Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Dihydro-beta-Erythroidine”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1977

Substance P and Renshaw cells: a new concept of inhibitory synaptic interactions.

1. The actions of microelectrophoretically administered substance P on Renshaw cells in pentobarbitone anaesthetized cats were investigated. 2. The effects on spontaneous and synaptic firing and interactions with a number of other agents including acetylcholine, acetyl-beta-methylcholine, acidic amino acids, morphine, dihydro-beta-erythroidine and strychnine were studied in attempts to elucidate the mechanism of action of substance P. 3. Substance P usually selectively depressed the excitation by ACh, and also reduced submaximal synaptically evoked discharges which activate nicotinic receptors, but failed to modify excitation caused either by acetyl-beta-methylcholine, which activates muscarinic receptors, or excitation caused by glutamate or homocysteate. Substance P also depressed excitation by morphine which acted via the nicotinic receptors. 4. The inhibitory effect was not blocked by strychinine and was considered to be unlikely to be due to interaction between the polypeptide and either glycine or GABA receptors. 5. On some cells substance P caused excitation which was blocked by dihydro-beta-erythroidine. Mixed excitatory-inhibitory effects were observed on some of these neurones. 6. The results are discussed in relation to the possibility that substance P could function as a synaptic inhibitory mediator with an unusual selectivity of action.

Acetylcholine↗
PubMed1975

Acetylcholine receptors on Renshaw cells of the rat.

Experiments have been performed on Renshaw cells of rats to investigate the receptors mediating both the responses to electrophoretically applied cholinergic excitants and the synaptic excitation following stimulation of the ventral roots. The effects of atropine and dihydro-beta-erythroidine, muscarinic and nicotinic antagonists respectively, have been tested on both types of excitation. Most importantly we found that in the rat the ventral root evoked response can be blocked by atropine as well as by DHbetaE. It was not possible to categorise the responses to the cholinergic agents in terms of muscarinic and nicotinic receptors. In addition we have failed the late (muscarinic) excitation seen in the cat.

Acetylcholine↗
PubMed1977

Responses of identified spinal neurones to acetylcholine applied by micro-electrophoresis.

1. The responses of identified cells in the cat Clarke's column and dorsal horn to micro-electrophoretically applied cholinomimetics and anti-cholinergic substances have been investigated. 2. Both antidromically identified (DSCT neurones) and synaptically activated neurones from the region of the Clarke's column of the spinal cord were excited by ACh. However, the proportion of ACh excited cells was greater in units synaptically activated by ipsilateral dorsolateral funiculus stimulation (78%) than in DSCT neurones (50%). In addition, about 55% of neurones activated either antidromically or synaptically by ipsilateral dorsal column stimulation were excited by ACh. 3. In contrast to a relatively weak excitatory potency on the DSCT neurones (maximum firing frequency did not exceed 130% of the control activated by ipsilateral dorsolateral funiculus stimulation (maximum firing frequency reached 430% of the control level). 4. ACh has a relatively quick and rapidly reversible excitatory effect on Clarke's column neurones and some types of dorsal horn interneurones, which can be obtained also with nicotine. However, the action of nicotine is frequently delayed in onset and recovery. This excitatory action of ACh can be blocked or markedly depressed by dihydro-beta-erythroidine. These results and those obtained with acetyl-beta-methylcholine and atropine seem to suggest that the receptors mediating excitation of the cholinoceptive spinal cells activated either antidromically or synaptically by ipsilateral dorsolateral funiculus stimulation besides predominantly nicotinic have also weak muscarinic properties. 5. Desensitization with repeated applications of ACh and nicotine has been observed in both DSCT neurones and units antidromically activated by ipsilateral dorsal column stimulation. 6. About 11% of units antidromically activated by ipsilateral dorsolateral funiculus stimulation were depressed by ACh. In addition, the depressant effect of ACh was more frequently encountered in the cells unresponsive either to the dorsolateral funiculus or dorsal column stimulation. ACh depression was also seen in units activated either antidromically or synaptically by ipsilateral dorsal column stimulation. In contrast, none of the units synaptically activated by the ipsilateral dorsolateral funiculus stimulation were depressed by ACh. The same was true for spinal neurones receiving convergent peripheral inputs activated either antidromically or synaptically by ipsilateral dorsolateral or dorsal column stimulation. 7. The findings that ACh depression of all tested DSCT neurones is blocked by atropine and readily evoked by acetyl-beta-methylcholine indicates that receptors mediating the effect are of muscarinic type.

