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Results for “Ganglionic Stimulants”

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At least 559 records · Page 31Linked to original sources
PubMed1989

Train-of-four as an index of neuromuscular block in cats: changes induced by atropine.

1. The present study reevaluates the effect of atropine on the rate of recovery from tetanic fade caused by intraarterial administration of neostigmine or antinicotinic agents in cat anterior tibial muscle preparations submitted to a train-of-four (TOF) pattern of nerve stimulation. The study also compares the sensitivity of the TOF and tetanic responses as indices of residual nondepolarizing block. 2. Neostigmine, hexamethonium and d-tubocurarine all produced short-lived TOF fade. Both single and TOF twitches were increased by neostigmine and depressed by the antinicotinic agents. 3. Prior administration of atropine reduced the TOF fade induced by the antinicotinic drugs but potentiated that caused by anticholinesterase drugs. 4. These results indicate that TOF fade is not the most sensitive index for studying neuromuscular blockade when drugs other than neuromuscular blockers are also present.

Analysis of Variance↗
PubMed1980

Mechanism of noradrenaline release from rabbit atria induced by nicotinic agonists.

The release of noradrenaline and its metabolic products by the nicotinic agonists nicotine, 1,1-dimethyl-4-phenylpiperazinium (DMPP) and acetylcholine (in the presence of atropine) was investigated in rabbit atria in which the transmitter stores were labelled with (3H)-noradrenaline. The proportions of noradrenaline and its metabolic products released by nicotine (50 microM), DMPP (100 microM) and acetylcholine (1.6 mM, in the presence of atropine (6 microM)) were similar to those released by sympathetic nerve stimulation: (3H)-noradrenaline itself comprised more than 90% of the tritiated compounds released by these agents. None of the nicotinic agonists affected the activity of monoamine oxidase extracted from rabbit atria. The results suggest that nicotinic agonists and sympathetic nerve stimulation release noradrenaline from the same sites and by similar mechanisms, presumably by exocytosis of the contents of transmitter storage vesicles.

Acetylcholine↗
PubMed2000

Mitochondrial calcium accumulation following activation of vanilloid (VR1) receptors by capsaicin in dorsal root ganglion neurons.

Stimulation of the vanilloid (capsaicin) receptor (VR1), currently viewed as a molecular integrator of chemical and physical noxious stimuli, evoked intracellular Ca2+ transients in a capsaicin-sensitive subpopulation of rat dorsal root ganglion neurons. These were comprised of an initial fast rise (seconds) followed by a long-lasting intracellular Ca2+ recovery (tens of minutes). The rate of intracellular Ca2+ recovery was dependent on the magnitude of intracellular Ca2+ transients. Opening of voltage-operated Ca2+ channels in the same neurons by K+ depolarization evoked intracellular Ca2+ elevation of a similar amplitude and rate of rise; however, the recovery of intracellular Ca2+ to the prestimulated level was significantly faster. A mitochondrial uncoupler (10 microM carbonyl cyanide m-chlorophenylhydrasone) was used to reveal the role of mitochondria in intracellular Ca2+ buffering. Carbonyl cyanide m-chlorophenylhydrasone-evoked elevation in intracellular Ca2+ was greater in neurons previously stimulated with capsaicin compared with KCl. Neither extracellular Ca2+ nor ATP depletion influenced significantly the carbonyl cyanide m-chlorophenylhydrasone-sensitive intracellular Ca2+ elevation in neurons loaded with Ca2+ via vanilloid 1 receptor stimulation. The effects of carbonyl cyanide m-chlorophenylhydrasone suggest that the amount of Ca2+ buffered by mitochondria is greater when extracellular Ca2+ enters the neuron via the vanilloid 1 receptor channel than via voltage-operated Ca2+ channels. The long duration of intracellular Ca2+ decline in neurons stimulated with capsaicin, which depends on the amount of Ca2+ buffered by mitochondria, may reflect a specific mechanism of Ca2+ buffering following activation the pain receptor VR1.

Animals↗
PubMed2004

Age-related differences in the response of blood stroke volume to stimulation of the sympathetic ganglion in rats with beta-adrenoceptor blockade.

Blood stroke volume in rats aging 21 and 56 days decreased during beta-adrenoceptor blockade with propranolol, but increased again by the 15th minute after treatment. Suprathreshold stimulation of the stellate ganglion decreased the stroke volume and increased the heart rate in control animals. Electrical stimulation after beta-adrenoceptor blockade was followed by a further decrease in stroke volume in young rats. In 100-day-old animals this parameter remained unchanged, while the cardiac output improved.

