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K R Delaney

Publications and source records attributed to K R Delaney.

36 records · Page 2Linked to original sources
PubMed1994

Ca2+ accumulations in dendrites of neocortical pyramidal neurons: an apical band and evidence for two functional compartments.

Apical dendrites constitute a prominent feature of the microcircuitry in the neocortex, yet their function is poorly understood. Using fura-2 imaging of layer 5 pyramidal neurons from slices of rat somatosensory cortex, we have investigated the Ca2+ influx into dendrites under intracellular, antidromic, synaptic, and receptor-agonist stimulation. We find three spatial patterns of Ca2+ accumulations: an apical band in the apical dendrite approximately 500 microns from the soma, an accumulation restricted to the basal dendrites, soma, and proximal apical dendrite, and a combination of both of these. We show that the apical band can be activated antidromically and synaptically and that, under blocked Na+ and K+ conductances, it generates Ca2+ spikes. Thus, the apical band may serve as a dendritic trigger zone for regenerative Ca2+ spikes or as a current amplifier for distal synaptic events. Our results suggest that the distal apical dendrite should be considered a separate functional compartment from the rest of the cell.

Animals↗
PubMed1994

Dynamics of propagating waves in the olfactory network of a terrestrial mollusk: an electrical and optical study.

1. The procerebral (PC) lobe of the terrestrial mollusk Limax maximus contains a highly interconnected network of local olfactory interneurons that receives ipsilateral axonal projections from superior and inferior noses. This network exhibits an approximately 0.7-Hz intrinsic oscillation in its local field potential (LFP). 2. Intracellular recordings show that the lobe contains at least two classes of neurons with activity phase locked to the oscillation. Neurons in one class produce periodic bursts of spikes, followed by a period of hyperpolarization and subsequently a depolarizing afterpotential. There is a small but significant chance for a second burst to occur during the depolarizing afterpotential; this leads to a double event in the LFP. Bursting neurons constitute approximately 10% of the neurons in the lobe. 3. Neurons in the other class fire infrequently and do not produce periodic bursts of action potentials. However, they receive strong, periodic inhibitory input during every event in the LFP. These nonbursting cells constitute the major fraction of neurons in the lobe. There is a clear correlation between the periodic burst of action potentials in the bursting neurons and the hyperpolarization seen in nonbursting neurons. 4. Optical techniques are used to image the spatially averaged transmembrane potentials in preparations stained with voltage-sensitive dyes. The results of simultaneous optical and electrical measurements show that the major part of the optical signal can be interpreted as a superposition of the intracellular signals arising from the bursting and nonbursting neurons. 5. Successive images of the entire PC lobe show waves of electrical activity that span the width of the lobe and travel its full length along a longitudinal axis. The direction of propagation in the unperturbed lobe is always from the distal to the proximal end. The wavelength varies between preparations but is on the order of the length of the preparation. 6. One-dimensional images along the longitudinal axis of the lobe are used to construct a space-time map of the optical activity, from which we calculate the absolute contribution of bursting and nonbursting neurons to the optical signal. The contribution of the intracellular signals from the two cell types appears to vary systematically across the lobe; bursting cells dominate at middle and proximal locations, and nonbursting cells dominate at distal locations. 7. The direction and form of the waves can be perturbed either by microsurgical manipulation of the preparation or by chemical modulation of its synaptic and neuronal properties.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

A quantitative measurement of the dependence of short-term synaptic enhancement on presynaptic residual calcium.

