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PubMed1998

Effects of nicotine and mecamylamine on rat dorsal raphe neurons.

This study investigates the hypothesis that serotonin mediates certain nicotine effects, such as mood improvement and the suppression of the ponto-geniculo-occipital spikes of rapid eye movement sleep. The influence of nicotine (10-300 microM) on the firing rate of dorsal raphe neurons and on serotonin release was therefore, studied in rat midbrain slices. Nicotine increased the firing rate, 10-90%, in 67.5% recorded neurons and decreased it, 8-100%, in the remaining 32.5%. Serotonin release increased 2-7 times after nicotine administration, regardless of firing frequency, but the absolute value of serotonin release was 3 times higher during the decreases than during the increases in firing rate. Mecamylamine (1-20 microM) transiently stimulated the dorsal raphe neurons and competitively antagonized the nicotine-induced serotonin release. The results support the working hypothesis and additionally show that mecamylamine also stimulates dorsal raphe neurons.

Action Potentials↗
PubMed1990

Hypophysial portal blood flow during preganglionic stimulation of the superior cervical ganglion under condition of systemic arterial blood pressure stabilization in rat.

The presence of hypothalamic hormones in the pituitary portal blood is regarded as the principal factor by which the hypothalamus controls pituitary secretion. In contrast to numerous investigations on hypothalamic hormone release, the regulation of the hypophysial-portal blood flow (HPBF) has been scarcely studied. Hypophysial-portal vessels were exposed according to the Worthington's method [1966]. The 10-min blood samples were collected before and during unilateral or alternative bilateral electrical stimulation of the preganglionic fibers of the superior cervical ganglia (SCG). During blood samples collection the stable systemic arterial blood pressure was maintained by a barostat. The HPBF was estimated according to the determination of the hemoglobin in samples of washed and collected blood from the cut pituitary portal vessels. The mean HPBF was 3.5 microliters/min. Electrical stimulation of SCG. did not change HPBF. This indicates that sympathetic efferents do not participate in the regulation of HPBF under conditions of stabilization of the systemic arterial blood pressure.

Animals↗
PubMed2002

Acute ventilatory and circulatory reactions evoked by nicotine: are they excitatory or depressant?

Either excitatory or inhibitory cardio-respiratory responses induced by nicotine have been reported. We evaluated the joint and separate contributions of peripheral arterial chemoreceptors and pulmonary vagal afferences to nicotine-induced cardio-respiratory responses in 11 pentobarbitone-anaesthetized cats. Nicotine, given i.v. in doses of from 1 to 200 microg/kg, evoked dose-dependent transient increases in tidal volume (VT) and arterial blood pressure (BP), but the highest doses evoked brief apnoea, immediately followed by intense hyperventilation, as well as discrete early hypotension followed by late hypertension. Bilateral section of the aortic and carotid nerves abolished all hyperventilatory responses to nicotine, giving way to apnoea followed by few cycles of reduced VT and profound hypotension followed by slight hypertension in response to intermediate doses (50-100 microg/kg). Subsequent bilateral vagotomy (BV) suppressed apnoeic and hypotensive responses. In other cats initially subjected to BV, only increases in VT and BP were observed in response to nicotine, effects which were no longer observed after additional carotid and aortic deafferentation. These data suggest that excitatory effects of nicotine on respiration and BP are reflexes evoked by stimulation of peripheral arterial chemoreceptors, while inhibitory effects are also reflex responses but evoked from stimulation of pulmonary vagal afferences.

Animals↗
PubMed1991

[The effect of stimulation of the A5 cell group in the medulla oblongata on cardiac activity in the cat].

The anesthetized cats, heart rate and dp/dt max. were elevated in the result of the A5 cell group electrical stimulation. Similarly, the L-glutamate injections, too, increased the heart rate and dp/dt max. After transection of the spinal cord (T8-10) and blocking of rostral ventrolateral medulla, this effect was still present and only blocked by i.v. infusion of phentolamine and hexametonium.

Animals↗
PubMed2004

Isolation of stimulants of gastrointestinal motility in beer.

