Biomedical subjects

S M Thompson

Publications and source records attributed to S M Thompson.

At least 91 records · Page 5Linked to original sources

PubMed1989

Activity-dependent disinhibition. II. Effects of extracellular potassium, furosemide, and membrane potential on ECl- in hippocampal CA3 neurons.

1. Single-electrode voltage-clamp recordings were made from CA3 pyramidal cells in organotypic hippocampal slice cultures for measurement of membrane currents underlying both the gamma-aminobutyric acid (GABA)-mediated, Cl- -dependent inhibitory postsynaptic potential (IPSC), evoked in response to stimulation of the mossy fiber pathway, and responses to iontophoretically applied GABA. Their reversal potentials are presumed to equal the equilibrium potential for Cl- (37). Mechanisms underlying activity-dependent increases in the intracellular concentration of Cl- ([Cl-]i) were investigated by describing active and passive pathways for Cl- influx and efflux. 2. During 99-s applications of GABA, driving force declined by 51% due to increases in [Cl-]i; thus passive Cl- influx through GABA-activated pathways can significantly affect [Cl-]i. 3. Decreasing the extracellular K+ concentration ([K+]o) from 5.8 to 1 mM caused a rapid hyperpolarizing shift in the mean IPSC reversal potential (EIPSC) from -67.6 to -81.9 mV, even when membrane potential (Vm) was maintained constant and depolarized with respect to EIPSC. 4. Decreasing [K+]o from 5.8 to 1 mM caused a rapid hyperpolarizing shift in the mean GABA reversal potential (EGABA) from -64.7 to -81.1 mV, even when Vm was maintained constant and depolarized with respect to EGABA. Reducing the extracellular Cl- concentration from 153 to 89 mM, while maintaining [K+]o constant at 1 mM, shifted the mean EGABA from -81.1 to -66.2 mV, an amount close to that predicted by the Nernst equation for Cl-. We conclude that reducing [K+]o caused a hyperpolarizing shift in EGABA and EIPSC by decreasing [Cl-]i. 5. The shift of EIPSC and EGABA upon alteration of [K+]o did not result from contamination of the responses by additional K+-mediated components because it was unaffected by block of K+ channels with intracellular Cs+. 6. Reducing the extracellular Na+ concentration from 141 to 70 mM had no effect on EGABA. 7. Furosemide, bath-applied at 5 X 10(-4) M while holding Vm depolarized with respect to EIPSC, caused a rapid, reversible decrease in IPSC driving force averaging 69%, consistent with the presence of a furosemide-sensitive outward Cl- -transport system. 8. Reducing [K+]o from 5.8 to 1 mM in the presence of 5 X 10(-4) M furosemide produced a smaller shift of EIPSC from -61.0 to -71.2 mV, however, after washout of furosemide from [K+]o = 1 mM saline, EIPSC shifted further to -89.8 mV.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1989

Activity-dependent disinhibition. III. Desensitization and GABAB receptor-mediated presynaptic inhibition in the hippocampus in vitro.