Acetylcholine↗
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↗
PubMed1975

Synaptic organization in teleost spinal motoneurons.

Glass microelectrodes were inserted into motoneurons innervating pectoral fin muscles to record action and synaptic potentials, evoked by electrical stimulation of ventral and dorsal roots, and the medulla oblongata. Ventral root stimulation evoked a small depolarizing response which had properties compatible with those of the EPSP; its amplitude changes were graded, being increased by membrane hyperpolarization and decreased by high frequency repetitive stimulation. The latency of the response was sufficiently longer than that of the antidromic spike to allow for a monosynaptic delay. Stimulation of the dorsal root produced EPSPs with relatively long latencies, suggesting mediation by a polysynaptic pathway. EPSPs with short latencies were evoked by stimulation of the medulla oblongata, indicating the presence of a monosynaptic excitatory connection. Action potentials, recorded from peripheral nerve after stimulation of the medulla oblongata, were facilitated by conditioning volleys via ventral roots. This facilitation was blocked by dihydro-beta-erythroidine hydrobromide and atropine sulphate, indicating the cholinergic nature of the EPSP of ventral root origin. The conduction velocities of motor axons and of the ventral roots fibers responsible for production of EPSPs were about the same. The EPSP of ventral root origin had a slower rising time course and lesser sensitivity to shifts of membrane potential than the EPSP of medulla oblongata origin, suggesting that the sites of generation of the former EPSP were on the peripheral dendrites. From the above results, it was concluded that the EPSP of ventral root origin was mediated by recurrent axon collaterals of motoneurons.

Action Potentials↗
PubMed1975

Micro-electrophoretic studies in the cat pulvinar region: effect of acetylcholine.

1. In the posterior half of the pulvinar of cats anaesthetized with halothane and nitrous oxide, the majority of neurons were fired by ACh released with small electrophoretic currents. In the anterior part of that nucleus, ACh had more variable effects: excitation, depression or none. 2. In comparison with L-glutamate, DL-homocysteic acid and DL-aspartic acid, ACh appeared to be the most potent excitant. 3. ACh-induced discharges were easily and reversibly blocked by low doses of atropine. In most cases, ACh effects could not be blocked selectively by mecamylamine or dihydro-beta-erythroidine. 4. Nicotine failed to mimic ACh, whereas carbachol was a potent excitant and was readily blocked by low doses of atropine. 5. The histochemical reaction to acetylcholinesterase was moderate in the pulvinar. 6. These observations support the view that pulvinar cells differ from other thalamic cells.

Acetylcholine↗
PubMed1976

Drug-induced rhythmical activity in the inferior olivary complex of the rat.

Experiments have been performed on pentobarbitone anesthetized or decerebrated rats. The nature of the synchronous rhythmical activity which occurs in the inferior olive following the electrophoretic or systemic administration of harmaline, harmine, dihydro-beta-erythroidine and various other compounds, is described. Harmine was shown to reduce the late phase of biphasic unitary action potentials and to evoke massed synchronous rhythmical activity on which the units were superimposed. The beta-carboline was more effective than ACh or DL-homocysteate (DLH) in increasing cell discharge rates. Synchronized rhythmical activity was recorded more than 500 mum from the site of ejection of the rhythm-inducing drugs. Developed rhythmical activity reduced the size of antidromic field potentials, but antidromic invasion could reset the rhythm of submaximal rhythmical activity. The effects of ACh and DLH, glycine, GABA, NA, DA and 5-HT were tested on established rhythmical activity. Of these, 5-HT was the only compound which almost invariably antagonized the rhythm. A number of tryptamine derivatives and reported 5-HT antagonists, as well as parachlorophenylalanine, have been tested, but the results were largely inconclusive. The hypothesis is advanced that the drug-induced rhythm results from the inhibition of a tonic inhibitory serotonergic input. This antagonism releases an innate tendency of olivary cells to discharge both rhythmically and synchronously.

Acetylcholine↗
PubMed1975

Acetylcholine-sensitive cells in the caudal medulla of the rat: distribution, pharmacology and effects of pentobarbitone.