Adrenergic beta-Antagonists↗
PubMed2001

Development of the evoked potentials in the thalamus and cerebral cortex after stimulation of the stellate ganglion afferents in kittens.

The primary evoked potentials (EP) were studied in newborn, 10-, 20-day-old, 1-month-old kittens in the thalamus and cerebral cortex after stimulation of the stellate ganglion (SG) afferents. The nerves were irritated with single square-wave pulses with an amplitude of 1.2-1.3 threshold for EP appearance. In all kittens, EP were registered in the same zones as in adult animals. In the thalamus, this zone was represented by the centromedial part of the ventralis posterior lateralis (n. VPL), contralaterally to the stimulation place. In the cerebral cortex, the EP were observed in the cerebral cortex, specifically in the somatosensory zones S1 and S2 also contralaterally to the stimulation place. In postnatal ontogenesis, the latency of evoked potentials decreases, amplitude increases and the form of these potentials transforms from negative in newborn kittens to positive-negative wave in 1-month-old animals. Maturation of the SG afferent pathways exists in parallel with the somatosensory ones and does not finish at 1 month of life.

Afferent Pathways↗
PubMed1979

Preeminence of the left stellate ganglion in the long Q-T syndrome.

In seven patients with Romano-Ward syndrome, stellate ganglion block or stimulation and pharmacologic interventions were made to assess their influence on duration of the O-T interval, electrical alteration of the T wave and ventricular tachydysrhythmias. Left stellate ganglion block and right stellate ganglion stimulation shortened Q-T interval, abolished alternans phenomena and suppressed tachydysrhythmias. Propranolol and phenytoin had a similar effect. In contrast, right stellate ganglion block, left stellate ganglion stimulation and prior administration of quinidine and procainamide had an opposite effect. These responses resemble observations in animal models which suggest that excessive or unopposed activity of the left, or subnormal activity of the right stellate ganglion, or both, account for the pathophysiologic manifestations of the long Q-T syndrome. They are also consistent with clinically correlated, cardiac neuropathologic findings in these patients. An analogous but acquired dysautonomia involving the left stellate ganglion and ischemic left ventricle may precipitate sudden coronary death.

Adult↗
PubMed1989

Preganglionic nerve stimulation increases mRNA levels for tyrosine hydroxylase in the rat superior cervical ganglion.

Increased synaptic stimulation of sympathetic neurons in vivo causes a delayed increase in the activity and the amount of tyrosine hydroxylase (TH). To determine whether these changes result from an increase in the messenger RNA for TH, the rat preganglionic cervical sympathetic trunk was electrically stimulated unilaterally for 90 min, and 48 h later RNA was extracted from stimulated and contralateral control superior cervical ganglia. Northern blots probed with a cDNA for TH demonstrated that nerve stimulation produced about a 2.5-fold increase in the amount of TH mRNA in the ganglion. These results indicate that synaptic stimulation leads to an increase in TH mRNA, either by increasing the rate of transcription of the TH gene or by increasing the stability of its mRNA.

Animals↗
PubMed1993

Rapid recovery of structure and function of the cholinergic synapses in the cat superior cervical ganglion in vivo following stimulation-induced exhaustion.

Cat superior cervical ganglia (SCG) were tetanically stimulated in vivo at 30-100 Hz until neural transmission was exhausted, and then were allowed to rest and recover. Changes in their cholinergic synapses were examined electrophysiologically and morphologically during the time of tetanic stimulation and during recovery. For morphometric analysis the presynaptic terminal was subdivided into two areas: an area directly over the active zone, termed zone-I, (bounded by a hemicircle with a diameter equivalent to the active zone length), and the remaining preterminal area, termed zone-II. In control ganglia before stimulation synaptic vesicle density in zone-I (SVD-I) averaged 90 microns-2 and the number of vesicles actually attached to the active zone (SVA) averaged about 2.5 per single profile of nerve terminal. Upon stimulation, the postganglionic potential immediately began to decline in amplitude and disappeared after 1 min of stimulation. Simultaneously, SVD-I declined to less than 35 microns-2 and SVA declined to less than 1 per section. Thereafter, stimulation was terminated and the ganglion was allowed to rest. Recovery of the postganglionic potential was monitored by stimulation at 1 Hz. The postganglionic potential reached control levels after only 1 min of rest. Likewise, the structural parameters, SVD-I and SVA, also rapidly recovered, reaching control levels after only 30 sec of rest, slightly faster than the postganglionic potential. This illustrates that stimulation-induced fatigue of transmitter output and depletion of synaptic vesicles recover to the control level at a high rate in synapses of the cat SCG with a normal supply of blood. In fact, morphological recovery may be slightly faster than electrophysiological recovery. Mechanisms of vesicle formation and migration to the presynaptic area are discussed in light of these observations.