BACKGROUND: Among various alcoholic beverages, it has reported that beer has a potent activity to stimulate gastric emptying. Our previous studies showed that beer congener stimulated gastrointestinal motility by directly stimulating muscarinic M3 receptor, present in smooth muscles of the gastrointestinal tract. However, active components that account for the action have yet to be identified. We attempted to isolate the stimulant(s) of gastrointestinal motility in beer. METHODS: Beer congener was prepared from beer and used to separate and purify active components by a series of liquid chromatography using affinity to muscarinic M3 receptor as an index. Gastrointestinal motility-stimulating activity was evaluated using a test for activity that causes contraction of longitudinal muscles in guinea pig ileum and a test for gastric emptying activity in mice. RESULTS: The active components (compounds A and B) were purified and isolated from beer by four liquid chromatography steps. The IC50 values of two active isolates to muscarinic M3 receptor were 0.65 x 10 g/ml and 2.30 x 10 g/ml, respectively. The concentrations of compounds A and B contained in beer were sufficient to explain most of the muscarinic M3 receptor binding activity of beer. The active fraction that contained both compounds A and B (which was 10 times as active as beer congener in muscarinic M3 receptor binding activity) dose-dependently contracted the longitudinal muscles of guinea pig ileum with an activity that was 20 times as potent as that of beer congener. The same active fraction significantly stimulated gastric emptying in mice with an activity 20 times as potent as that of beer congener. CONCLUSIONS: Two active components (compounds A and B) were isolated as gastrointestinal motility stimulants (muscarinic M3 agonists) in beer. These results suggest that the two isolated active components are the active entities of the gastrointestinal motility-stimulating effect of beer.

Animals↗
PubMed2002

Stimulant-like action of nicotine on striatal dopamine transporter in the brain of adults with attention deficit hyperactivity disorder.

Eleven adult patients with attention deficit hyperactivity disorder (ADHD) without medication, consuming 7-40 cigarettes per day, showed statistically significant lower values for striatal dopamine transporter (DAT) measured by [99mTc]TRODAT-1 SPECT compared to 11 non-smoking drug-naive patients with ADHD, matched for sex and age, despite higher ADHD scores for the smokers. Because stimulants have been shown to reduce primarily elevated DAT density in adults with ADHD, it can be suggested that nicotine acts in a similar way on striatal DAT as do stimulants.

Adolescent↗
PubMed1983

Presynaptic modulation of the release of dopamine from striatal synaptosomes: differences in the effects of high K+ stimulation, methamphetamine and nicotinic drugs.

We examined the effects of nicotinic drugs on the metabolites of [3H]dopamine (DA) released from rat striatal synaptosomes in comparison with the effects of high K+ and methamphetamine stimulation. The pattern of outflow of [3H]DA and its metabolites induced by nicotine stimulants, acetylcholine (ACh), nicotine and lobeline, was different from that induced by high K+ and methamphetamine.

Animals↗
PubMed1991

Tetanus and botulinum A toxins inhibit stimulated F-actin rearrangement in chromaffin cells.

Tetanus and botulinum A neurotoxins block exocytosis of noradrenaline in chromaffin cells. During exocytosis vesicles fuse with the plasma membrane. This requires an intact cytoskeleton. The cytoskeleton can be displayed by rhodamine-labelled phalloidin binding to F-actin. When chromaffin cells are stimulated with carbachol, F-actin forms clusters close to the plasma membrane. On withdrawal of the secretagogue the stimulated cells revert to their original appearance. The conversions, like exocytosis, depend on the presence of Ca2+, indicating the association of exocytosis with F-actin arrangement. When exocytosis is blocked in chromaffin cells by tetanus or botulinum A neurotoxins, F-actin fails to cluster during nicotinic stimulation. Thus, the toxins act somewhere between the rise in intracellular free Ca2+ and the rearrangement of F-actin.

Actins↗
PubMed1993

Nicotinic receptors in the cerebellar vermis modulate the gain of the vestibulospinal reflexes in decerebrate cats.