1. Single-electrode voltage-clamp recordings were made from CA3 pyramidal cells in organotypic hippocampal slice cultures for measurement of membrane currents underlying both the gamma-aminobutyric acid (GABA)-mediated, Cl- -dependent inhibitory postsynaptic potential (IPSC), evoked in response to stimulation of the mossy fiber pathway, and responses to iontophoretically applied GABA. Pre- and postsynaptic mechanisms mediating activity-dependent reductions in the conductance underlying the IPSC (gIPSC) were investigated. 2. During 99-s applications of GABA, the mean evoked conductance (gGABA) decreased 43% with an initial time constant of 51 s. Desensitization was never complete. 3. Ca2+-influx, activated with depolarizing voltage commands of 100-ms to 15-s duration in the presence of intracellular Cs+, had no effect on GABA responses. 4. Iontophoretic application of the GABAA-receptor agonist muscimol caused a rapid decrease of 80-100% in the amplitude of IPSCs evoked at depolarized membrane potentials (Vm). Recovery was 80% complete in 30 s. The second of two paired applications of muscimol, delivered at the same iontophoretic intensity, was reduced in amplitude 35%. This was shown to result from a decrease in driving force rather than from desensitization. We conclude that muscimol decreases IPSCs by causing an increase in the intracellular Cl- concentration. 5. Iontophoretic application of the GABAB-receptor agonist (+/-)-baclofen caused a decrease of only 30% in the amplitude of IPSCs evoked at depolarized Vms. This effect outlasted the post-synaptic effects of baclofen; recovery was 80% complete between 60 and 90 s. 6. Bath application of (-)-baclofen was found to decrease gIPSC without affecting the IPSC reversal potential. This effect was rapid in onset, could be observed at concentrations as low as 1 X 10(-7) M, and recovered quickly. The EC50 was roughly 5 X 10(-7) M and appeared similar to that for the baclofen-activated increase in postsynaptic conductance. No effect on responses to iontophoretically applied GABA was observed, demonstrating that baclofen decreases gIPSC by reducing presynaptic release via GABAB receptors. 7. Iontophoretic application of GABA reduced IPSCs in a dose-dependent manner. At low iontophoretic intensities, IPSCs were reduced only 30% and recovered slowly, as with baclofen iontophoresis. At higher iontophoretic intensities, IPSCs were more completely blocked. Recovery was initially fast, but took 60-90 s to be complete.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1988

Outward chloride/cation co-transport in mammalian cortical neurons.

The mechanism underlying outward chloride transport in guinea pig cingulate cortical neurons of in vitro slices was characterized with respect to its pharmacological antagonists and anion selectivity, and the nature of other ion movements coupled to Cl- transport. Changes in intracellular Cl- concentration, following iontophoresis of Cl- from KCl-filled intracellular recording electrodes, were estimated from changes in the amplitude of GABAergic, Cl(-)-mediated inhibitory postsynaptic potentials (IPSPs). The rate of outward Cl- transport was found to be reduced by bumetanide but not by SITS. SCN-, but not NO3-, was found to be actively transported. Increasing the extracellular K+ concentration ([K+]o) from 2.5 to 10 mM was found to inhibit Cl- extrusion. These data suggest that active Cl- extrusion from mammalian cortical neurons is mediated by an outwardly directed chloride/cation cotransport mechanism. Inhibition of this process by elevated [K+]o may be important in epilepsy.

Animals↗

PubMed1988

Relative contributions of passive equilibrium and active transport to the distribution of chloride in mammalian cortical neurons.

1. Active and passive factors affecting the chloride gradient of cortical neurons were assessed using intracellular recordings from neurons in slices of cingulate cortex maintained in vitro. The chloride equilibrium potential (ECl-) was estimated indirectly from the reversal potentials of responses to perisomatic gamma-aminobutyric acid (GABA) application and the Cl(-)-dependent inhibitory postsynaptic potential (IPSP). Under control conditions the mean resting potential (Vm; -69.7 mV) was not significantly different than the mean IPSP reversal potential (EIPSP; -70.1 mV). 2. Increasing the external potassium concentration ([K+]o) from 1 to 10 mM shifted the mean EIPSP from -80.4 to -61.8 mV. The mean EIPSP was approximately equal to the mean Vm at all [K+]oS. The conditions of Donnan equilibrium are not met in [K+]o less than 10 mM. 3. Polarization of Vm up to 20 mV away from EIPSP for 4 min with maintained current injection had no significant effect on EIPSP. 4. The GABA reversal potential was maintained 37-52 mV less negative than Vm after equilibration in saline in which the external chloride concentration had been reduced from 133 to 5 mM by substitution with isethionate. Vm and input resistance were not significantly different from control values in cells recorded under these conditions. 5. We conclude that Cl- is not passively distributed in cortical neurons, perhaps due to a low resting Cl- permeability. 6. Impalement with electrodes containing 2 M KCl resulted in a rapid 10 mV depolarizing shift in EIPSP that then remained relatively constant. Intracellular iontophoresis of Cl- resulted in a further depolarizing shift of EIPSP of 5-10 mV that returned to control in less than 1 min. The time course of recovery of IPSP amplitude could be fit with a single exponential having a mean time constant of 6.9 +/- 1.5 s and was independent of the amount of Cl- injected or stimulation frequency. 7. Reductions in temperature from 37 to 32 degrees C significantly increased the mean time constant of IPSP recovery from Cl- injection to 11.1 +/- 3.3 s, corresponding to Q10 = 2.6.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1987