Acetylcholine↗
PubMed1986

Stimulation of the trigeminal ganglion increases flow in the extracerebral but not the cerebral circulation of the monkey.

The trigeminal ganglion of 9 anesthetized paralysed artificially ventilated Macaca nemestrina monkeys was electrically stimulated with frequencies varying from 0.2 to 200 Hz. This stimulation led to a frequency-dependent decrease in external carotid resistance but no significant change in internal carotid resistance was recorded. The response is probably mediated as previously described in the cat, i.e. predominantly through the greater superficial petrosal branch of the facial nerve and a small proportion through antidromic activation of the trigeminal system. Elucidation of the physiological and pharmacological mechanisms underlying such a response may aid in a better understanding of the pathophysiology of vascular headache.

Animals↗
PubMed2001

Capsaicin stimulation of the cochlea and electric stimulation of the trigeminal ganglion mediate vascular permeability in cochlear and vertebro-basilar arteries: a potential cause of inner ear dysfunction in headache.

Trigeminal neurogenic inflammation is one explanation for the development of vascular migraine. The triggers for this inflammation and pain are not well understood, but are probably vasoactive components acting on the blood vessel wall. Migraine-related inner ear symptoms like phonophobia, tinnitus, fluctuation in hearing perception and increased noise sensitivity provide indirect evidence that cochlear blood vessels are also affected by basilar artery migraine. The purpose of this investigation was to determine if a functional connection exists between the cochlea and the basilar artery. Neuronally mediated permeability changes in the cochlea and basilar artery were measured by colloidal silver and Evans Blue extravasation, following orthodromic and antidromic stimulation of the trigeminal ganglion innervating the cochlea. Capsaicin and electrical stimulation induced both dose- and time-dependent plasma extravasation of colloidal silver and Evans Blue from the basilar artery and anterior inferior cerebellar artery. Both orthodromic and antidromic activation of trigeminal sensory fibers also induced cochlear vascular permeability changes and significant quantitative differences between the treated and control groups in spectrophotometric assays. These results characterize a vasoactive connection between the cochlea and vertebro-basilar system through the trigeminal sensory neurons. We propose that vertigo, tinnitus and hearing deficits associated with basilar migraine could arise by excitation of the trigeminal nerve fibers in the cochlea, resulting in local plasma extravasation. In addition, cochlear "dysfunction" may also trigger basilar and cluster headache by afferent input to the trigeminal system.

Animals↗
PubMed1980

Alleviation of atypical trigeminal pain by stimulation of the Gasserian ganglion via an implanted electrode.

Facial pain associated with disturbances of sensitivity as a sign of injury of the trigeminal nerve is difficult to treat. Drug therapy as well as blocking procedures are generally ineffective. Transcutaneous nerve stimulation offers a new possibility for pain alleviation but is inconvenient for the patient. A method for stimulation of the gasserian ganglion via an implanted electrode has been developed. Five cases are reported on and they all experienced excellent or good pain relief. Follow-up is 6-21 months.

Adult↗
PubMed1988

Critical flicker frequency as a function of stimulus area and luminance at various eccentricities in human cone vision: a revision of Granit-Harper and Ferry-Porter laws.

When the photopic luminous flux collected by ganglion cells was kept constant at all retinal locations by reducing average stimulus luminance in inverse proportion to photopic Ricco's area (F-scaling), critical flicker frequency to stimuli of 1.2-88 deg2 in area, presented at various eccentricities along the temporal meridian of the visual field, increased as a single logarithmic function of the number of retinal ganglion cells stimulated. Their number was calculated by multiplying stimulus area by the ganglion cell receptive field density of the human retina. When the number of ganglion cells stimulated was kept constant by enlarging the stimulus area in inverse proportion to the ganglion cell density (M-scaling), the logarithm of CFF to green, yellow, orange and red cone-targets increased as parallel linear functions of logarithmic flux, calculated by multiplying retinal illuminance by photopic Ricco's area.

Adult↗
PubMed2000

Cerebral vasodilatation induced by stimulation of the pterygopalatine ganglion and greater petrosal nerve in anesthetized monkeys.

