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Biomedical subjects

M Sasa

Publications and source records attributed to M Sasa.

At least 235 records · Page 13Linked to original sources
PubMed1980

Locus coeruleus-induced inhibition of dorsal cochlear nucleus neurons in comparison with lateral vestibular nucleus neurons.

The effects of conditioning stimulation of the locus coeruleus (LC) on the neuron activity of dorsal cochlear nucleus (DCN), which is rich in noradrenergic nerve terminals, were compared with those on the lateral vestibular nucleus (LVN), devoid of such terminals, to determine whether or not noradrenaline is responsible for the LC-induced inhibition. The conditioning stimuli applied to the LC had no effect on either the field potential or the spike generation of mono- and polysynaptic neurons in the LVN elicited by VIIIth cranial nerve stimulation. In contrast, the spike firing of the DCN neurons with VIIIth cranial nerve stimulation was significantly inhibited by LC conditioning stimulation. The inhibition of spike generation was mainly observed in the DCN neurons which fired spikes with a longer latency. The inhibition of DCN neurons by LC conditioning stimulation did not occur in the cats pretreated with reserpine; however, a rapid recovery of the inhibition was produced by intraventricular application of noradrenaline. These results are in good agreement with the histochemical findings and support our previous conclusion that noradrenaline acts as an inhibitory transmitter or modulator on the nuclei where noradrenergic nerve terminals derived from the LC are located. In addition, the vestibular input in the primary relay nucleus is apparently not regulated by noradrenaline originating in the LC.

Animals↗
PubMed1980

Local anesthetic activity of beta-adrenergic blocking drugs in the Crayfish giant axon, with reference to calcium ion.

The actions of beta-adrenergic blocking drugs, propranolol, pindolol, timolol, carteolol, sotalol and practolol, were examined regarding effects on crayfish giant axon in an attempt to determine the relationship among chemical structure and local anesthetic activity, and the interaction of these drugs with Ca++. The activities of local anesthetics such as procaine and lidocaine served for comparisons. A conventional microelectrode technique was used to obtain the resting membrane and action potentials. All drugs except sotalol and practolol dose-dependently inhibited the dV/dt and amplitude of the action potential with a slight decrease (less than 6 mV) in the resting membrane potential. The relative potencies of these drugs in the reduction of the dV/dt were as follows: propranolol 13.3, pindolol 1.7, procaine 1.0, lidocaine 0.91, timolol 0.71 and carteolol 0.22. Sotalol and practolol had little activity. The chemical structure of the drugs for local anesthetic action was closely related to that of the lipophilic aromatic group; the most potent activity seen in the naphthyl group. Potentiation of the local anesthetic activity in low Ca++ solution was obtained with pindolol, timolol, carteolol, sotalol and practolol. Reduction of the activity in high Ca++ solution was observed with propranolol, pindolol, timolol, procaine and lidocaine. These results suggest that external Ca++ competes with the local anesthetic action of the beta-adrenergic blocking drugs, at the site of the action potential generating mechanism.

Action Potentials↗
PubMed1980

Selective effect of ethanol on the vestibular nucleus neurons in the cat.

Effects of intravenous administration of ethanol on the neuronal activities of the lateral vestibular nucleus (LVN) and spinal trigeminal nucleus (STN) were investigated in cats. The LVN neurons were classified into three groups according to the latency of the first spike elicited by orthodromic vestibular nerve stimulation and antidromic vestibulospinal tract stimulation: monosynaptic, polysynaptic I and polysynaptic II neurons. Ethanol of 0.2--1.6 g/kg dose-dependently suppressed the orthodromic spike generation of the monosynaptic and polysynaptic II neurons without affecting their latency and antidromic spike generation of the former neuron. The mean spike numbers of the monosynaptic and polysynaptic II neurons were significantly decreased with ethanol over 0.4 g/kg. The polysynaptic I neuron, however, remained unaffected by the drug up to 0.8 g/kg. Similarly, the spike generation of the STN relay neuron and interneuron elicited by trigeminal nerve stimulation remained unaltered with ethanol given in doses up to 0.8 g/kg. These results indicate that small doses of ethanol more selectively interfere with synaptic transmission in the LVN monosynaptic and polysynaptic II neurons than transmission in the STN relay neurons and interneurons.

Action Potentials↗
PubMed1979

Convergence of sensory input from tooth pulp, optic chiasm and sciatic nerve onto locus coeruleus neurons in the rat.

Electrophysiological studies using rats were performed to determine whether or not neurons in the locus coeruleus (LC), subcoeruleus and parabrachial areas receive convergence of sensory input from tooth pulp (TP), optic chiasm (OC) and sciatic nerve (SN). Convergence of input from these nerves was observed in 23% and 33% of LC and subcoeruleus neurons, respectively, and from two nerves in 31% and 20% of LC and subcoeruleus neurons, respectively, while convergence was rarely detected in parabranchial neurons. These results suggest that there is a convergence of peripheral sensory input onto more than half the noradrenergic coerulear neurons.

