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J W Jacklet

Publications and source records attributed to J W Jacklet.

At least 19 recordsLinked to original sources
PubMed1989

An antibody to the Drosophila period protein recognizes circadian pacemaker neurons in Aplysia and Bulla.

The molecular mechanisms of the pacemakers underlying circadian rhythms are not well understood. One molecule that presumably functions in the circadian clock of Drosophila is the product of the period (per) gene, which dramatically affects biological rhythms when mutated. An antibody specific for the per protein labels putative circadian pacemaker neurons and fibers in eyes of two marine gastropods, Aplysia and Bulla. As was found for the Drosophila per protein, there is a daily rhythm in the levels of the per-like antigen in Aplysia eyes. Thus, certain molecular features of the per protein, as well as aspects of the temporal regulation of its expression, may be conserved in circadian pacemakers of widely divergent species.

Animals↗
PubMed1987

FMRF-amide-like immunoreactive efferent fibers and FMRF-amide suppression of pacemaker neurons in eyes of Bulla.

The eyes of certain marine gastropods including Aplysia and Bulla, contain circadian pacemakers, which produce a circadian rhythm of autogenous compound action potential (CAP) activity. The CAPs are generated by the synchronous spike discharge of a distinctive population of retinal pacemaker neurons whose axons convey the CAP activity to the CNS. When CAP activity is recorded from a preparation with eyes attached to the CNS, the CAP activity is modulated by efferent activity. In this study we have identified FMRF-amide-like immunoreactive efferent axons in the optic nerves of Bulla. These axons arborize in the basal retinal neuropil adjacent to the pacemaker neurons and are in a position to make synaptic contacts with their dendrites. Similar immunoreactive fibers are not observed in Aplysia eyes. Exogenous FMRF-amide at micromolar concentrations suppresses ongoing CAP activity in isolated eyes but does not suppress the ERG or phase shift the circadian rhythm of CAP activity. Intracellular recordings from the retinal pacemaker neurons reveal that FMRF-amide hyperpolarizes the membrane potential, suppresses spike discharge, and decreases the input resistance, suggesting that a K conductance is increased. Electrical stimulation of the region of the cerebral ganglion that contains FMRF-amide immunoreactive neurons suppresses ongoing CAP activity. All these results are consistent with the idea that the FMRF-amide immunoreactive central neurons and their axons provide a pathway for efferent modulation of the CAP rhythm generated by the retinal pacemaker neurons.

Animals↗
PubMed1987

Serotonin induced protein phosphorylation in the Aplysia eye.

Serotonin (5-HT) increases the phosphorylation of two low molecular weight phosphoproteins of 23,000 and 15,000 daltons molecular weight and decreases the phosphorylation of a 20,000 dalton phosphoprotein in the isolated Aplysia eye. The cAMP analog 8-benzylthio cAMP increases and decreases the phosphorylation of the 23,000 and 20,000 dalton 5-HT sensitive phosphoproteins, respectively. The effect of 5-HT on protein phosphorylation is not affected by the phase of the circadian rhythm of spontaneous compound action potentials generated in the eye.

Animals↗
PubMed1986

The exponent of the calcium power function is reduced during steady-state facilitation in neuron R15 of Aplysia.

Stimulation of the right pleurovisceral connective at frequencies greater than 0.2 Hz produces a steady-state facilitation of the Input 1 excitatory postsynaptic potential (EPSP) in neuron R15 of Aplysia. The magnitude of facilitation is reduced by increases in the concentration of extracellular calcium. Unfacilitated EPSPs (EPSP1) exhibited a power function dependence on the concentration of extracellular calcium with an exponent (XEPSP1) of approximately 3. The exponent for facilitated release (XEPSPss) was examined by comparing steady-state EPSP amplitudes obtained in different static concentrations of calcium (Method A), or by changing the calcium concentration during continuous stimulation and determining changes in steady state EPSP amplitudes (Method B). Method A failed to reveal any dependence of XEPSPss on stimulation frequency, while Method B revealed frequency-dependent changes in XEPSPss consistent with the hypothesis that presynaptic calcium accumulation is at least partly responsible for steady-state facilitation. At a stimulation frequency of 0.5 Hz, the XEPSPss value was significantly reduced to 2/3 of the XEPSP1 value.