Organization of subcortical pathways for sensory projections to the limbic cortex. I. Subcortical projections to the medial limbic cortex in the rat.

Subcortical afferent projections to the medial limbic cortex were examined in the rat by the use of retrograde axonal transport of horseradish peroxidase. Small iontophoretic injections of horseradish peroxidase were placed at various locations within the dorsal and ventral cingulate areas, the dorsal agranular and ventral granular divisions of the retrosplenial cortex and the presubiculum. Somata of afferent neurons in the thalamus and basal forebrain were identified by retrograde labeling. Each of the anterior thalamic nuclei was found to project to several limbic cortical areas, although not with equal density. The anterior dorsal nucleus projects primarily to the presubiculum and ventral retrosplenial cortex; the anterior ventral nucleus projects to the retrosplenial cortex and the presubiculum with apparently similar densities; and the anterior medial nucleus projects primarily to the cingulate areas. The projections from the lateral dorsal nucleus to these limbic cortical areas are organized in a loose topographic fashion. The projection to the presubiculum originates in the most dorsal portion of the lateral dorsal nucleus. The projection to the ventral retrosplenial cortex originates in rostral and medial portions of the nucleus, whereas afferents to the dorsal retrosplenial cortex originate in caudal portions of the lateral dorsal nucleus. The projection to the cingulate originates in the ventral portion of the lateral dorsal nucleus. Other projections from the thalamus originate in the intralaminar and midline nuclei, including the central lateral, central dorsal, central medial, paracentral, reuniens, and paraventricular nuclei, and the ventral medial and ventral anterior nuclei. In addition, projections to the medial limbic cortex from the basal forebrain originate in cells of the nucleus of the diagonal band. Projections to the presubiculum also originate in the medial septum. These results are discussed in regard to convergence of sensory and nonsensory information projecting to the limbic cortex and the types of visual and other sensory information that may be relayed to the limbic cortex by these projections.

Afferent Pathways↗

PubMed1987

Organization of subcortical pathways for sensory projections to the limbic cortex. II. Afferent projections to the thalamic lateral dorsal nucleus in the rat.

Afferent projections to the thalamic lateral dorsal nucleus were examined in the rat by the use of retrograde axonal transport techniques. Small iontophoretic injections of horseradish peroxidase were placed at various locations within the lateral dorsal nucleus, and the location and morphology of cells of origin of afferent projections were identified by retrograde labeling. For all cases examined, subcortical retrogradely labeled neurons were most prominent in the pretectal complex, the intermediate layers of the superior colliculus, and the ventral lateral geniculate nucleus. Labeled cells were also seen in the thalamic reticular nucleus and the zona incerta. Within the cerebral cortex, labeled cells were prominent in the retrosplenial areas (areas 29b, 29c, and 29d) and the presubiculum. Labeled cells were also seen in areas 17 and 18 of occipital cortex. Peroxidase injections in the dorsal lateral part of the lateral dorsal nucleus result in labeled neurons in all of the ipsilateral pretectal nuclei, but especially those that receive direct retinal afferents. Labeled cells were also seen in the ventral lateral geniculate nucleus and the rostral tip of laminae IV-VI of the superior colliculus. In contrast, peroxidase injections in ventral medial portions of the lateral dorsal nucleus result in fewer labeled pretectal cells, and these labeled cells are found exclusively in the pretectal nuclei that do not receive retinal afferents. Other labeled cells following injections in the rostral and medial portions of the lateral dorsal nucleus are seen contralaterally in the medial pretectal region and nucleus of the posterior commissure, and bilaterally in the rostral tips of laminae IV and V of the superior colliculus. Camera lucida drawings of HRP labeled cells reveal that projecting cells in each pretectal nucleus have a characteristic soma size and dendritic branching pattern. These results are discussed with regard to the type of sensory information that may reach the lateral dorsal nucleus and then be relayed on to the medial limbic cortex.

