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Biomedical subjects

R Spehlmann

Publications and source records attributed to R Spehlmann.

At least 19 recordsLinked to original sources
PubMed1984

Decreased sensitivity of neurons in the basolateral amygdala to dopamine and noradrenaline iontophoresis after a kindling stimulus.

The depressant effects of iontophoretically applied dopamine and noradrenaline on glutamate-induced neuronal firing in the amygdaloid complex of cats were significantly reduced 1 and 2 h after induction of a local epileptiform afterdischarge of the kind used in kindling. Neuronal excitation by glutamate and depression by GABA were not significantly changed. This suggests that kindling is associated with a reduction of the inhibitory effects of endogenous catecholamines.

Amygdala↗
PubMed1982

Cholinergic mechanisms in the production of focal cortical slow waves.

Microiontophoretic application of scopolamine and atropine usually induced or increased focal cortical slow waves of under 3 Hz and abolished or decreased focal fast waves of over 6 Hz whereas acetylcholine iontophoresis and electrical stimulation of the mesencephalic reticular formation had the opposite effect, suggesting that focal cortical slow waves may be due to the interruption of cholinergic input from the reticular formation.

Animals↗
PubMed1981

Microiontophoretic study of the GABA receptor in the feline caudate nucleus.

The effect of microiontophoretic application of GABA and its antagonist, picrotoxin, on the firing of neurons in the feline caudate nucleus (CN) was studied. Firing was elicited by stimulation of the CN a few millimeters from the recording site. Increasing ejection currents of GABA produced a dose-dependent decrease and eventual blockade of the firing of CN neurons. The GABA current which reduced firing by 50% (ED50) was 7 nA. The Hill coefficient for the action of GABA was calculated as 1.8, indicating that a minimum of two independent subunits of the GABA receptor might need to be simultaneously occupied to activate the conductance change which produces the depressant effect. Picrotoxin blocked the action of GABA in a manner suggestive of a competitive antagonism. Dose ratios for the effects of GABA alone and of GABA during picrotoxin iontophoresis showed the dissociation constant (KD) of picrotoxin for the GABA receptor in the CN to be approximately 5 microM. Our results agree with those reported for different parts of the nervous system in various species, suggesting that the receptor which mediates the depressant effect of GABA in the CN has properties similar to striatal GABA receptors characterized in in vitro studies.

Animals↗
PubMed1978

Selective blockade by scopolamine of synaptic responses in cat's caudate nucleus and its modification by lesions of the substantia nigra.

Because it is commonly believed that acetylcholine is a synaptic transmitter in the caudate nucleus and that the reduction of striatal biogenic amines in Parkinson's disease leads to acetylcholine supersensitivity in the caudate nucleus, we investigated the effects of the muscarinic blocking agent scopolamine on synaptic responses of neurons in the intact feline caudate nucleus and in the caudate nucleus depleted of dopamine by long-standing nigrostriatal lesions. In the intact caudate nucleus, micro-iontophoretic application of scopolamine selectively blocked the neuronal responses to stimulation of the caudate nucleus near the recording site without affecting the responses to stimulation of the sensorimotor cortex or the substantia nigra in the same fashion. This suggests that acetylcholine is a synaptic transmitter of caudate interneurons. Responses to thalamic stimuli were also blocked by scopolamine, suggesting that acetylcholine may be a transmitter of thalamic afferents although the course of these afferents is unclear. In the dopamine-depleted caudate nucleus scopolamine was more effective than in the intact caudate nucleus blocking the neuronal responses to stimulation of the caudate nucleus. This greater blocking effect by scopolamine suggests an increased effect of endogenous acetylcholine in this response and supports previous observations of an increased excitatory effect of iontophoretic acetylcholine in the dopamine-depleted caudate nucleus. These results suggest that the acetylcholine supersensitivity which follows nigrostriatal degeneration may be due to increased effectiveness of synaptic transmission by cholinergic interneurons in the caudate nucleus.

Acetylcholine↗
PubMed1977

Visual evoked potentials and postmortem findings in a case of cortical blindness.

A patient with cortical blindness due to extensive bilateral posterior cerebral infarcts showed occipital visual evoked potentials to flash stimulation on repeated testing. These responses were probably mediated by extrageniculocalcarine connections between the optic nerve and the secondary visual cortex of the occipital convexity.

Aged↗
PubMed1976

Dopamine acetylcholine imbalance in Parkinson's disease. Possible regenerative overgrowth of cholinergic axon terminals.

Parkinson's disease is characterised by an imbalance between acetylcholine and dopamine which probably results from the degeneration of a dopaminergic nigrostriatal pathway. A new hypothesis is proposed to explain the development of this imbalance. Applying the concept that degeneration of nerve-fibres in the central nervous system can lead to collateral sprouting of uninjured fibres, it is suggested that the death of dopaminergic nigrostriatal neurons results in sprouting of axons of cholinergic interneurons in the caudate nucleus. This overgrowth could result in the cholinergic innervation of neuronal membranes vacated by degenerated dopaminergic terminals. Thus, the apparent changes in the activity of dopaminergic and cholinergic systems can be accounted for by faulty regeneration in the central nervous system.

Acetylcholine↗
PubMed1976

Comparison of dantrolene sodium and diazepam in the treatment of spasticity.

The effects of dantrolene sodium and diazepam were compared in a double crossover study of 42 patients with spasticity due to stable multiple sclerosis. Both drugs reduced the findings of spasticity, clonus, and hyperreflexia, and the complaints of muscle stiffness and cramping. Each drug had different side effects which suggest indications and contraindications for its use in spastic patients.

Clinical Trials as Topic↗
PubMed1975

The effects of acetylcholine and dopamine on the caudate nucleus depleted of biogenic amines.

Because it has been proposed that the reduction of the striatal biogenic amines in Parkinson's disease leads to an imbalance between the actions of acetylcholine and dopamine, we have studied the effects of these substances, liberated from multibarrelled micropipettes, on the firing of single neurons in the feline caudate nucleus depleted of biogenic amines by long-standing nigrostriatal lesions. Compared with neurons in intact cats, those in cats with lesions were more easily excited by acetylcholine and less easily supressed by dopamine. These results suggest that the depletion of the striatal amines decreases the neuronal susceptibility to dopamine and increases that to acetylocholine, possibly by changing the sensitivity or the number of the neuronal receptors of these agents.

Acetylcholine↗
PubMed1975

A pharmacologic study of the stiff-man syndrome. Correlation of clinical symptoms with urinary 3-methoxy-4-hydroxy-phenyl glycol excretion.

We have investigated hypotheses that link the stiff-man syndrome to an imbalance of neurotransmitter systems. No evidence was found to support the concept of defective synaptic transmission at either cholinergic input to Renshaw inhibitory elements or at glycinergic inhibitory input to motoneurons from spinal interneurons, since neither physostigmine nor glycine altered symptomatology. Urinary excretion of the norepinephrine metabolite 3-methoxy-4-hydroxy-phenyl glycol showed a high correlation with clinical status. This suggests the involvement in the stiff-man syndrome of a central norepinephrine neuronal system that has net excitatory effects upon motoneurons, a system whose activity can be increased slightly by levodopa and decreased markedly by diazepam, with corresponding changes in stiffness.

Diazepam↗