Animals↗
PubMed1986

Involvement of protein synthesis in circadian clock of Aplysia eye.

The effects of the protein synthesis inhibitors anisomycin and puromycin were measured on protein synthesis and phase shifting of the circadian rhythm in the isolated Aplysia eye. Anisomycin pulses induce phase delays proportional in magnitude to the duration and percentage of protein synthesis inhibition. The phase-response curve to anisomycin pulses consisted of delays induced throughout the subjective night. Delays were maximal between circadian times (CT) 18 and CT 2; pulses initiated between CT 2 and CT 12 did not phase shift. Puromycin induced phase delays and advances. Delays were proportional to the duration and percentage of protein synthesis inhibition, occurring with increasing magnitude throughout the subjective night (CT 12-2). Peptidyl-puromycin formation may contribute to the magnitude of the delay. Advances, occurring between CT 2 and CT 8, required a greater drug concentration and pulse duration than delays and appeared to result from an effect other than protein synthesis inhibition. Our results support the hypothesis of a phase-dependent requirement for protein synthesis during the subjective night in this circadian clock.

Action Potentials↗
PubMed1985

Serotonin decreases a background current and increases calcium and calcium-activated current in pedal neurons of Hermissenda.

The effects of serotonin (5-HT) on membrane potential, membrane resistance, and select ionic currents were examined in large pedal neurons (LP1, LP3) of the mollusk Hermissenda. Calcium (Ca) action potentials were evoked in sodium-free artificial seawater containing tetramethylammonium, tetraethylammonium, and 4-aminopyridine (0-Na, 4-AP, TEA ASW). They failed at stimulation rates greater than 0.5/sec and were blocked by cadmium (Cd). Under voltage clamp the calcium current (ICa) responsible for them also failed with repeated stimulation. Thus, ICa inactivation accounts for refractoriness of the Ca action potential. The addition of 10 microM 5-HT to 0-Na, 4-AP, TEA ASW produced a slight depolarization and increased excitability and input resistance. Under voltage clamp the background current decreased. The voltage-dependent inward, late outward, and outward tail currents, sensitive to Cd, increased. ICa inactivation persisted. Under voltage clamp with Ca influx blocked by Cd, the addition of 10 microM 5-HT decreased the remaining current uniformly over membrane potentials of -10 to -100 mV. Thus, 5-HT reduces a background current that is active within the physiological range of the membrane potential, voltage insensitive, independent of Ca influx, noninactivating, and not blocked by 4-AP or TEA.

Action Potentials↗
PubMed1985

The circadian pacemaker in the Aplysia eye sends axons throughout the central nervous system.

Each eye of Aplysia contains a population of electrically coupled pacemaker neurons whose synchronous activity can be recorded from the optic nerve as a compound action potential (CAP). The CAP frequency continues to show a circadian rhythm even when the eye is isolated from the animal and maintained in constant conditions, and thus it contains an autonomous circadian pacemaker, which may reside in the pacemaker neurons. The pacemaker neurons, along with retinal photoreceptors, send axons out of the optic nerve, which connects to the cerebral ganglion of the central nervous system (CNS). Pacemaker neurons, but not photoreceptors, may contain an aminergic transmitter, possibly dopamine (DA). We describe the central projections of optic nerve fibers using horseradish peroxidase filling of the cut optic nerve, and transport of radiolabeled macromolecules after selective exposure of the eye to [3H] leucine, which labels both pacemaker neurons and photoreceptors. We were able to determine the projections of pacemaker axons by exposing the eye to [3H]-3,4-dihydroxyphenylalanine [( 3H] DOPA and [3H]DA, which is preferentially taken up and transported by the pacemaker neurons. Pacemaker axons project bilaterally to the cerebral, pedal, and pleural ganglia and may extend as far as the abdominal ganglion. We corroborate this anatomical evidence by recording an orthodromic CAP in the optic nerve that had originated in the eye and subsequently recording the CAP in the CNS connectives and nerves that contained [3H]DOPA-labeled fibers. These results suggest that circadian pacemaker information from the eye is widely distributed throughout the CNS, including neural structures known from studies by others to mediate circadian-regulated behaviors, such as locomotion. Thus, Aplysia can now be used as a model system to examine the influence of the central projections of an identified circadian pacemaker on behavior, such as locomotion, at the level of identified central neurons.