Afferent Pathways↗

PubMed1987

Ocular signs in Alport's syndrome.

The eyes of sixty one patients with Alport's syndrome or its variant, and of 25 unaffected relatives, were examined. Details of ocular signs associated with Alport's syndrome are presented and related to renal prognosis and family history.

Adolescent↗

PubMed1986

Relationships among sodium current, permeability, and Na activities in control and glucocorticoid-stimulated rabbit descending colon.

Effects of a potent synthetic glucocorticoid, methylprednisolone (MP), on transepithelial Na transport were examined in rabbit descending colon. Current-voltage (I-V) relations of the amiloride-sensitive apical Na entry pathway were measured in colonic tissues of control and MP-treated (40 mg im for 2 days) animals. Tissues were bathed mucosally by solutions of various Na activities, (Na)m, ranging from 6.2 to 75.6 mM, and serosally by a high K solution. These I-V relations conformed to the "constant field" flux equation permitting determination of the permeability of the apical membrane to Na, PmNa, and the intracellular Na activity, (Na)c. The following empirical relations were observed for both control and MP-treated tissues: Na transport increases hyperbolically with increasing (Na)m obeying simple Michaelis-Mentin kinetics; PmNa decreased hyperbolically with increasing (Na)m, but was unrelated to individual variations in (Na)c; (Na)c increased hyperbolically with (Na)m; both spontaneous and steroid-stimulated variations in Na entry rate could be attributed entirely to parallel variations in PmNa at each mucosal Na activity. Comparison of these empirical, kinetic relations between control and MP-treated tissues revealed: maximal Na current and PmNa were greater in MP tissues, but the (Na)m's at which current and PmNa were half-maximal were markedly reduced; (Na)c was significantly increased in MP tissues at each (Na)m while the (Na)m at half-maximal (Na)c was unchanged. These results provide direct evidence that glucocorticoids cause marked stimulation of Na absorption across rabbit colon primarily by increasing the Na permeability of the apical membrane. While the mechanism for the increased permeability remains to be determined, the altered relation between PmNa and (Na)m suggests possible differences in the conformation or environment of the Na channel in MP-treated tissues.

Animals↗

PubMed1986

A comparison of postoperative refractive results with and without intraocular lens power calculation.

Sixty-five patients underwent intracapsular cataract extraction with implantation of Binkhorst iris-clip intraocular lenses (IOLs). For 31 patients the IOL was of a standard power. Thirty-four patients had axial length measurement and keratometry preoperatively, and IOLs calculated to produce emmetropia or 1 dioptre of myopia were implanted. There was no significant difference in the range of postoperative refractive results between the two groups.

Aged↗

PubMed1986

Relations between chord and slope conductances and equivalent electromotive forces.

