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M V Bennett

Publications and source records attributed to M V Bennett.

At least 163 records · Page 9Linked to original sources
PubMed1976

Altered calcium conductance in pawns, behavioural mutants of Paramecium aurelia.

Pawns are behavioural mutants (in one of three genes) of Paramecium aurelia that have lost, to varying degrees, the reversal response which is thought to depend on the calcium influx during excitation. This report shows that all of the single and double mutants have reduced active inward (calcium) current, the reduction correlating with the degree of behavioural deficit. All of the mutants display normal resting potential, input impedance and delayed rectification. Mutants in genes pwA and pwC show normal anomalous rectification, but pwB mutants do not show anomalous rectification until the membrane is hyperpolarized further. We suggest that the pwA gene plays a role in depolarization sensitivity (the 'gate') and the pwB gene a role affecting either the wall of the channel itself or the total number of channels.

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PubMed1975

Depletion of vesicles and fatigue of transmission at a vertebrate central synapse.

Synapses from Mauthner to giant fibers in the hatchetfish are chemically transmitting excitatory axo-axonic synapses located in the medulla. The synapses are 4--10 mum in diameter and easily identified for electron microscopy. Presynaptic vesicles are clustered near the contact regions and are round, clear and 40-60 nm in diameter. Stimulation of the Mauthner fiber at 10/sec for 10 min greatly reduces PSP amplitude and causes profound changes in presynaptic structures. Synaptic vesicles become few in number and there is a marked accumulation of irregular membranous structures. These changes are reversible. During the recovery period, the number of synaptic vesicles progressively increases to control values, and the number of irregular membranous structures declines. Further, stimulation during cooling induces depletion of vesicles together with a great increase in the surface area of the presynaptic membrane and in the number of coated vesicles. Internal irregular membranous structures are few. Our data provide evidence for the vesicular release of transmitter and are consistent with there being a mechanism of membrane recycling in which vesicle membrane fuses with the presynaptic membrane and is reclaimed from it by coated vesicles that then coalesce to form irregular membranous structures from which new synaptic vesicles are formed.

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PubMed1975

Fatigue and recovery of transmission at the Mauthner fiber-giant fiber synapse of the hatchetfish.

When the Mauthner fiber-giant fiber synapse of the hatchetfish is activated at gradually increasing frequencies, postsynaptic potentials (PSPs) in the giant fiber become progressively smaller, but complete failures of transmission are not observed even when PSP size is as small or smaller than miniature PSPs (mPSPs) simultaneously recorded. On the assumption of a Poisson distribution of amplitudes, calculations from the absence of failures and from variance suggest that guantum number remains at least as high as 5--10 and that quantal size is greatly reduced. During tetanic stimulation the frequency of mPSPs first increases and then decreases again, sometimes to a very low frequency. However, mPSP amplitude is reduced by no more than about 50%, which indicates that quanta giving rise to mPSPs come from a different population of vesicles than those comprising evoked PSPs. During rest following a tetanus, calculated quantal size in evoked PSPs recovers within several hundred milliseconds to mPSP size simultaneouly recorded. Most of this recovery time represents time for filling, since vesicles can be supplied at much higher rates during tetanic stimulation. After one second rest PSP amplitude exceeds threshold but recovery for later PSPs in a short train requires many minutes. The slowness of this recovery is consistent with the morphological demonstration of slow recovery of the vesicle population after depletion. These data are interpreted in terms of vesicle release, depletion and membrane recycling. Following depletion new vesicles are released after only partial filling which accounts for small quanta. Very small mPSPs are not seen because filling time is short compared to time for release as mPSPs. Since quantal size can be gradually reduced, release can interrupt filling, and filling and release sites are likely to be the same. The data in combination with the morphological observations support the hypothesis of vesicular release of transmitter and provide new evidence as to rates and sites for filling of vesicles.

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PubMed1975

Morphology of spinal electromotor neurons and presynaptic coupling in the gymnotid Sternarchus albifrons.

