TES (adjusted to pH 7.2 with NaOH). The DM
cells investigated are a group of four large-diameter DUM neurones.
Nicotine, strychnine hydrochloride, d-tubocurarine chloride, mecamylamine, oxotremorine, scopolamine, atropine sulfate, collagenase type V, and
hyaluronidase type I-S were obtained from Sigma Chemical Co. (St. Louis,
MO). The purified snake toxins a-bungarotoxin and K-bungarotoxin were
obtained from Biotoxins (St. Cloud, FL). Pirenzepine was obtained from Dr.
Karl Thomae GmbH, Biberach a.d. Riss, Germany. Bicuculline methiodide
was purchased from Cambridge Research Biochemicals (Cambridge UK).
Depolarization of dorsal midline cells was detected following exposure to
certain nicotinic and muscarinic cholinergic agonists. Nicotine, a potent
nicotinic acetylcholine receptor agonist, depolarized the cell body membrane
of dorsal midline neurones at concentrations above 10 nM. Peak depolarization (about 30 mV) was observed at 10 p M nicotine, and was accompanied by
an increase in membrane conductance. The EC50 value for nicotine on dorsal
midline neurones (0.2 pM) reveals that these cell bodies are slightly more
sensitive to this agonist than the cell body membrane of motor neurone Df
(EC50 = 3 pM) in the same ganglion [7]. A typical depolarization response
induced by syringe pump application of nicotine is shown in Figure 1.
Oxotremorine, a muscarinic agonist, also depolarized cell bodies of dorsal
midline neurones. Compared to nicotine-induced responses, the oxotremorine-induced depolarizations displayed a slower onset and longer duration
2 min
Fig. 1. Depolarization of a dorsal midline neuronal cell body by bath-applied nicotine (10 pM,
arrowhead indicates onset) and oxotremorine (100 pM, filled circle indicates onset). The voltage
responses were recorded intracellularly from the same cell. Agonists were injected via a syringe pump
(10 s application) into the continuously flowing saline. Resting membrane potential was -64 rnV.
4Q -
0 -
Loglo ILigandl
Fig. 2. Dose-response curves for depolarizing actions of bath-applied cholinergic agonists on dorsal
midline neurones. The mean peak amplitude of depolarization i s recorded for various concentrations
of bath-applied nicotine (0)carbarnylcholine
oxotrernorine (A).
Vertical bars represent twice
t h e standard error of the mean (n = 3).
(Fig. 1).Dose-response curves for the depolarizing actions of bath-perfused
nicotine, oxotremorine, and carbamylcholine were constructed (Fig. 2). Depolarizing responses to nicotine and carbamylcholine saturated at a higher
level than responses to oxotremorine. All were more effective than acetylcholine. The presence of the anticholinesterase neostigmine (1 pM) enhanced
sensitivity to acetylcholine.This was further increased by a 5 min pretreatment
of the tissue with a mixture of the enzymes collagenase (0.5 mg/ml) and
hyaluronidase (0.5 mglml) (Fig. 3). Thus, the low sensitivity of dorsal midline
cells to exogenous acetylcholine appears to be due to enzymatic breakdown
of the neurotransmitter, and physical barriers.
Actions of nAChR Antagonists
Cholinergic antagonists were used to test for the existence of subpopulations of cholinergic receptors on dorsal midline neurones.
Mecamylamine and d-tubocurarine. Mecamylamine is a potent blocker
of vertebrate ganglionic nicotinic receptors [31] and nicotinic receptors of the
cockroach motor neurone Df [7]. When bath-applied at a concentration of 10
pM, mecamylamine was normally ineffective (n = 6 ) on dorsal midline
neurones, but following an application at 100 pM it blocked 90% the response
to nicotine (n = 8; Fig. 4a). Thus responses to nicotine on dorsal midline
neuronal cell bodies were less sensitive to mecamylamine than those of the
cell body of motor neurone Db for which an IC50 of 2.5 pM was estimated [7].