Animals↗
PubMed1979

Microiontophoretic studies on noradrenergic inhibition from locus coeruleus of spinal trigeminal nucleus neurons.

Microiontophoretic studies using cats anesthetized with alpha-chloralose and local anaesthetic were undertaken in an attempt to determine whether or not norepinephrine (NE) derived from the locus coeruleus (LC) acts on neurons of the spinal trigeminal nucleus (STN) as an inhibitory transmitter. Both conditioning stimulation of the LC and iontophoretic application of NE inhibited orthodromic spike generation by interior alveolar nerve stimulation in 9 out of 14 STN relay neurons, without affecting antidromic spikes elicited by stimulation of the contralateral medial lemniscus. Glutamate-induced spike firing of the STN relay neurons, however, remained unaltered with iontophoretic application of NE up to 200 nA. The LC conditioning stimulation inhibited orthodromic spikes in 22 out of 25 type-B interneurons in the STN, while iontophoretic NE application seldom had an effect on orthodromic spikes and spontaneous firing of the interneurons. Only 5 out of the 25 interneurons exhibited an inhibition of orthodromic spike generation and spontaneous firing with iontophoretic NE. These neurons fired spikes upon orthodromic stimulation with a relatively short latency, compared with the spike latency of neurons unaffected by iontophoretic NE. The present results strongly suggest that NE released from the terminals of the LC neurons inhibits transmission of STN relay neurons, probably by acting on primary afferent terminals to produce presynaptic inhibition.

Action Potentials↗
PubMed1978

Role of the locus coeruleus in transmission onto anterior colliculus neurons.

The present study was an attempt to elucidate the role of locus coeruleus (LC) on neuronal activities in the anterior colliculus of rats anesthetized with alpha-chloralose. The spike latency of neurons in the deep grey and white layers of anterior colliculus elicited by stimulation of the optic chiasm (OC), lateral geniculate body (LGB) and visual cortex (VC) was longer than that of neurons in the more superficial layers: optic and intermediate grey layers. When conditioning stimuli were applied to LC, a significant inhibition of spike generation upon OC, LGB and VC stimulation was observed on neurons of deep grey and white layers, but not on those of optic and intermediate grey layers. The conditioning stimulation did not alter spike generation, either in the neurons of deep grey and white layers or those of optic and intermediate grey layers, following stimulation of the superficial grey layer. These results strongly suggest that noradrenaline originating in the LC could produce an inhibition of neuronal activities in the deep grey and white layers, and such is probably the result of inhibition of neurons located in the superficial layer of the anterior colliculus.

Animals↗
PubMed1978

Equillibrium disorders with diffuse brain atrophy in long-term toluene sniffing.

A Japanese male who became habituated to sniffing toluene exhibited ataxia, tremor, incoordination and equilibrium disorders. There was pendular nystagmus with a normal caloric response. There were an inhibition of optokinetic nystagmus and a failure to follow over 0.1 Hz sine waves on eye tracking test. Angiogram and pneumoencephalogram revealed an atrophy of the midbrain and cerebrum, and degeneration of the cerebellum was suspected.

Adult↗
PubMed1978

Selective effect of cinnarizine on the vestibular nucleus neurons.

Effects of cinnarizine were studied on the lateral vestibular nucleus (LVN) and spinal trigeminal nucleus (STN) of cats anesthetized with alpha-chloralose. Cinnarizine did not produce any obvious alterations of the field potential and spike generation of type B interneurons in STN elicited by trigeminal nerve stimulation as well as the field potential in LVN by vestibular nerve stimulation. Spike generation of monosynaptic LVN neurons elicited by the suprathreshold stimulus to the vestibular nerve was unaffected by cinnarizine up to 4 mg/kg. When the subthreshold stimulus was applied to the vestibular nerve, however, the spike number of LVN monosynaptic neurons was significantly increased after cinnarizine treatment. The enhancement of spike firing by cinnarizine upon both supra- and subthreshold stimuli to the vestibular nerve was found to be more pronounced in LVN polysynaptic neurons than monosynaptic ones. Since the effect of cinnarizine on LVN neurons was not dose-dependent, it is suggested that the enhanced responsiveness of the neurons by the drug might be due to an increase of blood flow, but not to a direct excitation of the neurons themselves.

Animals↗
PubMed1977

Attenuation of morphine analgesia in rats with lesions of the locus coeruleus and dorsal raphe nucleus.