1. The possibility that the cholinergic afferent system terminating in the vermal cortex of the cerebellar anterior lobe acts on the target neurons by utilizing nicotinic receptors has been investigated in decerebrate cats by testing the effects of local microinjection of cholinergic nicotinic agonists and antagonists on posture as well as on the dynamic characteristics of the vestibulospinal (VS) reflexes. 2. Unilateral injection into the vermal cortex of the culmen of nicotine (0.25 microliter at the concentration of 0.05-0.5 microgram/microliter saline) decreased the extensor tonus in the ipsilateral forelimb, while the extensor tonus in the contralateral forelimb increased. The some agent significantly increased the gain of the first harmonic component of the EMG responses of the ipsilateral and more prominently also of the contralateral triceps brachii to animal tilt. However, the phase angle of the responses remained bilaterally unmodified. The effects described above were first observed 5-10 min after the injection, reached the peak after 40-60 min and persisted for at least 2-3 h before disappearing. 3. The effective area was located between the second and the fourth folium of the cerebellar vermis rostral to the fissura prima, at the laterality of 1.4-1.8 mm. This area, which upon cathodal stimulation suppressed the spontaneous EMG activity of the ipsilateral triceps brachii, actually corresponds to the zone B of the cerebellar cortex which exerts a direct inhibitory influence on the lateral vestibular nucleus. Moreover, the effects were dose-dependent. 4. Microinjection of nicotinic antagonists of both the ganglionic type (hexamethonium, 0.25 microliter at 4 micrograms/microliters saline) and the neuromuscular type (d-tubocurarine, 0.25 microliter at 7 micrograms/microliters saline) produced a postural asymmetry opposite in sign to that elicited by nicotine. The same agents also decreased the response gain of the triceps brachii of both sides to animal tilt recorded either under normal conditions or after previous injections of nicotine. 5. The experiments indicate that the cholinergic system is involved in the control of posture as well as in the gain regulation of the VS reflexes. Previous histochemical studies had shown that the cholinergic fibers terminate not only on Purkinje (P)-cells, but also and more prominently as mossy fibers ending on granular cells. This system may thus affect the discharge of P-cells and related inhibitory interneurons not only ipsilaterally but also contralaterally to the side of the injection.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Responsiveness of noradrenergic neurons in rat experimental hypertension.

We investigated possible abnormalities of cholinergic-noradrenergic neurotransmission in superior cervical ganglia in vitro in spontaneously hypertensive, Dahl salt-sensitive and deoxycorticosterone-salt-hypertensive rats by measuring the de novo synthesis of catecholamines from their labeled precursor tritiated tyrosine in response to cholinergic stimulation. Labeled tyrosine was incorporated into dopamine and its main neuronal metabolite dihydroxyphenylacetic acid as well as into norepinephrine. Dihydroxyphenylacetic acid and norepinephrine, but not dopamine, generation was linear with time under basal and stimulated conditions. However, norepinephrine incorporation remained similar before and after cholinergic stimulation of ganglionic neurons. Only young, prehypertensive spontaneously hypertensive rats showed altered responses when compared with their controls. Although endogenous dihydroxyphenylacetic acid content and baseline tyrosine incorporation into dihydroxyphenylacetic acid were lower in 4-week-old spontaneously hypertensive rats than in age-matched Wistar-Kyoto rats, cholinergic stimulation increased labeled dopamine and dihydroxyphenylacetic acid generation significantly more in juvenile spontaneously hypertensive rats. Such a hyperresponsiveness was not observed in either young Dahl rats or in any of the other models when they became hypertensive. These results probably reflect a genuine hyperreactivity of postganglionic noradrenergic neurons to acetylcholine or their increased catecholamine-synthesizing ability after centrally evoked enhanced sympathetic outflow known to occur during the early development of hypertension in spontaneously hypertensive rats.

Animals↗
PubMed1984

[Intracellular reactions of neurons of the primary auditory area of the cerebral cortex in the cat to tones of different frequency and electric stimulation of nerve fibers of the spiral ganglion].

In experiments with nembutal-anaesthetized cats it was found that neurons in the AI auditory cortical area responded to sound stimulation by EPSP, EPSP-spike-IPSP, EPSP-IPSP and IPSP. The majority of neurons studied responded to tones of characteristic frequency or to above-threshold tones whose frequencies were close to the characteristic ones as well as to electrical stimulation of spiral ganglion fibres innervated a central part of the receptive field by the sequence: EPSP-spike-IPSP. Tones whose frequency differed significantly from the characteristic one and electrical stimulation of the peripheral parts of the receptive field evoked responses in the form of EPSP-IPSP or IPSP. The tone frequency band that under threshold stimulation evoked a spike in a neuron was significantly narrower than the tone frequency band that evoked EPSP or IPSP. Two types of IPSPs were observed: components of the EPSP-spike-IPSP sequence evoked by excitation of receptors in the centre of the receptive field and primary or following EPSP evoked only if receptors locating in peripheral parts of the receptive field were excited.

Animals↗
PubMed2003

Regulation of atrial natriuretic peptide secretion by cholinergic and PACAP neurons of the gastric antrum.