Mecamylamine (10 pM n = 4;100 pM, n = 6 )failed to block oxotremorine-in-
nAChRs of Dorsal Midline Neurones
ACh + NeoQtgmine + E I T Z ~ ? S *
40 -
0 -
Fig. 3. Dose-response curves for depolarizing actions of bath-applied acetylcholine on dorsal
midline neurones. The desheathed preparations are bathed in saline (O),
saline containing 1 fl
neostigmine (O), or saline containing neostigmine after pretreatment of the preparation with a
mixture of collagenase (0.5 mg/ml) and hyaluronidase (0.5 mg/ml) for about 5 min (A).In the
presence of the enzymes and the anticholinesterase neostigrnine, dorsal midline cells respond to
lower concentrations of acetylcholine.
15 mln
21 mln
Fig. 4. Actions of bath-applied mecamylamine on nicotine-induced (1 0 KM nicotine, arrowheads
indicate onset) and oxotremorine-induced (1 00 pM oxotremorine, filled circles indicate onset)
depolarizations of dorsal midline neurones. Mecamylamine (1 00 p,M) totally blocked the nicotineinduced depolarizations (a) and was without effect on oxotremorine-induced depolarizations (b).
Resting membrane potential was -85 mV.
Bai eta!.
duced depolarization of dorsal midline neurones (Fig. 4b). Another nAChR
antagonist, d-tubocurarine (100 kM, n = 4), was found to block the depolarizing response to nicotine, but failed to block oxotremorine-induced
responses of the same neurones.
a-Bungarotoxin and K-bungarotoxin. a-Bungarotoxin, a blocker of vertebrate muscle nicotinic acetylcholine receptors, is effective on insect nicotinic
receptors of motor neurone Df [7]. K-Bungarotoxin ( = neuronal bungarotoxin)
is an antagonist of many vertebrate neuronal nicotinic acetylcholine receptors.
This toxin also blocks the nicotinic receptors of motor neurone Df [32]. On
dorsal midline neurones, a-bungarotoxin (0.1 pM) and K-bungarotoxin (0.1
pM) failed to block the depolarizing actions of nicotine (n = 3 for each toxin;
Fig. 5 ) . A higher concentration of a-bungarotoxin (0.5 pM, n = 1) also failed
to block nicotine-induced depolarization even after a 107 min exposure.
However, following pretreatment with collagenase (0.5 mg/ml) and hyaluronidase (0.5 mg/ml), a higher dose of a-bungarotoxin (3 pM) did block
responses to nicotine. So the dorsal midline cells are much less sensitive to
a-bungarotoxin than Df, but are not completely insensitive.
Actions of "Non-nAChR" Antagonists
Bicuculline. Bicuculline, a specific antagonist for vertebrate GABAA receptors [33], was found to be an antagonist at acetylcholine receptors on cell
body membranes of dissociated locust neurones [34], and cockroach motor
neurone Df in situ (S.D. Buckingham and D.B. Sattelle, unpublished observations), On cockroach dorsal midline neurones, a high dose of bicuculline
(100 p M ) partially and reversibly blocked nicotinic responses (Fig. 6), while a
lower concentration of bicuculline was without effect.
Strychnine. Low concentrations of a vertebrate glycine receptor antagonist [35], strychnine (10 pM), failed to block nicotine-induced depolarizations
on dorsal midline neurones (n = 5). However, following perfusion with 100
1.ox10 - 7 ~
127 mln
1.ox10 - 7 ~
145 min
Fig. 5. Effects of bath-applied a-bungarotoxin and K-bungarotoxin on nicotine-induced responses
of dorsal midline neurones in desheathed metathoracic ganglia. Perfusion with saline containing
a-bungarotoxin (0.1 FM) and K-bungarotoxin (0.1 IJM) is without effect on the nicotine-induced
responses (arrowheads indicate the onset of 10 pM nicotine). Resting membrane potentials were
about -75 mV for both experiments.
nAChRs of Dorsal Midline Neurones
26 min
26 min
1.ox10 - 4 ~
18 min
19 min
10 mln
Fig. 6. The effects of bicuculline and strychnine on the nicotine (1 0 pM)-induceddepolarizations
on the dorsal midline neurones. Bicuculline (100 pM) partially and reversibly blocks the
nicotine-induced depolarization. Strychnine (1 00 p.M) reversibly blocks the response to nicotine.