We simultaneously measured presynaptic free calcium ion concentration ([Ca2+]i) and synaptic strength at the crayfish claw opener neuromuscular junction (nmj) under a variety of experimental conditions. Our experiments were designed both to test the hypothesis that elevated [Ca2+]i is necessary and sufficient for the induction of a form of synaptic enhancement that persists for several seconds after tetanic stimulation--augmentation--and to determine the quantitative relationship between elevated [Ca2+]i and this enhancement. Action potential trains increased [Ca2+]i and enhanced transmission. During the decay phase of synaptic enhancement known as augmentation (time constant of decay approximately 7 sec at 20 degrees C with < 200 microM fura-2 in terminals), [Ca2+]i was elevated 700 nM or less above rest and an essentially linear relationship between [Ca2+]i and enhancement was observed. Introduction of exogenous Ca2+ buffers into the presynaptic terminal slowed the buildup and recovery kinetics of both [Ca2+]i and the component of synaptic enhancement corresponding to augmentation. The slope of the relationship relating delta [Ca2+]i to augmentation was not changed. The time course of augmentation and recovery of [Ca2+]i remained correlated as the temperature of the preparation was changed from about 10 degrees C to 20 degrees C, but the quantitative relationship of enhancement to [Ca2+]i was increased more than two- to threefold. During moderate frequency trains of action potentials, a slowly developing component of the total synaptic enhancement was approximately linearly related to residual [Ca2+]i measured with fura-2. The quantitative relationship between [Ca2+]i and this component of synaptic enhancement during trains was the same as that during synaptic augmentation after trains.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1994

The role of presynaptic calcium in short-term enhancement at the hippocampal mossy fiber synapse.

The mossy fiber synapse between dentate granule cells and CA3 pyramidal cells in the guinea pig hippocampus shows a robust short-term synaptic enhancement. We have simultaneously measured presynaptic residual free calcium ([Ca2+]i) and postsynaptic field potentials at this synapse to examine the role of [Ca2+]i in this enhancement. Single action potentials produced an increase in [Ca2+]i of 10-50 nM that decayed to resting levels with a time constant of about 1 sec. Trains of action potentials produced larger [Ca2+]i increases that returned more slowly to resting levels. Following the onset of moderate frequency stimulus trains (0.1-5 Hz), synaptic transmission and [Ca2+]i both increased and eventually plateaued. During the steady-state phase a linear relationship between [Ca2+]i and synaptic enhancement was observed. During the initial buildup, however, [Ca2+]i rose more rapidly than synaptic enhancement. Similarly, during the decay phase immediately following termination of a stimulus train, [Ca2+]i returned to prestimulus levels faster than synaptic enhancement. High concentrations of the calcium buffer EGTA in the presynaptic terminal slowed the buildup and decay of both [Ca2+]i and synaptic enhancement produced by stimulus trains. Under these conditions, the time course of [Ca2+]i and synaptic enhancement were well matched. This suggests that, despite the differences in kinetic rates observed for normal buffering conditions, increases in [Ca2+]i play a causal role in short-term enhancement. An increase in [Ca2+]i of 10-30 nM produced a twofold enhancement. We propose a simple kinetic model to explain these results. The model assumes that synaptic enhancement is controlled by a Ca-dependent first-order reaction. According to this scheme, a change in [Ca2+]i alters neurotransmitter release, but the slow kinetics of the underlying reaction introduces a temporal filter, producing a delay in the change in synaptic enhancement.

Animals↗
PubMed1991

Presynaptic calcium in transmitter release and posttetanic potentiation.

This review gives some indication of the progress that has been made in understanding synaptic transmission by use of new methods for measuring and controlling presynaptic [Ca2+]i. Many unsolved problems remain. We still do not have a clear idea of the exact relationship between [Ca2+]i and transmitter release and whether this relationship is the same under all circumstances. The apparently different [Ca2+]i-dependence of evoked transmitter release and of PTP suggest multiple molecular sites of calcium action that remain to be identified. A complete and comprehensive model of transmitter release has yet to be devised, and questions raised by our experiments may indicate that it is still too early to try to construct a precise model. We also do not know just how serotonin acts to modulate transmitter release, only that it does not appear to alter either resting or entering calcium. Some of these questions may be approachable with the techniques described here; others are not and require different methods for their resolution. The work continues.

Action Potentials↗
PubMed1990

Calcium released by photolysis of DM-nitrophen stimulates transmitter release at squid giant synapse.