Afferent Pathways↗
PubMed1977

Neuronal circadian rhythm: phase shifting by a protein synthesis inhibitor.

A potent inhibitor of protein synthesis, anisomycin, was applied (10(-6)M) in 6-hour pulses at specific phases in the circadian rhythm of endogenous compound action potential (CAP) activity recorded from the eye of Aplysia in vitro. The phase of the circadian rhythm was systematically advanced or delayed (up to 15 hours) depending on the specific phase at which the pulse was applied. The resultant phase response curve implicates protein synthesis on the eukaryotic ribosome as a fundamental part of the controlling processes that constitutes the circadian clock.

Action Potentials↗
PubMed1977

Facilitation at neuromuscular junctions: contribution to habituation and dishabituation of the Aplysia gill withdrawal reflex.

The gill withdrawal reflex of Aplysia has been used as a model for studying the neuronal mechanisms of habituation, a behavioral plasticity. We have assessed the contribution of neuromuscular facilitation, an elementary synaptic plasticity, during habituation of the reflex by recording gill muscle potentials, which we show are caused by excitatory junctional potentials. These potentials show systematic frequency-dependent changes in amplitude. The gill withdrawal evoked by central motor neuron firing during each habituation trial is determined by facilitation of the excitatory junctional potentials during the trial and the facilitated state of the initial excitatory junctional potential in a trial, determined by neuron activity prior to the trial. The neuromuscular junctions, therefore, act like a frequency-dependent amplifier of central motor activity. They are fully responsive to the dynamic changes of motor neuron firing that occurs during habituation and especially after dishabituation.

Action Potentials↗
PubMed1976

Habituation of reflexes in Aplysia: contribution of the peripheral and central nervous systems.

We studied the contribution of the Aplysia peripheral nervous system, in the siphon and gill, to habituation of the gill withdrawal reflex. After removal of one central ganglion, the parietovisceral, repeated stimulation of the siphon caused habituation of the reflex as it had with the ganglion intact, showing that there is a peripheral pathway between the siphon and gill with competence to mediate habituation. Repeated electrical stimulation of two efferent nerves to the gill, after removal of the parietovisceral ganglion, resulted in habituation of withdrawal movements, which shows that the terminals of the ganglion neurons in the gill are a site of habituation. Also, stimulation of one nerve dishabituates the withdrawal movements elicited by the other. These identify two sites of habituation in the gill in addition to sites in the parietovisceral ganglion.

Animals↗
PubMed1976

Localization of catecholamines in the eyes and other tissues of Aplysia.

A green fluorescence indicative of catecholamines (CA) was localized in the secondary cells (nonreceptor neurons), neuropile and optic nerve of the eye and other tissues in Aplysia by using the formaldehyde-induced fluorescence method for the demonstration of biogenic amines. The specificity of the induced fluorescence was confirmed by its absence in tissue not exposed to formaldehyde vapor, relatively rapid decay upon exposure to UV light and its chemical reduction by sodium borohydride. The fluorescence was greatly reduced in eyes treated with reserpine (depletes serotonin and catecholamines). Furhter confirmation that the green fluorescence in the eye was due to a CA and not to serotonin was obtained by showing that it was decreased or eliminated by alpha-methyl-para-tyrosine (an inhibitor of catecholamine synthesis), increased by incubation in dopamine and exhibited a peak emission (470 nm) characteristic of CA fluroescence. CA fluorescence was also observed in the neuropiles of the cerebral, pedal, pleural and parieto-visceral ganglia and in cells in the pedal ganglion, statocyst, mantle, anterior tentacles and siphon. The finding of CA in secondary neurons of the eye was unusual since CA-containing cells have not been observed in other gastropod eyes. The distribution of CA in Aplysia, in tissue other than the eye, is similar to that of other gastropod molluscs.

Animals↗
PubMed1972

Habituation and dishabituation: interactions between peripheral and central nervous systems in Aplysia.

The withdrawal response of the isolated siphon of Aplysia habituates to a light stimulus and dishabituates to a tactile stimulus, and vice versa, with or without connections to the central nervous system. The peripheral nervous system can dishabituate or enhance the response mediated by the central nervous system and vice versa. Normally the adaptive siphon withdrawal response of the intact animal must be mediated by the integrated activity of the peripheral and central nervous systems.

Action Potentials↗