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B Lancaster

Publications and source records attributed to B Lancaster.

31 records · Page 2Linked to original sources
PubMed1986

Intracellular electrophysiology of CA1 pyramidal neurones in slices of the kainic acid lesioned hippocampus of the rat.

Intracellular recordings were made from hippocampal CA1 pyramidal cells in slices where the CA3/CA4 region had been lesioned using intracerebroventricular kainic acid. In 55% of the cells studied orthodromic excitation evoked bursts of action potentials. This bursting activity was associated with a decrease in or loss of the early phase to the hyperpolarisation which normally follows orthodromically evoked action potentials. The recurrent inhibitory post-synaptic potential produced by antidromic activation of pyramidal cells was also reduced or absent. A late phase to the orthodromic hyperpolarisation was reduced in cells from lesioned slices. However, in normal slices treated with bicuculline this potential showed an apparent increase. The afterhyperpolarisation which follows a short current evoked burst of action potentials was reduced in bursting cells from lesioned slices. In addition, a silent period in the firing pattern produced by long depolarising current pulses was reduced or absent in these cells. These results together with observations made with bicuculline suggest that the bursting activity in lesioned slices is largely due to a loss of inhibition mediated by gamma-aminobutyric acid. It is proposed that the kainic acid-lesioned in vitro hippocampus may be a suitable preparation for studying the electrophysiology of temporal lobe epilepsy.

Adaptation, Physiological↗
PubMed1986

A method for the rapid exchange of solutions bathing excised membrane patches.

In this communication we describe a technique for rapidly exchanging solutions bathing excised membrane patches, and present examples of its implementation using both outside-out and inside-out patches. The ability to make step changes in the concentration of channel-activating ligands (e.g., acetylcholine, calcium) offers a novel and direct means of measuring kinetic processes in the 10-100-ms range. The responses to step ligand concentration changes are well suited to ensemble variance analysis, yielding estimates of the number of channels in a patch, and testing assumptions of channel independence and homogeneity. Kinetic analysis of the pseudomacroscopic currents obtained by averaging large numbers of responses can be compared and correlated with analysis of the microscopic behavior of single channels, using the same membrane patch for both approaches. Practical and theoretical limitations associated with the method are briefly discussed.

Animals↗
PubMed1986

Calcium-dependent current generating the afterhyperpolarization of hippocampal neurons.

A single-electrode voltage-clamp technique was employed on in vitro hippocampal slices to examine the membrane current responsible for the slow afterhyperpolarization (AHP) in CA1 pyramidal cells. This was achieved by using conventional procedures to evoke an AHP in current clamp, followed rapidly by a switch into voltage clamp (hybrid clamp). The AHP current showed a dependence on extracellular K+, which was close to that predicted for a K+ current by the Nernst equation. The AHP current could be blocked by Cd2+ or norepinephrine. Although the AHP current showed a requirement for voltage-dependent Ca2+ entry, the current did not show any clear intrinsic voltage dependence. Once activated, AHP current is not turned off by hyperpolarizing the membrane potential. The effects of norepinephrine, Cd2+, and tetraethylammonium (TEA) were used to identify an AHP current component to the outward current evoked by depolarizing voltage commands from holding potentials that approximate to the resting potential for these cells. The AHP current can contribute significantly to the outward current during the depolarizing command. Upon repolarization it is evident as a slow outward tail current. This slow tail current had the same time constant as AHP currents evoked by hybrid clamp. Fast components to the tail currents were also observed. These were sensitive to Cd2+ and TEA. They probably represent a voltage-sensitive gKCa, sometimes termed C-current. The strong sensitivity to voltage and TEA displayed by the conventionally described gKCa (IC) are properties inconsistent with the AHP. It seems likely that the AHP current (IAHP) represents a Ca2+-activated K+ current separate from IC and that these two currents coexist in the same cell.

Action Potentials↗
PubMed1986

Slow synaptic transmission in frog sympathetic ganglia.

Bullfrog ganglia contain two classes of neurone, B and C cells, which receive different inputs and exhibit different slow synaptic potentials. B cells, to which most effort has been directed, possess slow and late slow EPSPs. The sEPSP reflects a muscarinic action of acetylcholine released from boutons on B cells, whereas the late sEPSP is caused by a peptide (similar to teleost LHRH) released from boutons on C cells. During either sEPSP there is a selective reduction in two slow potassium conductances, designated 'M' and 'AHP'. The M conductance is voltage dependent and the AHP conductance is calcium dependent. Normally they act synergistically to prevent repetitive firing of action potentials during maintained stimuli. Computer stimulation of the interactions of these conductances with the other five voltage-dependent conductances present in the membrane allows a complete reconstruction of the effects of slow synaptic transmission on electrical behaviour.

Animals↗
PubMed1985

Two distinct Ca-dependent K currents in bullfrog sympathetic ganglion cells.

