Biomedical subjects
Publications and source records attributed to S Lindström.
Appropriate management of patients with urinary incontinence requires access to a variety of methods. Electrical stimulation, although so far proportionally small in the armamentarium of methods, is founded on physiologic principles and has the advantage of being curative without significant side effects.
Excitatory postsynaptic potentials (EPSPs) were evoked in principal cells of the cat's dorsal lateral geniculate nucleus by electrical stimulation of cortico-geniculate fibres. The EPSPs had a pronounced frequency sensitivity. They were barely detectable at stimulation frequencies below 3 Hz but increased dramatically in size at higher frequencies. At 30-50 Hz their amplitude typically exceeded that of EPSPs from optic tract fibres. A prominent EPSP potentiation was also obtained with pair pulse stimulation. The findings are discussed in relation to the hypothesis that the cortico-geniculate system serves as a variable gain regulator for the visual input to the cortex.
1. Reflex effects of cold stimulation of the lower urinary tract were studied in cats anaesthetized with alpha-chloralose. The bladder and the urethra were catheterized for separate fluid instillations and the bladder pressure was monitored together with the evoked efferent nerve responses in pelvic nerve filaments. 2. A bladder cooling reflex could be evoked from both the bladder and the urethra. The response was an efferent discharge in preganglionic pelvic motor fibres to the bladder. 3. Bladder mechanoreceptors that drive the normal micturition reflex were not directly involved in the cooling reflex. Their tension sensitivity was decreased by cooling and the efferent reflex response typically occurred before any activation of these receptors. The efferent activity of the cooling reflex also survived an intentional unloading of the mechanoreceptors, a manipulation that abolishes the normal micturition reflex. 4. The dynamic threshold temperature of the cooling reflex was about 30-32 degrees C, which was at the thermal neutral point of the bladder in our experimental situation. 5. The bladder-evoked component of the reflex was greatly reduced or abolished by an intravesical infusion of the local anaesthetic Xylocaine. It was also abolished by total bladder denervation. 6. The vesical component of the reflex was unchanged by bilateral transections of the hypogastric nerves but abolished by pelvic nerve transection. The cooling reflex from the distal urethra was abolished by transection of the pudendal nerves. 7. It was proposed that the cooling reflex originates from cold receptors in the bladder and urethral walls and that the responsible afferent fibres are unmyelinated C fibres. The function of the reflex may be to rid the body of a thermal ballast when under cooling stress.
1. Inhibitory connections of X- and Y-type principal cells in the cat's dorsal lateral geniculate nucleus were studied with intracellular recording techniques in barbiturate-anaesthetized animals. Cells were identified as principal cells by antidromic activation from the visual cortex and as X or Y types by their responses to visual stimulation. 2. Graded electrical stimulation was used to obtain selective activation of X and Y ganglion cell axons. The optic nerves were stimulated through ring electrodes behind the eye bulbs and the evoked nerve volley was monitored by an optic tract electrode. The nerve volley consisted of two well-segregated components, an early, low-threshold Y component and a late, high-threshold X component. 3. All principal cells received monosynaptic excitation and disynaptic feed-forward inhibition from optic nerve fibres. The excitatory and inhibitory postsynaptic potentials were evoked by Y axons in Y cells and by X axons in X cells. Thus, the feed-forward inhibitory pathway to principal cells is type selective. 4. Recurrent inhibition was evoked in all cells by antidromic activation of principal cell axons in the visual cortex. The recurrent inhibitory potentials had significantly shorter latencies in Y than in X cells but with considerable overlap between the two samples. This overlap presumably reflects a similar overlap in antidromic conduction times for X and Y principal cell axons. 5. Recurrent inhibitory potentials evoked in the orthodromic direction by optic nerve stimulation originated from Y axons in Y principal cells and from X axons in X cells as would be expected for a type-selective recurrent inhibitory pathway. 6. It is concluded that X and Y principal cells in the dorsal lateral geniculate nucleus have similar but functionally separate inhibitory circuits.
Five binocularly activated cells near the interlaminar layers of the dorsal lateral geniculate nucleus have been studied with intracellular recording techniques. Four neurons were relay cells and antidromically activated from the visual cortex. They received monosynaptic excitation and disynaptic inhibition from Y type retinal ganglion cells in both eyes and disynaptic recurrent inhibition. The fifth cell was similar to perigeniculate neurons. It received disynaptic excitation from retinal ganglion cells in both eyes and monosynaptic excitation from antidromically activated relay cell axons. It was also inhibited from all these sources after an additional synaptic delay. The cell had a large receptive field, about twice the center size of neighboring relay cells, and gave on-off responses from the entire response area. Such displaced perigeniculate like cells may explain why relay cells issue occasional axon collaterals within the dorsal lateral geniculate nucleus.