Nonlinear current-voltage relations for ion movement across biological membranes have been observed and significantly complicate the interpretation of electrical measurements on these transport processes. To enable analysis of the electrical measurements two formalisms have evolved, chord and slope, by which equivalent conductances and electromotive forces (emfs) can be obtained. Because, in the presence of nonlinear relations between current and voltage, the chord conductances and emfs are generally not equal to their slope counterparts, it is imperative that they not be intermixed (8). However, when the functional relationship between the current and voltage is known, such as the Goldman-Hodgkin-Katz (GHK) flux equation, it becomes possible to compare the voltage dependencies of these parameters and examine interrelationships between them. In this communication analytical expressions are derived for the chord and slope conductances and emfs for transport of a single ionic species that obeys the GHK flux equation. Using these expressions, it is possible to convert electrical equivalent circuit parameters derived for one formalism to electrical equivalent parameters of the other formalism. Therefore data obtained using either formalism can be used to obtain values for intracellular activity and membrane permeability to the transported ion. Parallel analyses can be applied to other models of ion transport.

Animals↗

PubMed1986

Activation of electrogenic sodium pump in hippocampal CA1 neurons following glutamate-induced depolarization.

Intracellular recordings were obtained from guinea pig hippocampal CA1 pyramidal neurons maintained in vitro. Focal applications of glutamate produced depolarizations followed by prolonged hyperpolarizations. The mechanisms underlying this postglutamate hyperpolarization (PGH) were investigated. PGH did not reverse polarity with hyperpolarization to potentials at or near the presumed K+ equilibrium potential. A transient increase in conductance was associated with the PGH; control values returned well before the termination of PGH. Application of Mn2+, an antagonist of voltage-dependent calcium conductance, blocked synaptic transmission and the afterhyperpolarization (AHP) that follows a directly evoked train of action potentials but did not diminish the PGH or the transient conductance increase. Intracellular application of the calcium chelator ethyleneglycol-bis(beta-aminoethylether)-N,N'-tetraacetic acid blocked AHP but did not affect PGH. Reductions in temperature from 37 to 27-32 degrees C reduced the amplitude of PGH and prolonged its duration but increased the amplitude and duration of AHP. The transient conductance increase associated with PGH was unaffected. Application of strophanthidin, a specific antagonist of Na+-K+-ATPase, reversibly blocked PGH and led to large increases in the amplitude and duration of the AHP. It is concluded that PGH is produced by activation of the electrogenic sodium pump by glutamate-induced excitation. As such, PGH is a useful physiological assay of electrogenic sodium transport. In addition, maintenance of the Na+ gradient by the sodium pump is important for the buffering of Ca2+ influx.

Animals↗

PubMed1985

Temperature dependence of intrinsic membrane properties and synaptic potentials in hippocampal CA1 neurons in vitro.

The temperature dependence of intrinsic membrane conductances and synaptic potentials in guinea pig hippocampal CA1 pyramidal neurons were examined in vitro as they were cooled from 37 degrees C to between 33 and 27 degrees C. Cooling reversibly increased resting input resistance in a voltage-independent manner (Q10 = 0.58 to 0.75). The amplitude and duration of orthodromically evoked action potentials were increased by cooling (Q10 = 0.87 and 0.52 to 0.53, respectively), whereas the maximum rates of rise and fall were reduced (Q10 = 1.27 to 1.49 and 2.19 to 2.44, respectively). The amplitude and duration of the afterhyperpolarization which follows a directly evoked train of action potentials were substantially increased at low temperatures. It is possible to attribute this increase to an augmentation of Ca2+ influx during the train and also to a slowing of Ca2+ removal from the cytoplasm. Spike frequency adaptation during prolonged depolarizing pulses was enhanced at low temperatures. In addition, there was a decrement in spike amplitude during the train of action potentials. These observations all suggest an increase in Ca2+-activated K+ conductance at low temperature. A late, slow, hyperpolarizing synaptic potential in response to orthodromic stimulation became apparent at low temperature. This potential had an apparent reversal potential more negative than the early inhibitory postsynaptic potential, suggesting that it was mediated by a K+ conductance, possibly activated by Ca2+ influx. We conclude that reductions in temperature of as little as 5 to 10 degrees C from normal can significantly alter the intrinsic and synaptic physiology of hippocampal neurons and should, therefore, be considered an important variable in in vitro brain slice experiments.