Atrial natriuretic peptide (ANP) released from enterochromaffin cells helps regulate antral somatostatin secretion, but the mechanisms regulating ANP secretion are not known. We superfused rat antral segments with selective neural agonists/antagonists to identify the neural pathways regulating ANP secretion. The nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium (DMPP) stimulated ANP secretion; the effect was abolished by hexamethonium but doubled by atropine. Atropine's effect implied that DMPP activated concomitantly cholinergic neurons that inhibit and noncholinergic neurons that stimulate ANP secretion, the latter effect predominating. Methacholine inhibited ANP secretion. Neither bombesin nor vasoactive intestinal polypeptide stimulated ANP secretion, whereas pituitary adenylate cyclase-activating polypeptide (PACAP)-27, PACAP-38, and maxadilan [PACAP type 1 (PAC1) agonist] each stimulated ANP secretion. The PAC1 antagonist M65 1) abolished PACAP-27/38-stimulated ANP secretion; 2) inhibited basal ANP secretion by 28 +/- 5%, implying that endogenous PACAP stimulates ANP secretion; and 3) converted the ANP response to DMPP from 109 +/- 21% above to 40 +/- 5% below basal, unmasking the cholinergic component and indicating that DMPP activated PACAP neurons that stimulate ANP secretion. Combined atropine and M65 restored DMPP-stimulated ANP secretion to basal levels. ANP secretion in the antrum is thus regulated by intramural cholinergic and PACAP neurons; cholinergic neurons inhibit and PACAP neurons stimulate ANP secretion.

Animals↗
PubMed1998

Behavioral and neurochemical components of nicotine sensitization following 15-day pretreatment: studies on contextual conditioning.

The effects of contextual conditioning on the induction of nicotine sensitization of locomotor activity, stereotypy and nucleus accumbens dopamine release were studied using a 15-day pretreatment regimen. Six groups of Sprague-Dawley rats were employed to test for the effects of drug pretreatment, conditioning and novelty. Groups 1-4 were treated with daily nicotine (0.6 mg/kg, s.c.) or saline injections that were either paired with the test chamber or given in the home cage, followed by saline injections in the home cage. Group 5 received saline in the test chamber followed by nicotine in the home cage (unpaired). Group 6 was naive to handling and drug treatment. Pretreated animals were implanted with 2 mm microdialysis probes, via chronic guide cannulae, after completing the 15th day of treatment, and were tested for their response to nicotine (0.6 mg/kg, s.c) or saline on day 16. Naive animals were implanted with microdialysis probes and tested in a similar manner. Nicotine-stimulated locomotor activity was sensitized in the paired, unpaired and homecage pretreatment groups whereas nicotine-stimulated stereotypy was sensitized only in the paired pretreatment group. Nicotine-stimulated nucleus accumbens dopamine release was sensitized in the paired and unpaired pretreatment groups. Saline-stimulated nucleus accumbens dopamine release, but not locomotor activity or stereotypy, was also found in the nicotine-pretreated, paired group. These findings demonstrate the development of sensitization to nicotine-induced locomotor activity, stereotypy and nucleus accumbens dopamine release after a 15-day pretreatment regimen. Each of these responses to nicotine were differentially modulated by contextual conditioning. It is suggested that nicotine-stimulated dopamine release in sensitized animals represents the conditioned component of nicotine sensitization.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2002

Ganglion cell responses to retinal light stimulation in the absence of photoreceptor outer segments from retinal degenerate rodents.

PURPOSE: To determine whether a severely degenerated retina without photoreceptor outer segments and a non-recordable electroretinogram (ERG) can still show retinal ganglion cell (RGC) responses to retinal light stimulation. METHODS: The authors measured ERGs and retinal surface RGC responses from six week old rd mice and three month old homozygous S334ter line3 rats. Animal eyes were also studied by light microscopy, transmission electron microscopy, and immunohistochemistry (rats). RESULTS: The corneal ERGs were non-recordable and no photoreceptor outer segments were found in either retinal degeneration model. A few cell bodies (without outer segments) that were immunoreactive for cone opsin and rhodopsin were found in the outer nuclear layer of the rats. Light-driven ON-RGC responses, however, were recordable from six week old rd mice. In addition, light-driven ON and OFF-RGC responses were recordable from three month old homozygous S334ter line 3 rats. CONCLUSIONS: This study suggests that despite the apparent absence of photoreceptor outer segments and a non-recordable ERG, ganglion cell responses to retinal light stimulation may remain preserved in some severe retinal degenerate transgenic rodents.

Animals↗
PubMed1960

Activity patterns of interneurons in the caudal ganglion of the crayfish.