Healthy bullfrog sympathetic ganglion cells often show a two-component afterhyperpolarization (AHP). Both components can be reduced or abolished by adding Ca-channel blockers or by removing external Ca. Application of a single electrode "hybrid clamp"--i.e., switching from current- to voltage-clamp at the peak of the AHP, reveals that the slow AHP component is generated by a small, slow, monotonically decaying outward current, which we call IAHP. IAHP is blocked by Ca-removal or by apamin and is a pure K current. It is slightly sensitive to muscarine and to tetraethylammonium ion but is much less so than muscarine-sensitive (IM) and fast Ca-dependent (IC) K currents. It also can be recorded in dual-electrode voltage-clamp experiments, where it is seen as a slow, small component of the outward tail current that follows brief depolarizations to 0 mV or beyond. IC is seen as an early, fast, large component of the same tail current. Both components are blocked by Ca removal, but only the IC component is blocked by low doses of tetraethylammonium ion. Thus, bullfrog ganglion cells exhibit two quite distinct Ca-dependent K currents, which differ in size, voltage-sensitivity, kinetics, and pharmacology. These two currents also play quite separate roles in shaping the action potential.

Action Potentials↗
PubMed1984

Chronic failure of inhibition of the CA1 area of the hippocampus following kainic acid lesions of the CA3/4 area.

The chronic effects of the lesioning agent, kainic acid, on paired pulse inhibition in the CA1 area were investigated in the hippocampus both in vivo and in vitro. Pretreatment of animals with a unilateral intracerebroventricular (i.c.v.) injection of kainic acid resulted in a lesion of the CA3/4 area of the hippocampus ipsilateral to the injection site. On activating the surviving Schaffer collateral afferents in the contralateral hippocampus, normal paired-pulse inhibition of the extracellularly recorded population spike in CA1 was observed. On activating the surviving commissural afferents to the CA1 area ipsilateral to the lesion, no such inhibition could be observed. However, paired-pulse inhibition was recorded in the dentate gyrus ipsilateral to the lesion in response to stimulation of the perforant path. The chronic failure of inhibition following the unilateral i.c.v. injection of kainic acid further supports the use of this method to provide a chronic model in the rat for the study of epileptogenesis in the hippocampus.

Animals↗
PubMed1984

In vivo and in vitro studies on putative interneurones in the rat hippocampus: possible mediators of feed-forward inhibition.

Extracellular and intracellular recordings have been made from non-pyramidal neurones in the rat hippocampus in vivo and in vitro. These cells were situated in the stratum pyramidale but were orthodromically activated with a lower threshold than pyramidal neurones in response to stimulation of the Schaffer collateral/commissural afferents. Cells fired earlier than pyramidal neurones in response to suprathreshold stimulation and, in contrast to pyramidal cells, often fired a burst of action potentials. The non-pyramidal neurones also appeared to be orthodromically activated on stimulating the alveus and fired later than antidromically activated pyramidal cells. A very short action potential duration and the ability to fire at high frequencies in response to long depolarizing current pulses also distinguished these neurons from pyramidal cells. It is suggested that these non-pyramidal cells are interneurones which could mediate an early feed-forward activity onto pyramidal cells such as feed-forward inhibition. They may also be recurrently activated and hence could conceivably mediate a recurrent inhibition.

Action Potentials↗
PubMed1984

The synaptically evoked late hyperpolarisation in hippocampal CA1 pyramidal cells is resistant to intracellular EGTA.

It has been suggested that the late hyperpolarisation following synaptic activation of hippocampal CA1 pyramidal neurons is activated by calcium influx. This hypothesis was examined using microelectrodes containing EGTA. Intracellular injection of EGTA blocked the afterhyperpolarisation which normally followed cell firing produced by injection of a depolarising current or the ionophoresis of glutamate onto the apical dendrites. In contrast, the hyperpolarisation following synaptic activation was resistant to EGTA. The results suggest that this potential is not dependent on intracellular Ca2+. Other possible mechanisms are discussed.

Animals↗
PubMed1983

Long-term potentiation in Schaffer collateral and commissural systems of the hippocampus: in vitro study in rats pretreated with kainic acid.

Experiments were carried out on hippocampal slices from rats pretreated with a unilateral intraventricular injection of kainic acid. The kainic acid produced a lesion of the CA3 area in the hippocampus ipsilateral to the site of injection. The resulting neuroanatomically modified hippocampal slices allowed the independent study of the Schaffer collateral and commissural afferents that synapse onto CA1 pyramidal cells. The Schaffer collateral and commissural afferents were both found to independently support long-term potentiation (LTP), and the properties of the LTP were similar to those observed in slices cut from unlesioned hippocampi.

Afferent Pathways↗
PubMed1983

Long-term potentiation in commissural and Schaffer projections to hippocampal CA1 cells: an in vivo study in the rat.

Rats were given unilateral injections of kainic acid into the lateral ventricle to produce a unilateral lesion of CA3 pyramidal cells in the hippocampus. This procedure allowed the commissural and associational Schaffer projections of the surviving contralateral CA3 field to be studied separately for their ability to sustain long-term potentiation (l.t.p.) of synaptic efficacy. Both Schaffer and commissural projections showed l.t.p. of the population excitatory post-synaptic potential (e.p.s.p.) and the population spike. No significant difference was seen in the degree or duration of l.t.p. sustained by the two projections.

Afferent Pathways↗