Action Potentials↗

PubMed1984

Electrophysiology of Necturus urinary bladder: II. Time-dependent current-voltage relations of the basolateral membranes.

As reported previously (S.R. Thomas et al., J. Membrane Biol. 73:157-175, 1983) the current-voltage (I-V) relations of the Na-entry step across the apical membrane of short-circuited Necturus urinary bladder in the presence of varying mucosal Na concentrations are (i) time-independent between 20-90 msec and (ii) conform to the Goldman-Hodgkin-Katz constant field flux equation for a single cation over a wide range of voltages. In contrast, the I-V relations of the basolateral membrane under these conditions are (i) essentially linear between the steady-state, short-circuited condition and the reversal potential (Es); and (ii) are decidedly time-dependent with Es increasing and the slope conductance, gs, decreasing between 20 and 90 msec after displacing the transepithelial electrical potential difference. Evidence is presented that this time-dependence cannot be attributed entirely to the electrical capacitance of the tissue. The values of gs determined at 20 msec are linear functions of the short-circuit current, Isc, confirming the relations reported previously, which were obtained using a more indirect approach. The values of Es determined at 20 msec are significantly lower than any reasonable estimate of the electromotive force for K across the basolateral membrane, indicating that this barrier possesses a significant conductance to other ions which may exceed that to K. In addition, these values increase linearly with decreasing Isc and approach the value of the electrical potential difference across the basolateral membrane observed when Na entry across the apical membrane is blocked with amiloride or when Na is removed from the mucosal solution. A possible explanation for the time-dependence of Es and gs is offered and the implications of these findings regarding the interpretation of previous microelectrophysiologic studies of epithelia are discussed.

Animals↗

PubMed1984

Dentin permeability. Effects of desensitizing dentifrices in vitro.

Patients using placebo dentifrices in clinical trials usually show a significant decrease in dentin sensitivity over a 2- to 4-week period. If their sensitivity were due to hydrodynamic fluid movement, then the results suggest that there was a decrease in their dentin permeability. This hypothesis was tested in vitro by measuring the ease with which fluid could flow (i.e., hydraulic conductance) across dentin discs before and after brushing the discs with a variety of dentifrices, including most of the marketed densensitizing dentifrices. All dentifrices decreased the hydraulic conductance of dentin. An experimental dentifrice containing oxalate as the active ingredient was far more effective than any of the marketed dentifrices. The results tend to support the hypothesis that, at least part of the reduction in clinical sensitivity in patients with hypersensitive dentin is due to the abrasive action of the dentifrice.

Dentifrices↗

PubMed1984

The effect of Timolol Maleate on tonic accommodation, tonic vergence, and pupil diameter.

The beta-adrenoceptor antagonist Timolol Maleate (0.5%) was employed topically to determine whether the resting (or "tonic") position of accommodation is a consequence of steady-state equilibrium between parasympathetic and sympathetic innervation of the ciliary muscle. Ten subjects were used, eight men and two women, with an age range of 19-37 (mean = 23.2). All subjects wore an optimum refractive correction giving visual acuities of 20/20 or better. Darkroom measurements of tonic accommodation (TA), tonic vergence (TV), and pupil diameter were determined with a Badal laser optometer , a nonius alignment device and infra-red photography, respectively. Far and near points of accommodation and oculo-motor balance tests were determined by standard optometric techniques and intraocular pressure (IOP) was measured by applanation tonometry. Both TA (mean = 1.66 D) and TV (mean = 2.10 deg) assumed intermediate resting positions in the absence of visual stimulation. A double-blind protocol between Timolol and Saline demonstrated a mean myopic shift in TA of +0.85 D over 40 min with Timolol. All other experimental parameters, apart from IOP, were unaffected by Timolol. It is concluded that sympathetic innervation to the ciliary muscle plays a significant role in determining the TA position and that this innervation is mediated by inhibitory beta adrenoceptors.