Resting membrane potentials were -70 mV (upper traces) and -72 rnV (lower traces). Arrowheads
indicate onset of nicotine application.
pM strychnine the response to nicotine was almost totally blocked. Nicotineinduced responses recovered from strychnine block after rebathing with
normal saline (n = 4; Fig. 6).
Actions of mAChR Antagonists
Scopolamine and atropine. The muscarinic antagonist scopolamine (10
pM) blocked the depolarizing actions of oxotremorine (100 pM, n = 6), but
failed to modify the response to 10 pM nicotine (n = 6; see Fig. 7). Following
block by scopolamine, the response to oxotremorine sometimes recovered on
rebathing the preparation in normal saline, but in other preparations recovery
was incomplete even after a prolonged (2 h) wash. Thus, scopolamine blocked
only the slower, oxotremorine-induced depolarization.
Another muscarinic antagonist atropine (1 rnM, n = 1; 100 pM, n = 5)
reversibly blocked oxotremorine-induced depolarization. Atropine (100 pM)
failed to block the response of dorsal midline neurones to nicotine, in contrast
with the findings for motor neurone Dr [7].
Pirenzepine. Pirenzepine is a specific blocker for the Mi subtype of
muscarinic acetylcholine receptors [36]. Bath-applied pirenzepine (50 yM)
blocked the response of dorsal midline neurones to oxotremorine, but not to
nicotine. Rebathing with normal saline resulted in partial recovery of the
response (Fig. 8). Thus, pirenzepine-sensitive mAChRs are present on dorsal
midline neuronal cell bodies.
Bai et at.
14 min
17 min
Fig. 7 . Actions of scopolamine on the oxotremorine (100 pM)-induced and nicotine (10
pM)-induced depolarizations of a dorsal midline neurone are illustrated. The response to
oxotremorine application (filled circles) i s totally blocked by scopolamine (10 pM), while the
response of the same cell to nicotine (arrowheads) i s unaffected. Resting membrane potential
was -80 rnV.
Acetylcholine receptors on dorsal midline neuronal cell bodies in the
cockroach have been described. Electrophysiological studies have shown
that both nicotine and oxotremorine depolarize these cells. The response
to nicotine rapidly follows the onset of bath-application of the ligand and
sometimes induces a short burst of action potentials. In contrast, the
response to oxotremorine develops more slowly, resulting in a prolonged
In vertebrates there are two quite distinct forms of cholinergic receptor
which serve quite distinct functions [37]. Fast-acting nicotinic receptors of
muscle and CNS [38,39] are normally associated with an increase in cation
(mainly Na', K', and Ca+ +) conductance, though recently a nicotinic
response coupled to a K+-selective channel has been detected [40]. By
contrast, a modulatory role is often attributed to vertebrate muscarinic recepControl
+Pirenz ine
50x10&P M
15 min
14 min
Fig. 8 . Pirenzepine, an MI subtype-specific muscarinic antagonist (50 pM), blocked oxotrernorine
(1 00 pM, filled circles)-induced depolarizations. After rebathing the preparation in normal saline, the
oxotremorine-induced depolarizations partially recovered. Resting membrane potential was -80 mV.
nAChRs of Dorsal Midline Neurones
tors which can control the rate and amount of information transfer in selected
pathways in the nervous system. Muscarinic actions of acetylcholine may
involve a variety of conductance mechanisms and involve a number of
different receptor subtypes [37], including activation or depression of certain
(particularly K + ) cation conductances.
One interpretation of our results is that a cholinergic receptor with "mixed"
(i.e., muscarinichicotinic) pharmacological properties is present on dorsal
midline neurones. Binding studies have indicated that putative receptors with
a mixed pharmacology may be present in insect nervous tissue [4143].
Adopting this model to account for all the findings for the dorsal midline cells,
it is difficult to reconcile the scopolamine, atropine, and pirenzepine block of
the slower oxotremorine-induced depolarization with the absence of any
action of these antagonists on nicotine-induced depolarization. Also, the
nicotinic antagonists mecamylamine and d-tubocurarine blocked nicotine-induced depolarization, but did not impair the depolarization in response to
oxotremorine recorded from the same cell.