1. The distribution of cholinoceptive and non-cholinoceptive cells in various nuclei of the caudal medulla of the rat is described. 2. The nature of the responses of cells of the paramedian reticular nucleus and of the perihypoglossal nuclei to electrophoretically applied acetylcholine (ACh) was investigated. 3. In unanaesthetized decerebrate preparations ACh responses were usually of a "fast onset-fast offset" nature. Dihydro-beta-erythroidine was a more effective antagonist than atropine. 4. In rats anaesthetized with barbiturate nearly all the tach responses showed a slower onset and prolonged action. Atropine was the more effective antagonist. 5. The synaptic responses of cells of the paramedian reticular and perihypoglossal nuclei to stimulation of glossopharyngeal, superior laryngeal, lingual and hypoglossal nerves were investigated. It is concluded that ACh does not mediate the responses at the level of these nuclei.

Acetylcholine↗
PubMed1976

General anaesthetics and the acetylcholine-sensitivity of cortical neurons.

1The effects of general anaesthetics on neuronal responses to iontophoretically-applied acetylcholine have been examined in slices of guinea-pig olfactory cortex maintained in vitro. 2 Acetylcholine excited 61% of the prepiriform neurones tested. The excitation was blocked by atropine, but not by dihydro-beta-erythroidine or gallamine. 3 Alphaxalone reversibly depressed the acetylcholine-sensitivity of prepiriform neurones. Pentobarbitone did not consistently depress the acetylcholine sensitivity of these cells. 4 Ether, methoxyflurane, trichloroethylene and halothane caused a dose-related augmentation of acetylcholine-induced firing. 5 These results show that general anaesthetics do not necessarily depress the sensitivity of nerve cells to all excitatory substances and that different anaesthetics may affect a particular excitatory process in various ways.

Acetylcholine↗
PubMed1976

Observations on the pharmacology of cholinoceptive neurones in the rat brain stem.

The pharmacology of spontaneously active cholinoceptive neurones in the brain stem of rats anaesthetized with urethane has been investigated using microiontophoresis to administer muscarinic and nicotinic agonists and antagonists. 2. Acetylcholine (ACh) excited most cells but occasionally depressed their activity. Muscarine, and the muscarinic agonists methacholine and bethanechol produced prolonged excitation or inhibition of cells whereas nicotine produced prolonged excitations but no inhibitions. 3 Atropine selectively antagonized ACh excitations and both excitation and inhibition of neuronal activity produced by muscarine and muscarinic agonists, but not the excitations produced by nicotine, glutamate or DL-homocysteic acid. 4 Dihydro-beta-erythroidine (DHBE) and tubocurarine antagonized both ACh and nicotine excitations but not those induced by glutamate or DL-homocysteic acid. Inhibitions by ACh or muscarine were not affected. 5 It is concluded that excitations of cholinoceptive neurones in the rat brain stem may be mediated by activation of both muscarinic and nicotinic receptors whereas inhibitions are mediated by activation of a muscarinic receptor.

Acetylcholine↗
PubMed1977

An excitatory action of iontophoretically administered lithium on mammalian central neurones.

1 The action of iontophoretically administered lithium was studied on spinal Renshaw cells an interneurones and on supraspinal neurones in cerebral cortex, thalamus, hypothalamus and brain stem in anaesthetized cats and rats. 2 There was a correlation between the effects of Li+ and those of acetylcholine (ACh), although rather more cells were unaffected by Li+ than by ACh. 3 The usual effect was an excitation of rather slow onset, but occasionally effects were produced with time courses similar to those of ACh. The excitation was blocked by ACh antagonists and was best demonstrated with dihydro-beta-erythroidine on Renshaw cells. 4 The postsynaptic excitant action of ACh on Renshaw cells was reduced by Li+. 5 Depressant actions of Li+ were encountered on cells also depressed by ACh. 6 It is concluded that Li+ may facilitate cholinergic transmission at some sites in the CNS by increasing the release of ACh by an unknown mechanism. Similar effects at non-cholinergic synapses might also occur but would appear to be of less importance. Since facilitation of neuronal firing with Li+ was usually observed, the depressant effects on postsynaptic responses to ACh may be of little consequence.

Acetylcholine↗
PubMed1975

The relative importance of central nervous catecholaminergic and cholinergic mechanisms in drinking in response to antiotensin and other thirst stimuli.