1. Transmitter release at the squid giant synapse was stimulated by photolytic release of Ca2+ from the 'caged' Ca2+ compound DM-nitrophen (Kaplan & Ellis-Davies, 1988) inserted into presynaptic terminals. 2. Competing binding reactions cause the amount of Ca2+ released by DM-nitrophen photolysis to depend on the concentrations of DM-nitrophen, total Ca2+, Mg+, ATP and native cytoplasmic Ca2+ buffer. Measurements of presynaptic [Ca2+] changes by co-injection of the fluorescent indicator dye Fura-2 show that DM-nitrophen photolysis causes a transient rise in Ca2+ followed by decay within about 150 ms to an increased steady-state level. 3. Rapid photolysis of Ca2(+)-loaded nitrophen within the presynaptic terminal was followed in less than a millisecond by depolarization of the postsynaptic membrane. As with action potential-evoked excitatory postsynaptic potentials (EPSPs), the light-evoked response was partially and reversibly blocked by 1-3 mM-kainic acid which desensitizes postsynaptic glutamate receptors. 4. Release was similar in magnitude and rate to normal action potential-mediated EPSPs. 5. The release of transmitter by photolysis of Ca2(+)-loaded DM-nitrophen was not affected by removal of Ca2+ from the saline or addition of tetrodotoxin. Photolysis of DM-nitrophen injected into presynaptic terminals without added Ca2+ did not stimulate release of transmitter nor did it interfere with normal action potential-mediated release. 6. Stimulation of presynaptic action potentials in Ca2(+)-free saline during the light-evoked response did not elicit increased release of transmitter if the ganglion was bathed in Ca2(+)-free saline, i.e. in the absence of Ca2+ influx. Increasing the intensity of the light or stimulating presynaptic action potentials in Ca2(+)-containing saline increased the release of transmitter. Therefore the failure of presynaptic voltage change to increase transmitter release resulting from release of caged Ca2+ was not due to saturation or inhibition of the release mechanism by light-released Ca2+. 7. Decreasing the temperature of the preparation increased the delay to onset of the light-evoked response and reduced its amplitude and rate of rise to an extent similar to that observed for action potential-evoked EPSPs.

Acetates↗
PubMed1989

Calcium in motor nerve terminals associated with posttetanic potentiation.

We have used fura-2 fluorescence to study the effects of repetitive stimulation producing posttetanic potentiation (PTP) at crayfish neuromuscular junctions on presynaptic calcium concentration. Fura-2 was injected into the preterminal axon of the excitor motor neuron to the claw opener muscle of a walking leg. Pictures of presynaptic terminals on the muscle surface were obtained with a charge-coupled device camera, ratioed, and converted to spatial images of intracellular calcium concentration. Stimulation of the motor nerve for 7-10 min at 20-33 Hz produced potentiation during the tetanus and PTP following the tetanus. Presynaptic calcium levels in terminal boutons and varicosities rose to about 2 microM during the tetanus and decayed at first rapidly and then slowly back to levels near the initial concentration of about 200 nM. The decay rate of potentiated synaptic transmission was the same as the decay rate of the elevated calcium concentration during the posttetanic period dominated by PTP, when facilitation and augmentation had dissipated. A 13-fold potentiation corresponded to a 500 nM elevation of calcium to about 700 nM. The linear dependence we observed is not consistent with the power law formulation of a residual calcium hypothesis for PTP. During the tetanus, the enhancement of synaptic transmission due to facilitation, augmentation, and potentiation exceeded that expected from the correspondence between PTP and posttetanic calcium levels. This may occur because during the tetanus there is insufficient time for calcium to equilibrate spatially between action potentials, and the submembrane calcium will be higher than the volume-average calcium levels that we detect. Following low-frequency trains (typically 8 Hz for about 35 sec), enhanced synaptic transmission and elevated presynaptic calcium decayed rapidly, within a few seconds. Short high-frequency trains (50-100 Hz for 1-2 min) elicited an additional hours-long elevation of presynaptic calcium, corresponding to, and perhaps responsible for, part of the long-term potentiation of transmission that such stimulation produces at this synapse.

Animals↗
PubMedDate not supplied

Milieu therapy: a therapeutic loophole.

TOPIC: The confusion over, and ultimate demise of, milieu therapy. SOURCE: Literature review. GOAL: To chronicle the conceptual problems and other events leading to the decline in the use of milieu therapy. CONCLUSION: Inpatient nurses would do best to leave the concept of milieu therapy behind and focus on clarifying how specific nursing interventions are operationalized and tied to patient outcomes.