Responses of ascending interneurons from the caudal ganglion of crayfish have been recorded from single units isolated by dissection from the ventral nerve cord; in addition, post-synaptic activity within the ganglionic neuropile has been studied with intracellular micropipettes. The following classes of interneurons have been found: (1) Large fibers which responded to tactile stimuli with single spikes or phasic bursts. These units usually showed broad receptive fields; and spontaneous activity, when present, showed transitory depressions following responses to natural stimuli. (2) A group of fibers, including many small ones, which responded to proprioceptive stimuli with tonic discharges of varying adaptation rate. (3) Interneurons which showed responses both to tactile stimuli and to activation of the sixth ganglion photoreceptor; and (4) units with constant frequency discharges which were unmodifiable by any of the above afferent inputs. Intracellular recording of post-synaptic activity has shown (1) that widely graded excitatory post-synaptic potentials occur; (2) that multiple firing from single synaptic potentials is usual; (3) that the post-synaptic responses to phasic natural stimuli and to electrical stimulation of ganglionic roots are similar. The existence of widely graded post-synaptic potentials and of extensive receptive fields suggests a high degree of convergence from primary afferents to interneurons. The activation of such post-synaptic units involves integrative synaptic transfer, without 1:1 correspondence between pre- and post-fiber activity.

Animals↗
PubMed1984

Muscarinic and nicotinic effects on yawning and tongue protruding in the rat.

Physostigmine, an anticholinesterase agent, elicited yawning with a marked protrusion of the tongue and teeth chattering. Yawning and chattering were also observed after pilocarpine, a cholinergic agonist predominantly acting upon muscarinic receptors. Apomorphine at low doses (0.1-0.5 mg/kg), which preferentially activates presynaptic dopamine autoreceptors, elicited yawning, whereas at high doses (1-2 mg/kg) it produced stereotypy. Yawning induced by both cholinergic agonists and apomorphine was inhibited by scopolamine, a muscarinic receptor blocking agent, but not by methylscopolamine, a peripheral anticholinergic agent and mecamylamine, a nicotinic receptor blocking agent. Low dose (0.02 mg/kg) of haloperidol, which has been reported to block presynaptic dopamine autoreceptors, inhibited apomorphine-induced yawning but did not affect cholinergic agonist-induced yawning. Physostigmine-elicited tongue protruding was inhibited by mecamylamine. The results imply that yawning behavior is essentially associated with the stimulation of central muscarinic receptors, and that physostigmine also induces tongue protruding by activating the central nicotinic receptors.

Animals↗
PubMed1982

Oxytocin release from neurohypophysis evoked by preganglionic stimulation of the rat superior cervical ganglion.

1. In male rats under urethane/chloralose anaesthesia the pituitary gland was exposed by transpharyngeal approach. The following methods were applied: (a) posterior pituitary lobe incubation in situ with the anterior lobe removed and the posterior lobe elevated so that only the vessels between the lobe and the meninges are broken, and continuous exchange of the incubation fluid; (b) removal of the entire pituitary and continuous exchange of the fluid washing the cut proximal end of the pituitary stalk. 2. 20 to 30-min samples of incubation or washing fluid were collected for 3-5 hrs and oxytocin was assayed according to Van Dongen and Hays (1966). 3. Preganglionic stimulation of the superior cervical ganglion caused significant increase (ca. 25 times) of oxytocin release from the posterior pituitary lobe. 4. Preganglionic stimulation of the superior cervical ganglion did not alter oxytocin content in the fluid washing the cut proximal end of the pituitary stalk. 5. The sympathetic neurons of the superior cervical ganglia could evoked oxytocin release from the neurohypophysis but did not change its outflow from the hypothalamus to the neurohypophysis.

Animals↗
PubMed2005

Effects of nicotine on hippocampal and cingulate activity during smooth pursuit eye movement in schizophrenia.

BACKGROUND: Abnormal smooth pursuit eye movement (SPEM) in schizophrenic patients is a well known phenomenon, but the neurophysiological mechanisms underlying the deficit are unknown. Nicotine temporarily improves SPEM and has been associated with reduced hippocampal hemodynamic activity in schizophrenics. Nicotine's effect on brain activity in control subjects performing SPEM has not been studied. The purpose of this work was to determine if nicotine differentially affects brain activity in schizophrenic and control subjects during pursuit eye tracking. METHODS: 16 subjects with schizophrenia and 16 control subjects underwent functional MR imaging during SPEM after receiving placebo or nicotine gum. Four brain regions were analyzed for main effects of group, drug, and interactions: hippocampus, cingulate gyrus, frontal eye fields, and area MT. RESULTS: Nicotine reduced hippocampal activity in both groups, but the effect was greater in control subjects. A group by drug interaction was observed in the anterior cingulate gyrus, where nicotine decreased activity in control subjects and increased activity in schizophrenic subjects. There were no significant effects of group, drug, or interactions in frontal eye fields or area MT. CONCLUSIONS: Nicotine may improve SPEM performance in people with schizophrenia through cholinergic stimulation of the hippocampus and cingulate gyrus. Potential mechanisms include improved inhibitory function and attention.

Administration, Oral↗