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J T Hackett

Publications and source records attributed to J T Hackett.

At least 37 records · Page 2Linked to original sources

Organization and development of brain stem auditory nuclei in the chick: ontogeny of postsynaptic responses.

The onset of responsiveness to eighth nerve stimulation was examined in n. magnocellularis and n. laminaris, (second- and third-order neurons) of the chick brainstem auditory system. Extracellular microelectrode mapping techniques were used to examine postsynaptic responses in in vitro brainstem preparations. Two specific questions were addressed. First, what is the earliest time at which postsynaptic action potentials can be evoked in n. magnocellularis and n. laminaris by eighth nerve stimulation? Second, does responsiveness to eighth nerve stimulation develop along a spatial gradient in n. magnocellularis and, if so, how does this gradient compare with other developmental events observed in the chick auditory system? Postsynaptic responses in n. magnocellularis were first recorded at 11 days of incubation. Nucleus laminaris responses to direct stimulation of n. magnocellularis were also first recorded at 11 days, although n. laminaris responses to eight nerve stimulation were not seen until 12 days of incubation. A gradient of response development within n. magnocellularis was indicated by mapping of responsive sites on days 11-13. At 11 days, responses to eighth nerve stimulation were restricted to the most anteromedial portion of n. magnocellularis. Between 11 and 13 days, cells in increasingly more posterolateral portions of n. magnocellularis became responsive. This anteromedial-to-posterolateral gradient in n. magnocellularis is correlated with the basal-to-apical gradient of morphogenesis observed in the basilar papilla and morphogenetic gradients previously observed in n. magnocellularis and n. laminaris.

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Synaptic excitation of the second and third order auditory neurons in the avian brain stem.

Synaptic potentials were examined in the second- and third-order auditory neurons of nucleus magnocellularis and nucleus laminaris in the chick. Brain stems of mature chick embryos were explanted and maintained in vitro for 4 to 8 h. Field potentials, extracellular spike potentials and intracellular potentials evoked by 8th-nerve stimulation were examined. Eighth-nerve stimulation reliability elicited four identifiable field potentials which could be attributed to: (i) the afferent volley of the 8th-nerve axons, (ii) postsynaptic responses of n. magnocellularis neurons, and (iii) ipsilaterally and, (iv) contralaterally-evoked n. laminaris postsynaptic responses. Intracellular-recorded postsynaptic potentials were characterized by a rapid rise time and short duration. They were apparently monosynaptic with a synaptic delay of 0.4 ms. In each n. magnocellularis neuron the 'fast' excitatory postsynaptic potentials were composed of 1 to 3 all-or-none components. 'Slow' excitatory postsynaptic potentials were characterized by a longer latency, a longer duration and graded amplitude variation in proportion to the intensity of 8th-nerve stimulation. Both 'fast' and 'slow' excitatory postsynaptic potentials had similar reversal potentials. Since the 8th nerve makes monosynaptic connection with n. magnocellularis neurons, it is likely that at this synapse the 'fast' excitatory postsynaptic potentials were produced, while the 'slow' potential may be attributable to the convergence of many boutonal synapses of unknown origin. Intracellular injections of horseradish peroxidase into n. magnocellularis revealed that its efferents bifurcate below the nucleus and send one axon to the contralateral n. laminaris while the other axon forms a highly divergent projection to the ipsilateral laminar nucleus. The intracellular records obtained from n. laminaris are consistent with this anatomical finding in that graded excitatory postsynaptic potentials were elicited by 8th-nerve stimulation.

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Does the Mauthner cell conform to the criteria of the command neuron concept?

The relationship between the Mauthner (M) cell action potential of the bullfrog tadpole and the rapid tail-flip was studied with electrophysiological and video-recording techniques. Single action potentials were elicited in the M-cell by vibratory stimulation or electrical stimulation of the eighth cranial nerve. These impulses were followed by a tail-flip to the side contralateral to the M-soma. Similarly, a tail-flip was produced by direct intracellular stimulation of the M-cell. Hyperpolarization of the M-soma blocked orthodromic action potentials and prevented the tail-flip. Therefore, the M-cell action potential appears to be sufficient and necessary to produce a rapid tail-flip which is associated with a naturally observed startle behavior.

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Calcium dependency of excitatory chemical synaptic transmission in the frog cerebellum in vitro.

Chemical synaptic transmission was studied with microelectrode techniques in isolated frog cerebella maintained in vitro. Purkinje cell (PC) EPSPs, elicited by selective monosynaptic electrical stimulation of both the parallel fiber (PF) and climbing fiber (CF) inputs, could be inverted by depolarizing (outward) current injections. Evoked synaptic transmission at both junctions was reduced by lowering the extracellular concentration of calcium ions ([Ca2+]) below 2 mM. Raising [Ca2+] above 2 mM to 8 mM did not further increase synaptic transmission. Mg2+, Sr2+, and Ba2+ did not substitute for Ca2+ in the transmission process.

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Selective antagonism of frog cerebellar synaptic transmission by manganese and cobalt ions.

Parallel fiber-Purkinje cell synaptic transmission of the frog cerebellum can be selectively blocked by Mn2+ and Co2+. The interaction of these cations with Ca2+ indicates that they act, as has been found for other chemical synapses, at the presynaptic terminals where Ca2+ is required for release of neurotransmitters. Climbing fiber-Purkinje cell synaptic transmission was similarly blocked by Mg2+, Mn2+ and Co2+.

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Dose-dependent dual effect of morphine on electrophysiologic correlates of positive reinforcement (reward contingent positive variation: RCPV) in the cat.

In cats trained to press a lever for milk reward, the postreinforcement EEG synchronization (PRS) and the associated epicortical steady potential shift, known as "Reward Contingent Positive Variation (RCPV) restricted to the occipital cortex, were studied prior to and after administration of morphine sulfate. Contrary to what has ordinarily been described as a typical feline response to morphine, such as restlessness, aggressiveness, rage, and exaggerated startle reaction to environmental stimuli, associated with an increased tonus of the brainstem-hypothalamic arousal system and desynchronized EEG patterns, doses of 0.1-0.4 mg/kg, IM, caused a strong monophasic enhancement of the PRS-RCPV phenomenon. Doses of 0.6-1.0 mg/kg, IM, had clearly a biphasic action: the initial enhancement of the PRS-RCPV responses was followed by their strong suppression. Chlorpromazine (0.1-1.6 mg/kg, i.e.) promptly restored the EEG responses. During the peak effect of the enhancing doses of morphine, the reward-related EEG phenomena also occurred prior to or after the nonrewarded bar press when the animals licked the empty cup. This dissociation of the PRS-RCPV from consumption was much more conspicuous in animals whose control frequency of the PRS oscillations was higher, and after morphine showed more significant slowing. Despite the strong facilitation of the PRS-RCPV in the presence of light, morphine, in contrast to LSD-25, was not able to restore the reward-induced phenomena in the dark.

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Calcium: is it required for transmitter secretion?

Ethanol multiplies miniature end-plate potential frequency independently of calcium ion concentrations and also multiplies calcium-dependent depolarization-evoked quantal release, to the same extent. This result implies a final common pathway, requiring little or no calcium, for both kinds of transmitter secretion. Chlorpromazine and hypertonicity act similarly to ethanol, but also depress depolarization-secretion coupling.

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