Although brain cell viability depends largely on cerebral circulation, mechanisms of blood flow control, such as autoregulation, or of the pathogenesis of functionally impaired blood supply to brain regions, such as in cerebral vasospasm after subarachnoid hemorrhage, have not been clearly defined. Our recent studies support the hypothesis that nitric oxide, released from nitrergic nerves, plays a crucial role as a neurotransmitter in vasodilating cerebral arteries from primate and subprimate mammals. In the present study, we demonstrated, by using arterial angiography, that electrical stimulation of the pterygopalatine ganglion produced vasodilatation of ipsilateral cerebral arteries of anesthetized Japanese monkeys. The response was abolished by intravenous injections of N(G)-nitro-L-arginine, a nitric oxide synthase inhibitor. Denervation of the ganglion elicited cerebral vasoconstriction, indicating that vasodilator nerves from the vasomotor center were tonically active. Stimulation of the greater petrosal nerve, upstream of the pterygopalatine ganglion, also elicited cerebral vasodilatation, which was abolished by treatment with the nitric oxide synthase inhibitor and with hexamethonium, indicating that the nerve is in connection via synapses with the nitrergic nerve innervating cerebral arteries. Endogenous nitric oxide released from the nerve may contribute to the maintenance of blood flow in major cerebral arteries necessary to supply blood to the different brain regions. Without this influence, cerebral arteries might be constricted to the extent that blood flow is impeded. This is the first direct evidence indicating an important role of nitric oxide liberated by pre- and postganglionic nerve stimulation in the control of cerebral arterial tone in primates.

Animals↗
PubMed1993

Effects of electrical stimulation of the superior cervical ganglion on cochlear blood flow in guinea pig.

It has been proposed that cochlear blood flow (CBF) is controlled in part by the sympathetic nervous system. In the present study the effect of electrical stimulation of the superior cervical ganglion (SCG) on CBF in guinea pigs was investigated using laser Doppler flowmetry (LDF). Animals were anesthetized with diazepam and fentanyl and the SCG was exposed. A custom-designed bipolar cuff electrode was fixed around the ganglion and 1 ms biphasic current pulses were injected at 0.15 mA to 1.5 mA, 6 Hz. Bilateral CBF was monitored, while the ganglion was stimulated for 3 or 5 min before and after the ascending sympathetic trunk and nerve branches from SCG were sectioned. Electrical stimulation of 0.5 mA caused the ipsilateral CBF (CBFi) to decrease 11.7% +/- 1.3 from the baseline (BL), while the contralateral CBF (CBFc) increased slightly due to the change in systemic blood pressure (BP). A linear relation was observed between the level of current stimulation and evoked reduction in CBF. Cervical sympathetic trunk section (between the SCG and the middle cervical ganglion) did not influence the pattern or the amplitude of CBF change in response to electrical stimulation of SCG. Sectioning the efferent fibers of the medial inferior and medial superior branch of the SCG only minimally reduced the amplitude of the CBF decrease evoked by electrical stimulation. However, sectioning the superior lateral branch abolished this decrease.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Lens injury stimulates adult mouse retinal ganglion cell axon regeneration via both macrophage- and lens-derived factors.

In the present study the effects of lens injury on retinal ganglion cell axon/neurite re-growth were investigated in adult mice. In vivo, lens injury promoted successful regeneration of retinal ganglion cell axons past the optic nerve lesion site, concomitant with the invasion of macrophages into the eye and the presence of activated retinal astrocytes/Muller cells. In vitro, retinal ganglion cells from lens-lesioned mice grew significantly longer neurites than those from intact mice, which correlated with the presence of enhanced numbers of activated retinal astrocytes/Muller cells. Co-culture of retinal ganglion cells from intact mice with macrophage-rich lesioned lens/vitreous body led to increased neurite lengths compared with co-culture with macrophage-free intact lens/vitreous body, pointing to a neurotrophic effect of macrophages. Furthermore, retinal ganglion cells from mice that had no lens injury but had received intravitreal Zymosan injections to stimulate macrophage invasion into the eye grew significantly longer neurites compared with controls, as did retinal ganglion cells from intact mice co-cultured with macrophage-rich vitreous body from Zymosan-treated mice. The intact lens, but not the intact vitreous body, exerted a neurotrophic effect on retinal ganglion cell neurite outgrowth, suggesting that lens-derived neurotrophic factor(s) conspire with those derived from macrophages in lens injury-stimulated axon regeneration. Together, these results show that lens injury promotes retinal ganglion cell axon regeneration/neurite outgrowth in adult mice, an observation with important implications for axon regeneration studies in transgenic mouse models.

Animals↗