Thus, the cholinergic pharmacology of dorsal midline cells strongly indicates the coexistence of distinct muscarinic and nicotinic receptor types on the
same neurone. Other observations support this view, namely the striking
differencesin the rise-time and duration of the depolarizing actions of nicotine
and oxotremorine. Also the dose-response curves for nicotine and oxotremorine saturated at different levels. Three pharmacologically distinct acetylcholine receptors have been detected on identified neurones in the pleural
ganglion of Aplysia californica [44].They are distributed in different combinations on functionallydistinct neurones. Benson [45]has shown the coexistence
of two distinct cholinergic receptors on unidentified dissociated locust neurones corresponding to nicotinic and muscarinic subtypes. Recently, dual
muscarinic and nicotinic actions have been seen on Drosophila neurones [lo],
though it remains to be determined whether or not they are present on the
same cell.
The responses to nicotine of thoracic dorsal midline cells differ from those
of motor neurone Df (Table 1).The nicotinic receptors of dorsal midline cells
appear less sensitive to nicotinic antagonists, such as mecamylamine and
d-tubocurarine, and in particular a-bungarotoxin. In view of the effects of
enzyme treatment on the acetylcholine dose-response curve, poor accessibility of chemicals onto the cell surface of dorsal midline neurones may account
for this reduced sensitivity, though intrinsic differencesin receptor pharmacology cannot be ruled out [9]. Also, dorsal midline neurones in situ [present
study] appear less sensitive to cholinergic ligands than isolated cells [21],
which may be due to improved drug access to the neuronal membrane in
dissociated, enzyme-treated cells.
Pharmacologically distinct subtypes of muscarinic receptors, termed MI
and M2, have been established in both vertebrates [36] and in insects [ll].
Pirenzepine, a novel muscarinic antagonist, binds with high affinity to the MI
type receptor, and can be employed to distinguish between the two receptor
types. In insects, muscarinic binding sites in synaptic membranes display a
low affinity for pirenzepine, indicating that M2 receptors predominate in
nerve terminals. Conversely, pirenzepine-sensitive receptor subtypes are
Bai et at.
TABLE 1. Pharmacology of Nicotinic Receptors of Functionally Distinct Cockroach
Neurones Studied In Situ*
Cell type
*Abbreviations: + = agonist; - = ineffective blocker at concentrations up to 100 $4; -a =
ineffective blocker at concentrations up to 100 nM; DM = dorsal midline neurone; D, = slow
extensor motor neurone; GI2 = giant interneurone 2; LFHSN = lateral filiform hair sensory
neurone; n.t. = not tested. All other abbreviations are as in the text.
"S.D. Buckingham and D.B. Sattelle, unpublished observations.
more abundant on the cell bodies [ll].In a brief report, Benson [46] has
confirmed the existence of Mi-like receptors on isolated, unidentified locust
neuronal somata, which are blocked by QNB, scopolamine, and pirenze ine
The EC5o for pirenzepine in these experiments was 7.1 ? 4.5 x 10- M,
whereas rnethoctramine, an M2 type mAChR blocker, was without effect.
Recent binding studies on mAChRs from 3 insect species, including cockroach, have shown high affinity for 4-DAMP, an M3-selective antagonist [47].
Furthermore, there is a preferential coupling of vertebrate MI and M2 receptors to the regulation of phosphoinositide hydrolysis and adenylate cyclase
systems respectively [16]. In insects there is evidence that M2 type receptor
may be involved in autoregulation of ACh release and they may be negatively
linked to adenylate cyclase [113.
It will be of interest to extend these studies, using a uniquely identifiable
dorsal midline neurone (DUM5rl) recently described in the cockroach metathoracic ganglion [48]. Further experiments are needed to characterize the
different nicotinic and muscarinic receptors and their associated signal transduction mechanisms in the nervous systems of insects, but here we provide
evidence for the coexistence of representatives of each class on dorsal unpaired median neurones of the cockroach metathoracic ganglion.
Y .
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cockroaches, acetylcholine, neuronet, dorsal, periplaneta, receptors, thoracica, american, midline
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