1. Intracranial or subcutaneous doses of atropine or atropine methyl nitrate that were fully effective at preventing drinking in response to intracranial carbachol did not block angiotensin-induced drinking. 2. The nicotinic antagonist dihydro-beta-erythroidine given intracranially affected neither angiotensin- nor carbachol-induced drinking. 3. The dopaminergic antagonists haloperidol and spiroperidol injected intracranially blocked angiotensin-induced drinking but did not affect carbachol-induced drinking. 4. Angiotensin- and carbachol-induced drinking were unaffected by alpha- or beta-adrenergic antagonists except at toxic doses. 5. Destruction of catecholaminergic neurones with 6-hydroxydopamine markedly reduced angiotensin-induced drinking, but had relatively little effect on carbachol-induced drinking. 6. Intracranial haloperidol reduced the amount of water drunk in response to overnight deprivation of water, but did not affect feeding in response to overnight starvation or to intracranial noradrenaline. 7. Drinking following overnight water deprivation was unaffected by intracranial alpha- or beta-adrenergic antagonists. 8. Preventing dopaminergic transmission with intracranial haloperidol decreased the water to food ratio of the rat's intake after overnight starvation, whereas increasing the dopamine levels with the combination of FLA-63 and L-DOPA increased the ratio. 9. Intraventricular dopamine in large amounts caused the water-replete rat to drink. 10. It is concluded that among the many functions of dopaminergic systems in the brain is a role in the control of water intake, and that these systems participate in an important way in drinking in response to angiotensin.

Acetylcholine↗
PubMed1976

Inhibitory effects of acetylcholine on neurones in the feline nucleus reticularis thalami.

1. Short iontophoretic pulses of acetylcholine (ACh) inhibited almost every spontaneously active cell encountered in the nucleus reticularis thalami of cats anaesthetized with a mixture of halothane, nitrous oxide and oxygen. On 200 cells the mean current needed to eject an effective inhibitory dose of ACh was 67 +/- 2 nA. When the ACh-evoked inhibition was mimicked by gamma-aminobutyric acid (GABA) or glycine on the same cell, the current required to release ACh was found to be approximately twice as great as that required to release an equally effective dose of GABA or glycine. 2. ACh inhibitions developed with a latency which was very much shorter than that for ACh excitation in cells of the ventrobasal complex. The latency of the ACh-evoked inhibition was as rapid as the onset and offset of the excitation of the same cells glutamate and their inhibition by GABA or glycine. 3. The firing pattern of ACh-inhibited neurones in the nucleus reticularis was characterized by periods of prolonged, high frequency bursts, and their mean firing frequency was 22 Hz. Raster dot displays and interspike interval histograms showed that whereas ACh suppressed the spikes that occurred between bursts much more readily than those that occurred during bursts, all spikes were equally sensitive to the depressant action of GABA and glycine. Large doses of ACh provoked or exaggerated burst activity. 4. ACh-evoked inhibition was extremely sensitive to blockade by short iontophoretic applications of atropine, which had no effect on the inhibitions evoked on the same cell equipotent doses of GABA or glycine. The ACh-evoked inhibitions were also antagonized by dihydro-beta-erythroidine released with slightly larger currents. When tested on the same cell, small iontophoretic applications of picrotoxin and bicuculline methoiodide blocked the inhibition evoked by GABA but had no effect on that evoked by ACh. Iontophoretic strychnine only rarely affected the inhibition evoked by ACh, while readily blocking the inhibition evoked on the same cell by an equipotent dose of glycine. In two cats, intravenous strychnine (1-2 mg/kg) had no effect on the ACh-evoked inhibition, while greatly reducing the sensitivity of the cell under study to glycine. 5. Only four out of forty-eight ACh-inhibted cells tested were inhibited by iontophoretic applications of either guanosine or adenosine 3':5'-phosphate. 6. Cells of the nucleus reticularis have been shown to have an inhibitory action on the thalamic relay cells, which are excited by ACh. It is suggested that the presence of both ACh excited and inhibited cells in different nuclei of the thalamus could be of considerable functional significance in gating sensory transmission through the thalamus.

Acetylcholine↗
PubMed1977

Synaptic excitation and inhibition resulting from direct action of acetylcholine on two types of chemoreceptors on individual amphibian parasympathetic neurones.