Animal experiments indicate that the awake state is supported by activating structures in the caudal reticular core of the mesencephalon and in the caudolateral hypothalamus. Different aspects of the normal wakefulness may be mediated by separate neuronal subsystems. This segregation may explain why atypical combinations of symptoms may occur in head injured patients.
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Inhibitory interactions between interneurones of the lateral geniculate nucleus (LGN) of the cat were studied with an indirect method based on intracellular recordings of synaptic responses in principal cells. Recurrent inhibitory postsynaptic potentials (IPSPs), evoked by antidromic activation of principal cell axons in the visual cortex, were depressed by a preceding stimulation of the optic tract or the visual cortex. Disynaptic feed-forward IPSPs, evoked by optic tract stimulation, were likewise depressed after cortex stimulation. The duration of the depression was in both cases about 100 ms. The effect was not due to conductance changes in the recorded principal cells or to activation of cortico-geniculate fibres. The observations indicate that perigeniculate neurones, the recurrent inhibitory interneurones of the LGN, have mutual inhibitory connexions and that they also project to intrageniculate interneurones, the inhibitory cells in the feed-forward pathway to principal cells. These conclusions were supported by intracellular recordings from a few interneurones. No evidence was found for interaction between feed-forward interneurones activated from separate eyes or for a projection from intrageniculate interneurones to perigeniculate cells. The results point to an unexpected similarity in the organization of the recurrent inhibitory system of principal cells in the LGN and of spinal motoneurones. It is suggested that the recurrent system of the LGN serves as a variable gain regulator in analogy with a recently proposed model for the spinal system.
Evoked potentials were recorded in the visual cortex of the cat after electrical stimulation of the lateral geniculate nucleus (l.g.n.). The primary response, mediated by geniculo-cortical fibres, was depressed at stimulation frequencies above 7 Hz and replaced by a late potential, the incremental response, which gradually increased in amplitude with successive stimuli. The incremental response was a negative-positive potential in the depth of the cortex with the negative component having maximal amplitude in layer 4. The response reversed polarity in layer 1 to become a positive-negative potential at the surface. The latency of the negative component of the incremental response was about 3.5-4 ms in layer 4, compared to about 1.5 and 2.5 ms for the mono- and disynaptic components of the primary response. The incremental response could only be evoked from the l.g.n. and the optic radiation, not from the optic tract, superior colliculus or other surrounding structures. Within the l.g.n., the effect was only evoked from stimulation sites in approximate retinotopic register with the recording site in the cortex. Low threshold points were found in the A laminae, completely overlapping with the low threshold points for the primary response. Thresholds increased steeply when the stimulation electrode was lowered into the C laminae. The incremental response could still be evoked ten days after the destruction of all cells in the l.g.n. complex by kainic acid. It is concluded that the described incremental response is identical to the augmenting response of Dempsey & Morison (1943) and is mediated by intracortical axon collaterals of antidromically activated cortico-geniculate neurones.
Antidromic activation of layer 6 cortico-geniculate cells from the lateral geniculate nucleus (l.g.n.) was used to study synaptic effects mediated by their intracortical axon collaterals. A specific stimulation procedure, earlier shown to suppress geniculo-cortical synaptic effects and to enhance synaptic effects from layer 6 cell collaterals was employed to differentiate between inputs from the two pathways. Single cells in different cortical layers were recorded both extra- and intracellularly with glass micro-electrodes. Antidromic activation of cortico-geniculate cells at 10-16 Hz induced massive, usually repetitive, spike discharges in almost all cells in layers 2-5. The shortest latency for this synaptic activation (3.4-7.5 ms) was found for simple cells in layer 4. Cells in layers 2, 3 and 5 responded with progressively longer latencies. Cortico-geniculate cells in layer 6 were atypical in that hardly any responded with synaptic discharges to the stimulation. Intracellular recordings from layer 4 cells revealed, besides a monosynaptic excitatory post-synaptic potential (e.p.s.p.) from geniculo-cortical fibres, a late e.p.s.p. with a latency of 3.0-4.2 ms. This e.p.s.p. could only be evoked from stimulation sites within the A laminae of the l.g.n. in retinotopic register with the recording site in the cortex. No corresponding potential was obtained by stimulation of the optic tract or the superior colliculus. The threshold intensity for the late e.p.s.p. in layer 4 cells was much higher than for the geniculo-cortical e.p.s.p.s from the same stimulation sites, indicating that the effect was mediated by thin fibres. The late e.p.s.p.s increased dramatically in size with repetitive stimulation of the l.g.n. at frequencies above 7 Hz, while the geniculo-cortical e.p.s.p.s remained unchanged. In all these properties, the late e.p.s.p.s resemble similar e.p.s.p.s evoked monosynaptically in principal cells of the l.g.n. by orthodromic activation of cortico-geniculate fibres. Large e.p.s.p.s were evoked also in complex cells of layers 2, 3 and 5 and in simple cells of layer 6 upon antidromic stimulation of cortico-geniculate fibres. The sample included many efferent neurones, identified as projection cells by antidromic activation from extracortical stimulation sites. The latency and behaviour of the e.p.s.p.s in these cells indicate that the effect was mediated indirectly via layer 4 cells. Presumably, the excitation travelled along an earlier identified chain of neurones, going from layer 4 to layers 2 and 3, from there to layer 5 and then to layer 6.(ABSTRACT TRUNCATED AT 400 WORDS)