The nociceptive reflex activity and analgesic effect of morphine were studied in rats using the hind paw stimulation test. The stimulation threshold was significantly increased in animals with bilateral destruction of the locus coeruleus (LC), and was reduced after lesion of the dorsal raphe nucleus (DR). LC lesions produced a selective lowering of noradrenaline (NA) content in the forebrain, while DR lesions resulted in a reduction in serotonin levels. Lesioning both LC and DR significantly reduced both NA and serotonin contents even when the stimulation threshold was not altered. Morphine produced a significant and dose-dependent elevation of the stimulation threshold in sham-operated animals, while morphine analgesia was almost completely inhibited by destruction of LC, DR and both the nuclei. These results imply that a depression of LC-mediated noradrenergic tone results in a decreased sensitivity to painful stimuli, whereas a reduction of raphe-derived serotonergic tone produces the opposite effect against LC. It is suggested, however, that both of these monoamines from the LC and DR are necessary for the analgesic effect of morphine.

Analgesics, Opioid↗
PubMed1976

Dorsal raphe stimulation produces inhibitory effect on trigeminal nucleus neurons.

Inhibitory effects of conditioning stimulation of the dorsal raphe nucleus (DR) on the neuron activity in the rostral part of spinal trigeminal nucleus (STN) were studied in cats for the purpose of comparison with the inhibition induced by locus coeruleus (LC) stimulation. DR conditioning stimulation reduced the orthodromic field potential in STN elicited by inferior alveolar nerve stimulation, and enhanced the antidromic field potential in the trigeminal nerve evoked by STN stimulation; but the inhibitory effects of DR stimulation were considerably weaker than those of LC stimulation. In tracking experiments near the raphe nucleus, conditioning stimulation of DR itself produced the most pronounced decrease in the STN field potential. Orthodromic spike number of STN relay neurons was significantly reduced by DR conditioning stimulation; however, the threshold for the conditioning stimulus to the DR was much higher than that to the LC. Antidromic spike generation of the STN neurons was unaltered by conditioning stimulation of both DR and LC. DR stimulation elicited a field potential in STN, which followed high frequency stimuli up to 200 HZ. A single fiber action potential was also obtained in STN by DR stimulation. STN stimulation produced a field potential in DR, which followed high frequency stimuli. It is suggested from these findings that conditioning stimulation of DR produces a direct inhibition of transmission in STN neurons; however, this stimulation has less effect on these neurons than does stimulation of the LC.

Animals↗
PubMed1976

Antagonizing effects of beta-adrenergic blockers on lucus coeruleus-induced inhibition of trigeminal nucleus neurons.

Effects of alpha- and beta-adrenergic blocking agents applied into the lateral ventricle were studied on the relay neuron in the rostral part of spinal trigeminal nucleus (STN) of cats. Conditioning stimulation of the locus coeruleus (LC) and sensory cortex (SC) inhibited the orthodromic spike generation in STN relay neuron without affecting the antidromic spike, as already reported, and re-confirmed herein. The LC-induced inhibition of orthodromic spike was significantly reduced by intraventricular administration of beta-blockers, MJ 1999 (5 mg) and propranolol (0.5 mg), while the SC-induced inhibition of orthodromic one was not modified by the beta-blockers. The antidromic spike in STN relay neuron per se remained unaffected by these treatments. Intraventricular administration of alpha-blockers such as phentolamine and phenoxybezamine produced no alterations of the LC- and SC-induced inhibition of orthodromic spike. As the beta-blockers produced a selective antagonism, noradrenaline originating in LC probably acts as an inhibitory transmitter on the STN relay neuron and is mediated by beta-receptor.

Action Potentials↗
PubMed1976

The role of thiamine on excitable membrane of crayfish giant axon.

Electrophysiological and biochemical studies were performed to determine the role of thiamine in the excitable membrane of the crayfish giant axons, as it has been suggested that thiamine plays a role in the excitability of the membrane which is unrelated to the metabolic process. Thiamine (5mM) significantly increased the rising rate of the action potential without affecting the resting membrane potential and threshold potential. A recovery of the enhancement was evidenced by a wash of the axon with physiological solution. Pyrithiamine (10 mM) reduced the rising rate of the action potential without affecting the membrane and threshold potential. The reduction of dV/dt by pyrithiamine remained unchanged after a wash of the axon with physiological solution, while dV/dt increased after thiamine treatment. The amount of thiamine found in the crayfish axons was comparable to that observed in the rat sciatic nerve. In addition, pyrithiamine reduced the thiamine content in axons and protein binding thiamine of the axons. It is thus concluded that thiamine in the excitable membrane of crayfish axons plays a significant role in production of the action potential and is essential for maintaining the membrane excitability of crayfish axons.

Action Potentials↗
PubMed1976

A study of the microfilarial periodicity at Bireuen, the type locality of Brugia malayi.

A field study was conducted in August 1974 at Bireuen, Indonesia, at the type locality of Brugia malayi from where the parasite was first described by Lichtenstein (1927) and Brug (1927), in order to determine the pattern of the microfilarial periodicity. From the results, it has been demonstrated that both the microfilariae of B. malayi as well as those of W. bancrofti in man from Bireuen area are the nocturnally periodic form. The microfilaria rates observed in the present survey were much lower than those recorded by Lichtenstein (1927) some 50 years ago in the same areas.

Blood↗