Accommodation, Ocular↗

PubMed1983

Organization of projections from the superior colliculus to the thalamic lateral posterior nucleus in the rat.

Injections of horseradish peroxidase into the lateral posterior nucleus (LP) of the rat thalamus resulted in retrograde labeling of neurons in the superior colliculus (SC). Approximately 80% of the labeled cells occurred in the stratum opticum and 20% in the stratum griseum superficiale. The system of projections is organized such that medial parts of SC project to dorsal LP and lateral parts of SC project to ventral LP.

Animals↗

PubMed1983

Projections from the pretectal complex to the thalamic lateral dorsal nucleus of the cat.

The subcortical projections to the lateral dorsal nucleus (LD) of the cat thalamus were studied with retrograde transport techniques. Deposits of horseradish peroxidase (HRP) or fluorescent tracers were placed unilaterally in LD of adult cats, using electrophoretic or pressure injection techniques. Following post-injection survival periods of 1, 2 or 3 days, HRP retrogradely labeled cells were identified in sections reacted with benzidine dihydrochloride; fluorescent labeled cells were identified by fluorescent microscopy. Injections in LD result in retrogradely labeled neurons in all nuclei of the pretectal complex, including the nucleus of the optic tract (NTO), the posterior pretectal nucleus (NPP), the anterior pretectal nucleus (NPA), the pretectal olivary nucleus (NOL), and the medial pretectal nucleus (NPM). Small electrophoretic injections of HRP were used to investigate a possible topographic organization of the pretectal projections. Results from a variety of injection sites indicate only a subtle rostral-caudal gradient. That is, small injection sites in rostral LD result in retrograde labeling of neuron somata in the rostral parts of NTO, NPA and NPP, and throughout NPM. Injections in caudal LD result in labeled cells more caudally situated in NTO, NPA, NPP, and throughout NPM. Injections in the pulvinar (Pul) also result in retrogradely labeled cells in the pretectal complex, particularly NTO, NPP, and NOL. Experiments with injections of distinguishable fluorescent tracers in LD and Pul reveal that many more cells project to Pul than to LD. These experiments also reveal that while neurons that project to LD are intermingled with neurons that project to Pul, the two projections originate from separate subpopulations of cells. These results are discussed in regard to phylogenetic comparison of pretectal projections and subcortical pathways of sensory input to the limbic system.

Afferent Pathways↗

PubMed1983

Relation between intracellular sodium and active sodium transport in rabbit colon: current-voltage relations of the apical sodium entry mechanism in the presence of varying luminal sodium concentrations.

The current-voltage relations of the amiloride-sensitive Na entry pathway across the apical membrane of rabbit descending colon, exposed to a high K serosal solution, were determined in the presence of varying mucosal Na activities, (Na)m, ranging from 6.2 to 99.4 mM. These relations could be closely fit to the "constant field" flux equation yielding estimates of the permeability of the apical membrane to Na, PmNa, and the intracellular Na activity, (Na)c. The following empirical relations emerged: (Na)c increased hyperbolically with increasing (Na)m; PmNa decreased hyperbolically with increasing (Na)m and linearly with increasing (Na)c; spontaneous variations in Na entry rate at constant (Na)m could be attributed entirely to parallel, spontaneous variations in PmNa; the rate of Na entry increased hyperbolically with increasing (Na)m obeying simple Michaelis-Menten kinetics; the relation between (Na)c and "pump rate," however, was sharply sigmoidal and could be fit by the Hill equation assuming strong cooperative interactions between Na and multiple sites on the pump; the Hill coefficient was 2-3 and the value of (Na)c at which the pump-rate is half-maximal was 24 mM. The results provide an internally consistent set of relations among Na entry across the apical membrane, the intracellular Na activity and basolateral pump rate that is also consistent with data previously reported for this and other Na-absorbing epithelia.

Animals↗