1. Synaptic transmission was studied in visually identified parasympathetic ganglion cells that modulate the heart beat of the mudpuppy Necturus maculosus).2. The brief pulse of acetylcholine (ACh) released from terminals of the vagus nerve after each impulse can produce two distinct post-synaptic responses in individual principal cells of the ganglion: (i) within a milli-second of release, ACh generates a rapid and strong excitatory post-synaptic potential (e.p.s.p.) that normally initiates a post-synaptic impulse; (ii) this excitation is usually followed by a slow hyperpolarizing inhibitory post-synaptic potential (i.p.s.p.) that lasts for several seconds. The magnitude and time course of the i.p.s.p. depends on the frequency and number of vagal stimuli. When the hydrolysis of ACh is inhibited by prostigmine, a train of nerve stimuli may be followed by an i.p.s.p. lasting half a minute or longer.3. The rapid e.p.s.p. and slow i.p.s.p. result from the direct action of ACh on two different types of chemoreceptors in the post-synaptic membrane of the principal cell. The e.p.s.p. can be preferentially blocked by the nicotinic antagonist dihydro-beta-erythroidine (5 x 10(-7)M), while the i.p.s.p. is selectively blocked by the muscarinic antagonist atropine (5 x 10(-9)M).4. Potentials resembling nerve-evoked e.p.s.p.s and i.p.s.p.s can be produced by iontophoretic release of ACh from micropipettes onto the post-synaptic membrane. Application of the muscarinic agonist bethanechol generates exclusively inhibitory responses.5. The reversal potential for the i.p.s.p. is about -105 mV, which is approximately the equilibrium potential for potassium (E(K)). When the external K(+) concentration is altered, the reversal potential for inhibition is shifted to the new value of E(K) as expected from the Nernst equation. Changes in the external Na(+) and Cl(-) concentrations have no appreciable effect on the reversal potential. Thus, the i.p.s.p. is the result of a conductance increase for K(+).6. The conductance change producing the i.p.s.p. is voltage sensitive. When the membrane potential is shifted from -40 to -60 mV, the i.p.s.p becomes larger and longer. Beyond -60 mV the inhibitory response decreases in proportion to the driving force on K(+) without any further change in time course.7. The inhibitory response produced by an iontophoretically applied pulse of bethanechol has a delayed onset of about 150 msec at 24 degrees C. The early portion of this response, including the delay, is proportional to t(3), where t is time. The proportionality factor (the apparent rate constant) decreases elevenfold when the temperature is lowered by 10 degrees C. This suggests that a multi-step process is involved in the activation of the conductance increase that leads to the inhibitory response. Inhibitory responses with similar kinetics were produced in heart muscles of the mudpuppy upon application of ACh.

Acetylcholine↗
PubMed1979

Selective antagonism of amino acid-induced and synaptic excitation in the cat spinal cord.

1. The effects of D-alpha-aminoadipate (DalphaAA), D-alpha-aminosuberate (DalphaAS) and other excitatory amino acid antagonists have been compared on the excitatory responses of neurones of the cat spinal cord to acetylcholine, a range of glutamate-related amino acids and stimulation of appropriate excitatory synaptic pathways. The ionophoretic technique was used for administration of excitants and antagonists. 2. DalphaAA and DalphaAS had little or no effect on acetylcholine-induced excitation of Renshaw cells. Responses of either Renshaw cells or dorsal horn neurones in the spinal cord to excitatory amino acids were depressed in the order: N-methyl-D-aspartate (NMDA), L-homocysteate, D-glutamate, ibotenate greater than D-homocysteate, L-aspartate, D-aspartate greater than L-glutamate, kainate and quisqualate. 3. These effects are consistent with the existence of different excitatory amino acid receptors, one type being sensitive to the actions of the antagonists, and activated predominantly by the NMDA group of excitants, with other receptors being relatively insensitive to DalphaAA and DalphaAS and activated predominantly by quisqualate and kainate. On this hypothesis, many amino acids are assumed to have mixed actions on DalphaAA-sensitive and -insensitive receptors. 4. 2-Amino-4-phosphonobutyrate (2APB) and L-glutamic acid diethyl ester (GDEE) produced different patterns of antagonism of excitatory amino acid-induced responses from those observed with DalphaAA and DalphaAS. Neither substance was as potent as DalphaAA or DalphaAS as an excitatory amino acid antagonist. 5. Both DalphaAA and DalphaAS selectively antagonized synaptic excitation of Renshaw cells evoked by dorsal root stimulation without affecting cholinergic excitation of these cells evoked by ventral root stimulation. These latter responses were selectively antagonized by dihydro-beta-erythroidine (DHbetaE). DalphaAA also antagonized synaptic excitation of unidentified dorsal horn neurones of the spinal cord evoked by dorsal root stimulation. Neither GDEE (particularly) nor 2APB were as effective as DalphaAA or DalphaAS as depressants of synaptic excitation. 6. Taken in conjunction with the results of in vitro studies on the specificity of action of Dalpha¿ and related substances, these observations suggest that certain synaptic excitations in the spinal cord are mediated by an excitatory amino acid transmitter, and that this transmitter interacts with receptors which are activated selectively by NMDA, less selectively by other amino acids, including L-aspartate, and probably only slightly by quisqualate, kainate and (exogenous) L-glutamate.