Brain-stem control of inhibitory circuits in the dorsal lateral geniculate nucleus (d.l.g.n.) of the cat was studied with extracellular recordings from functionally identified interneurones and with intracellular recordings from principal cells. Perigeniculate neurones, the recurrent inhibitory interneurones of the d.l.g.n., were inhibited by low-threshold stimulation within a wide bilateral field of the brainstem reticular formation extending from the rostral mesencephalon to the caudal medulla oblongata. The inhibition had a latency of 10-12 ms for stimulation sites in the mesencephalon and a duration of about 100 ms. The brain-stem stimulation evoked large hyperpolarizing potentials in intracellularly recorded perigeniculate neurones, indicating that the effect was due to post-synaptic inhibition. Intrageniculate interneurones, the feed-forward inhibitory interneurones of the d.l.g.n., were inhibited with a similar time course from the same region of the brain stem. Both feed-forward and recurrent inhibitory post-synaptic potentials (i.p.s.p.s) in principal cells were depressed by a preceding stimulation of brain-stem sites effective for the interneurones. The depression had about the same time course as the inhibition of the interneurones and it occurred without a concomitant change in the membrane potential of the recorded principal cells. A small depolarizing potential, with a latency of 10-20 ms, was observed in some principal cells after brain-stem stimulation. The potential reversed polarity when i.p.s.p.s were reversed by current injection into the recorded cell indicating that it was due to disinhibition of the principal cells. The possible neuronal pathway for the inhibition of the d.l.g.n. in interneurones is considered and it is proposed that the effect is mediated by a group of neurones located in the caudal mesencephalon and the rostral pons close to the fibres of the brachium conjunctivum.
Efferent nerve activity was recorded from pelvic nerve filaments to the urinary bladder of the cat. At intravesical pressures below 5-7 cm H2O there was no activity, but at higher pressure levels the parasympathetic neurones discharged in 10- to 15-second-long rhythmic bursts separated by silent periods. The frequency of the burst varied from about 1/min at 5 cm H2O to 6-7/min at 15-20 cm H2O. Each burst of activity was followed by a small bladder contraction. The nervous activity preceded the contraction by several seconds, indicating that the bladder response was caused by the efferent discharge. Prolonged continuous efferent activity could occur immediately after pressure changes, at pressures above 20-25 cm H2O or after inhibition caused by intravaginal stimulation. In these situations, rhythmic activity resumed as inhibition of the tonic discharge. This behaviour indicates that the rhythmicity is primarily determined by a central inhibitory mechanism. The findings are discussed in relation to the normal function of the neuronal feedback systems of the bladder and their possible role in the development of the clinical condition 'unstable bladder'.
A dialysis sampling probe was used to collect amino acids from the dorsal lateral geniculate nucleus (LGN) in vivo. The sampling probe was equipped with an electrode to allow local stimulation and recording of nerve activity. The amino acids in the dialysates were determined fluorimetrically by precolumn derivation and hplc-separation. Local electrical stimulation of the LGN caused a multifold increase in glutamate, aspartate and GABA levels. Smaller changes were observed for taurine, alanine and glycine. The results indicate that the dialysis sampling probe is rather atraumatic and can be used to detect stimulation-induced changes in extracellular amino acid concentrations.
Intravaginal electrical stimulation (IVS) induces a profound bladder inhibition and is successful in the treatment of incontinence due to detrusor instability. In this experimental study in cats, direct recordings of the efferent activity in thin hypogastric and pelvic nerve filaments to the bladder were used to analyze the neuronal mechanisms underlying this bladder inhibition. A longlasting reflex discharge, with a latency of 35 to 50 msec., was evoked in the hypogastric nerve by IVS. The reflex discharge was unaffected by imposed changes in intravesical pressure or by micturition contractions, but the response was very frequency-sensitive with an optimal transmission at about 5 Hz of stimulation. A "spontaneous" efferent activity could be recorded in the pelvic nerve filaments when the bladder pressure was elevated above 5 to 7 cm. H2O. The pelvic activity occurred in 10 to 20-second bursts, each followed by an abortive detrusor contraction. IVS of 5 to 10 Hz completely abolished this efferent pelvic activity by central inhibition. The findings are discussed in relation to the normal neuronal control of the bladder and to the clinical application of IVS.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.