Spinal electromotor neurons in the gymnotid Sternarchus albitrons were studied by light and electron microscopy. In this species, the electric organ discharge, which is of high and relatively constant frequency, is generated by specialized axons which arise from the spinal electromotor neurons. The cell bodies are located in medial regions of the spinal cord. They are round to ellipsoid in outline and dendrites are not peresent. The initial myelin segment often extends partially over the cell body. Fine glial lamellae are interposed between closely adjacent cells, and somato-somatic gap junctions are not observed. The large majority of axosomatic synapses are characterized by gap junctions. Single axons are commonly found to establish gap junctions with two adjacent neurons. Only a few synapses have the chracteristics associated with chemically mediated transmission. The morphological data provide evidence for electrotonic soupling between electromotor neurons by way of presynaptic fibres. The absence of dendrites in these neurons may provide a morphological correlate for their simple relay function.

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PubMed1975

Vestibular nystagmus and teleost oculomotor neurons: functions of electrotonic coupling and dendritic impulse initiation.

1. Nystagmus in the horizontal plane is evoked in fish by mechanical stimulation of the ampulla of the horizontal semicircular canal or by electrical stimulation of the nerve from this canal. The movements are conjugate and the slow phase is away from the side of stimulation. 2. Medial rectus motoneurons were recorded from intracellularly, during nystagmus. During the slow phase (induced by ipsilateral stimulation), impulses arise abruptly from the base line and appear to arise at a distance from the cell body. During the fast phase (evoked by contralateral stimulation), impulses appear to arise from large PSPs that must be generated at or near the cell body. 3. In the curarized fish, stimulation of the nerve from the contralateral horizontal canal evokes spikes that arise from large EPSPs and that are blocked relatively easily by hyperpolarizing currents. Stimulation of the nerve from the ipsilateral horizontal canal evokes spikes that arise abruptly from the base line and that are much more difficult to block by hyperpolarizing currents. Little if any underlying PSP is observed when these impulses are delayed or blocked. Thus impulses evoked by stimulation of contralateral and ipsilateral side are initiated near to and far from the cell soma, respectively. 4. If impulses evoked by contralateral stimulation fail to excite the cell body due to injury, antidromic spikes are not occluded. Thus contralateral stimulation initiates impulses in the dendrites. 5. Cell bodies of neighboring motoneurons are coupled electrotonically, and graded antidromic stimulation evokes graded depolarizing potentials which result from electrotonic spread of spike activity from adjacent neurons. These depolarizing potentials are adequate to excite the cells in the presence of a background EPSP evoked by contralateral canal stimulation. In this manner coupling tends to synchronize cells during the fast phase of the nystagmus. 6. Antidromic responses of neighboring cells fail to interact with dendritic inputs to a particular cell, although indirect evidence indicates antidromic spikes invade the impulse-initiating regions in the dendrites. Thus coupling between dendrites is negligible and dendritic inputs can mediate the smoothly graded movements of the slow nystagmic phase. Coupling between somata is too weak to cause significant interaction between dendritically evoked impulses (unless the cell bodies are depolarized by EPSPs). 7. Rhythmic firing can be recorded in a single presynaptic fiber corresponding to either the slow or the fast phase of nystagmus, but not to both. Oculomotor neurons appear to be "relay cells" that, during the fast phase of the nystagmus receive a synchronized synaptic input which is initiated in a higher level command nucleus.

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PubMed1973

Rapid degeneration of ampullary electroreceptor organs after denervation.

Electroreceptors (ampullary organs) of the transparent catfish (Kryptopterus bicirrhus) lie in the epidermis, and contain spherical receptor cells that receive purely afferent innervation from the lateral line nerve. Section of this nerve causes rapid degenerative changes to occur in the receptors. Fine structural alterations occur in the receptor cell synapses and nerve fiber 6-12 h postoperatively. Disruption of the receptor cells begins by 18 h and most are lost by 48 h. By 72 h supporting cells and secretory cells also show marked degeneration, and by 96 h they may be totally lost. The rapid degeneration of the electroreceptor organs of Kryptopterus should make them a useful preparation for analysis of neurotrophic functions.

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