2-Aminoadipic Acid↗
PubMed1979

Central nervous system responses to cigarette smoke inhalation in the cat.

Intact, pentobarbital anesthetized cats (with and without brainstem stimulating electrode implants) and unanesthetized Sherrington (gamma-driven) decerebrate cats "smoked" cigarettes of varying nicotine content (0.2-2.5 mg). Nicotine free lettuce leaf cigarettes were used as controls. "Smoking doses" of nicotine base (10-25 micrograms/kg) were administered i.v. for comparison. Smoke inhalation produced motor reflex depression which paralleled the nicotine content of the cigarettes "smoked". Patellar reflex facilitation due to mesencephalic reticular stimulation was reduced by doses of nicotine and cigarette smoke. Cigarettes (2.5 mg nicotine) and doses of nicotine (25-50 micrograms/kg, i.v.) significantly reduced rigidity and patellar reflex amplitude in the gamma-decerebrate cat. Dihydro-beta-erythroidine reduced the nicotine and cigarette smoke induced patellar reflex depression but not the diminution in the rigidity. Smoking doses of nicotine suppressed pentobarbital-induced EEG spindles in acutely prepared cats. Nicotine (10-25 micrograms/kg) produced EEG and behavioral arousal in cats with chronic deep electrodes. It was concluded that cigarette smoke produces its pharmacological effects via its nicotine content.

Action Potentials↗
PubMed1977

Pharmacology of the brachium conjunctivum: red nucleus synaptic system in the baboon.

Acetylcholine, biogenic amines, and certain amino acids were applied by microiontophoresis to parvicellular and magnocellular red nucleus (RN) neurons of baboon while recording brachium conjunctivum (BC)-evoked and amino acid-evoked unit discharge from these neurons. Glycine, gamma-aminobutyric acid, and beta-alanine were potent depressants of BC-RN synaptic transmission, amino acid-evoked firing, and spontaneous activity of all RN neurons studied. Glycine was clearly more potent than the other 2 depressant amino acids. L-Glutamic and DL-homocysteic acid were strong excitants of all RN neurons tested. Dopamine, noradrenaline, and 5-hydroxytryptamine depressed the excitability of both parvicellular and magnocellular RN neurons; no excitatory effects were observed with these biogenic amines on RN neurons. Acetylcholine increased the rate of firing of spontaneously discharging parvicellular RN neurons and facilitated the amino acid-induced firing of these same neurons. Acetylcholine did not facilitate BC-RN synaptic transmission nor could this transmission be blocked by cholinergic antagonists. Unlike parvicellular RN neurons, the responsiveness of magnocellular neurons was either unaltered by acetylcholine or slightly decreased. These experiments demonstrate a difference in the pharmacologic responsiveness of parvicellular and magnocellular RN neurons to acetylcholine but do not provide evidence for a cholinergic input to RN via the brachium conjunctivum.

Acetylcholine↗
PubMed1977

Tetanus toxin induced actions on spinal Renshaw cells and Ia-inhibitory interneurones during development of local tetanus in the cat.

In anaesthetized cats the activities of Renshaw cells (RCs) and Ia-inhibitory interneurones (IaINs) were recorded during the accumulation of tetanus toxin in the spinal cord following injection into the gastrocnemius muscle. The early response of the RCs increased during the period of development of local tetanus. With some cells there was a subsequent decrease in the early response in later periods of the observation time (16-44 hrs after intramuscular injection). The effects on the spontaneous activity of the RCs were in good correspondence to those on the early response. The hyperactivity of the RCs is proposed to be mediated mainly via disinhibited cholinergic gamma-motoneurones using muscarinic postsynaptic receptors. The "pause" which follows the early response and the recurrent inhibition of IaINs was not reduced during the development of local tetanus. These results indicate that the central action of tetanus toxin in local tetanus does not consist of a general loss of postsynaptic inhibition. It is suggested that tetanus toxin acts mainly on synaptic elements of the alpha- and gamma-motoneurones or on presynaptic nerve terminals in their vicinity. In later periods of disturbing influence on the cholinergic transmission at Renshaw cells seems to occur.

Animals↗