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Biomedical subjects

C Torda

Publications and source records attributed to C Torda.

At least 19 recordsLinked to original sources
PubMed1979

Relationship of geniculate and occipital PGO waves and the effects of nonvisual sensory activity.

The nature of occipital PGO waves (REM) was addressed by comparing the occipital PGO waves measured at the marginal gyrus with the geniculate PGO waves and the occipital PGO waves "directly" transmitted to the occipital cortex. The directly transmitted PGO waves lack the first short positive-going spike that precedes the negative phase of the occipital PGO waves. The "directly" transmitted PGO wave was recorded from cats with either deafferented or excised LG nucleus. The "directly" transmitted PGO wave resembled pontine negative-going PGO wave more regarding amplitude and wave shape changes than the occipital PGO waves of intact cats. The ascending negativity of pontine PGO waves is indirectly transmitted through phasic increase of the local excitatory processes, more in the LG than in the occipital cortex. The PGO waves seem to be affected by endogenous and exogenous nonvisual processes, more in the LG than the occipital cells alone. The occipital PGO waves seem to result from the vectorial sum of geniculate and "directly" transmitted occipital PGO waves.

Animals↗
PubMed1979

Attenuation in central neurons: its relationship to increased intracytoplasmic free calcium, calcium binding and memory storage.

A mechanism responsible for attenuation of dendritic spikes of nucleus reticularis gigantocellularis (NRG) origin was addressed. Stimulation of afferent neurons with pulses of 100 per sec frequency generated attenuation in specific neurons. Intrasomatic infusion of EGTA reversed the attenuation. The results suggest that attenuation results from intracytoplasmic accumulation of free Ca2+ due to differences in rate of Ca influx and Ca binding. This accumulation generates a concentration dependent prevention of Ca2+ (and Na+) influx that causes the attenuation. The free intracytoplasmic Ca2+ is removed mainly by binding on proteins and/or polypeptides, a mechanism that promotes memory storage.

Animals↗
PubMed1978

Studies on homosynaptic (posttetanic) potentiation: a cholinergic modulator of presynaptic origin.

Effects of soluble proteins (peptides, glycopeptides) extracted from presynaptic cholinergic vesicles of both rat brain and electric organ of Torpedo marmorata on postsynaptic spike generation were studied. The extracts potentiated postsynaptic effects of both endogenous and exogenous acetylcholine and had properties that fulfilled the minimum necessary requirements by Zetler of a modulator of a specific putative neurotransmitter effect. This modulator seems responsible for homosynaptic (posttetanic) potentiation. Therefore when cholinergic vesicle walls fuse with presynaptic terminal membrane during presynaptic stimulation, they verse into the synaptic cleft "modulator" substance(s) together with acetylcholine.

Action Potentials↗
PubMed1977

A cholinergic modulator.

Soluble proteins obtained from presynaptic cholinergic vesicles have been tested regarding their effects to modify postsynaptic spike generation. The results suggest that these proteins (or derivatives, incl. glycopeptides) may act as modulators in increasing the effectiveness and duration of postsynaptic spike generation. They may partake in generation of homosynaptic (posttetanic) potentiation.

Acetylcholine↗
PubMed1977

Hypothalamic adrenaline synthesis after stimulation of the medial forebrain bundle.

1 The problem of whether locally released noradrenaline can be methylated to adrenaline in the hypothalamus has been investigated. 2 During stimulation of the medial forebrain bundle (MFB) the hypothalamic adrenaline content increased somewhat, but the increase was not statistically significant (13%, mean of 10 experiments). 3 After inhibition of the activity of monoamine oxidase and catechol-O-methyltransferase this increase was much larger (80%, mean of 9 experiments). 4 Adrenalectomy did not prevent the rise in hypothalamic adrenaline after stimulation of the MFB. These results suggest that noradrenaline released during activity of noradrenergic hypothalamic structures may be methylated to adrenaline in the hypothalamus.

Adrenalectomy↗
PubMed1977

On newborn hypothalamic phenylethanolamine-N-methyltransferase.

Phenylethanolamine-N-methyltransferase activity of rat hypothalami was assayed. The enzyme was present at birth, in traces, and gradually increased during the first 2 postnatal months. Exposure to recurrent stressful situations increased PNMT activity in a statistically significant manner. Persistence of exposure to stressful events resulted in higher adult PNMT activity. Assays of hypothalamic tissue cultures revealed that part of PNMT activity increase was due to temporary potentiation by local factors, and partly to increase of tissue concentration of enzyme by increased protein synthesis. One of the submolecular chain reactions generated by stress (and able to induce protein synthesis) was identified as: release of ACTH during stress, activation of local adenylate cyclase by ACTH to synthesize cyclic AMP. When released, this cyclic AMP increased the local cyclic AMP: cyclic GMP ratio, a process known to induce protein synthesis. A potent and selective competitive inhibitor, SK&F 64139, when added to tissue cultures, prevented increase of PNMT activity by prolonged stimulation.

Animals↗
PubMed1977

A glycoprotein fraction "modulator" of norepinephrine effects in vivo.

The effects of a fraction (Part A of Fraction 8) of a glycoprotein isolated by Lee on the physiological effects of norepinephrine have been studied by measuring the spontaneous activity of Purkinje cells of rats. Fraction A appears to be a "modulator" of norepinephrine because (1) it potentiated the effects of exogenous and endogenous norepinephrine by increasing the amplitude of the response, (2) it significantly prolonged those effects beyond average duration, (3) its effects disappeared only gradually, (4) in the concentrations tested (physiologically available concentrations and up to 20 times greater), it lacked neurotransmitter effects of its own. The effects of Fraction A on endogenous norepinephrine were concluded from (a) its effects on the intact Purkinje cell, (b) its effects on Purkinje cells deprived of norepinephrine content by 6-OH-dopamine or alpha-methyl-paratyrosine, and (c) its effects on Purkinje cell activities induced by stimulation with rectangular pulses of the afferent noradrenergic inhibitory neurons.

Action Potentials↗
PubMed1976

Bioelectric observations on adult and newborn hypothalamic dendrites.

Bioelectric activities of hypothalamic dendrites of newborn kittens and adult cats were recorded in vivo. Stimulation of various hypothalamic areas with electrical stimuli, or by injection of norepinephrine, generated propagated spikes in both newborn and adult neurons. The morphologically immature hypothalamic dendrites were hypersensitive to stimuli and were able to generate propagated spikes not only of axon hillock (adults) but also of dendritic membrane origin. Some mechanisms responsible for the two types of spike formation (newborn and adult) have been identified.

Animals↗
PubMed1976

Effects of catecholamines on behavior.

The potential for at least partial reversible transition of aggression- and anxiety-type symptomatology suggested searching for a potential biochemical link between subcellular mechanisms involved in the execution of aggression and anxiety. The effects of norepinephrine combined with dopamine and of epinephrine on these two types of behavior were tested. Responses to foot-shock were used to test aggression, extinction of avoidance response was used to test anxiety-type behavior. The results suggested that one of the possible links between the intracerebral processes responsible for execution of aggression- and anxiety-type behaviors is transmethylation of norepinephrine and/or dopamine to epinephrine.

Aggression↗