Humans↗
PubMedDate not supplied

Nursing in child psychiatric milieus: Part I: What nurses do.

Because of the reduced length of inpatient hospitalization and the increasing emphasis on biopsychiatric treatments, milieu psychiatry is in decline. However, certain aspects of the therapeutic milieu are essential to the operation of child inpatient units. Children with acute psychiatric illness need a safe, structured, and supportive environment. Nurses are the professional group responsible for instituting and maintaining this type of environment, yet their specific functions are vaguely stated and often intuitively derived. A useful way to delineate and describe what nurses do is to organize nursing behaviors into five therapeutic processes: (a) safety, (b) structure, (c) support, (d) involvement, and (e) validation. By delineating essential milieu dimensions in this way, the form and purpose of nursing interventions are clarified.

Child↗
PubMedDate not supplied

Nursing in child psychiatric milieus: Part II: Mapping conceptual footholds.

In the first part of this paper, child inpatient nursing practice was organized into five therapeutic processes (safety, structure, support, involvement and validation). Using this organization of nursing care, three specific practice question are now addressed. One, how will nursing blend their traditional psychosocial orientation with biological psychiatry? Two, how might nurses best respond to the pressure to reduce the length of hospitalization yet still effectively intervene with troubled children? Three, does the traditional milieu therapy model have clinical utility for child inpatient nurses in the 1990's. It is suggested that nursing practice is best supported by multiple midrange theories which clarify children's behavior and give theoretical support to specific nursing interventions.

Biological Psychiatry↗
PubMedDate not supplied

Calming an escalated psychiatric milieu.

On inpatient psychiatric units, nurses control the tone, pace, and activity level of the environment. But under the influence of factors such as high patient acuity and negative group contagion, a milieu can become unacceptably loud and chaotic. A volatile milieu is a potentially dangerous environment because patients' anxiety and agitation can quickly lead to acting out and aggression. This article focuses on how nurses can regain control of a milieu spiralling into chaos by tightening the structure of the routine, anticipating potential problems, and maintaining a confident calm manner. The charge nurse orchestrates the staff group's response to escalation through detailed planning, decisive interventions, and strategic use of every available resource.

Child↗
PubMedDate not supplied

Parents' perceptions of their child's emotional illness and psychiatric treatment needs.

PROBLEM: The purpose of this study was to describe how parents define their child's emotional illness and psychiatric treatment needs. SUBJECTS: The sample consisted of 19 parents and one grandparent (N = 20) who had recently admitted their child to a short-term psychiatric unit. METHODS: Qualitative methods, utilizing a semistructured interview. Data were analyzed using the constant comparative method. Substantive codes were combined to derive the key concepts and themes in the interviews. FINDINGS: The findings of this study center on themes related to parents' efforts to control the current behavioral crisis, treatment acceptability, family needs, explanatory formulations, and securing the child's future. CONCLUSIONS: Implications for treatment include how nurses might tap into parents' perceptions to facilitate parent' professional communication.

Adolescent↗
PubMedDate not supplied

Developing a restraint-reduction program for child/adolescent inpatient treatment.

TOPIC: Meeting mandated guidelines to reduce, if not eliminate, the use of restraints with children and adolescents hospitalized on inpatient psychiatric units. PURPOSE: To present eight promising options for restraint reduction with inpatient children and adolescents, and the research that supports their efficacy. SOURCES: Review of the literature. CONCLUSION: By combining what is known about child/adolescent restraint use with restraint-reduction research in the adult field, several options for restraint reduction can be derived.

Adolescent↗
PubMedDate not supplied

Putting the unit to bed.

Bedtime on children's inpatient units taxes a staff's patience and energy. Many children are pressing their needs with great urgency. Unfortunately, by late evening staff members are frequently depleted and not emotionally available to the children. Inpatient nurses can address this situation by developing bedtime programs that focus on the particular nighttime needs of disturbed children. The Author details such a bedtime program and describes why it has been successful in helping patients get undisturbed sleep.

Child↗