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R Kretz

Publications and source records attributed to R Kretz.

27 records · Page 2Linked to original sources
PubMed1986

Presynaptic inhibition produced by an identified presynaptic inhibitory neuron. I. Physiological mechanisms.

We have examined the synaptic conductance mechanisms underlying presynaptic inhibition in Aplysia californica in a circuit in which all the neural elements are identified cells (Fig. 1). L10 makes connections to identified follower cells (RB and left upper quadrant cells, L2-L6). These connections are presynaptically inhibited by stimulating cells of the L32 cluster (4). L32 cells produce a slow inhibitory synaptic potential on L10. This inhibitory synaptic potential is associated with an apparent increased membrane conductance in L10. Both the inhibitory postsynaptic potential (IPSP) and the conductance increase are voltage dependent; the IPSP could not be reversed by hyperpolarizing the membrane potentials to - 120 mV. The hyperpolarization of L10 induced by L32 reduces the transmitter output of L10 and thereby contributes to presynaptic inhibition. However, this hyperpolarization accounts for about 30% of the effect because presynaptic inhibition can still be observed even when the hyperpolarization of L10 by L32 is prevented by voltage clamping. When L10 is voltage clamped, stimulation of L32 produces a slow outward synaptic current associated with an apparent increased conductance. Both the synaptic current and conductance change measured under clamp are voltage dependent, and the outward current could not be reversed. This synaptic current is not mediated by an increase in C1- conductance. It is sensitive to external K+ concentration, especially at hyperpolarized membrane potentials. With L10 under voltage clamp, stimulation of L32 also reduces a slow inward current in L10. This current has time and voltage characteristics similar to those of the Ca2+ current. Presynaptic inhibition is still produced by L32 when L10 is voltage clamped, and transmitter release is elicited by depolarizing voltage-clamp pulses. This component of presynaptic inhibition, which accounts for approximately 70% of the inhibition, appears to be due to a decrease in the Ca2+ current in the presynaptic neuron.

Abdomen↗
PubMed1986

Presynaptic inhibition produced by an identified presynaptic inhibitory neuron. II. Presynaptic conductance changes caused by histamine.

We have examined the morphology and pharmacology of the L32 neurons, identified cells that mediate presynaptic inhibition in the Aplysia abdominal ganglion, to gain insight into the putative transmitter released by the L32 cells. We analyzed the fine structure of the synaptic release sites of L32 cells stained with horseradish peroxidase. Each varicosity of L32 was found to contain two general classes of vesicles. One class of vesicles is large (mean long diameter of 98 nm) and contains an electron-dense core that typically filled or nearly filled each vesicle profile. The second class of vesicles is smaller (mean long diameter of 67 nm) and relatively electron lucent. The size, distribution, and morphology of the vesicle population in L32's terminals was similar to that described at the synapses of the identified histaminergic neuron C2 in Aplysia (2). These morphological observations suggested that L32 cells might be histaminergic. Among the various putative transmitters tested, histamine was most effective in mimicking the postsynaptic effects of L32 cells onto L10, and onto other follower cells of L32 in the abdominal ganglion. Histamine also caused inhibition of transmitter output from L10. Both the IPSP produced by L32 in L10 and the response of L10 to histamine could be reversibly blocked by cimetidine, a histamine antagonist in Aplysia (14). These results support, but do not establish the identification of histamine as the putative transmitter of L32 cells. Histamine mimics the action of L32 in mediating presynaptic inhibition allowing us to examine in more detail the conductance changes in L10 underlying presynaptic inhibition. Voltage-clamp analysis revealed that histamine blocked the voltage-dependent Ca2+ current and increased a voltage-dependent K+ current in L10, much as did L32. Both of these changes are likely to act synergistically to inhibit transmitter release. Reduction of Ca2+ current in L10 would directly inhibit transmitter release from L10 directly by decreasing the amount of Ca2+ entering during spike depolarization. The increase in K+ current would act indirectly to reduce transmitter release from L10, by hyperpolarizing L10 and decreasing the amplitude and duration of spikes in L10, as well as reducing the steady-state Ca2+ influx. These results support the idea that in Aplysia presynaptic inhibition is caused primarily by a direct transmitter-mediated reduction in presynaptic Ca2+ current and secondarily by a hyperpolarization of the presynaptic neuron due to a transmitter-mediated increase in a K+ current.(ABSTRACT TRUNCATED AT 400 WORDS)

Abdomen↗
PubMed1985

ON and OFF regions in layer IV of striate cortex.

In vertical penetrations through the striate cortex in the tree shrew (Tupaia belangeri), we found regions where neural activity was evoked predominantly by light ON. These were followed by regions where responses were evoked predominantly by light OFF. Histological reconstructions indicated that the ON regions were correlated with layer IVa and the OFF regions were correlated with layer IVb. Local application of cobalt chloride produced a transient cessation of visually evoked activity, suggesting that the electrodes sampled cortical activity rather than lateral geniculate nucleus afferents. These data demonstrate that separate ON and OFF regions are present in the tree shrew striate cortex and suggest that spatially separate, parallel ON and OFF afferent channels extend, in this species, at least through the first synapse in the striate cortex.

Animals↗
PubMed1984

Local cobalt injection: a method to discriminate presynaptic axonal from postsynaptic neuronal activity.

The local application of cobalt reversibly blocks the calcium channel conductance and therefore synaptic transmission. The blockage of synaptic transmission is a useful tool to discriminate between the origins of a response recorded with extracellular metal electrodes from central nervous system substructures. Incoming presynaptic fiber activity is not affected while activity from postsynaptic elements as intrinsic neurons and cell processes are blocked. In addition, local cobalt application does not change the stimulation conditions under which the system is tested.

Animals↗
PubMed1982

Ratfish retina--intracellular recordings and HRP injections in an isolated, superfused all-rod retina.

Hyperpolarizing responses to light were studied by intracellular recording in the isolated, superfused retina of the ratfish (Hydrolagus colliei). Two of these hyperpolarizing units were identified as horizontal cells by iontophoretic injection of horseradish peroxidase (HRP). These cells had rather large cell bodies (15 x 30 micrometer), elliptical dendritic arborizations measuring 150 x 300 micrometers and no axons. Since their physiological receptive fields were found to be at least 2.15 mm in diameter, it appears likely that either the photoreceptors or the horizontal cells are electrically coupled. Electron microscopy of HRP-injected horizontal cells showed their dendrites to end laterally in ribbon synapses of rods only and revealed dendro-dendritic contacts resembling gap junctions between injected and uninjected horizontal cells. The spectral sensitivity function of a dark-adapted horizontal cell can be described by a Dartnall nomogram based on a retinene pigment with lambda max = 473 nm. These findings are consistent with the histological observation that the ratfish retina appears to contain only rod photoreceptors.

Animals↗
PubMed1982

Post-tetanic potentiation at an identified synapse in Aplysia is correlated with a Ca2+-activated K+ current in the presynaptic neuron: evidence for Ca2+ accumulation.

We have examined the presynaptic changes underlying post-tetanic potentiation (PTP) in Aplysia by using voltage-clamp techniques combined with specific pharmacological blocking agents. The amplitude and time course of PTP parallel a slow outward clamp current that we have identified as a Ca2+-activated K+ current. Because this current is proportional to intracellular Ca2+ concentration our findings provide evidence for the "residual Ca2+ hypothesis," according to which PTP is caused by the accumulation of intracellular Ca2+ after tetanus. To obtain further evidence for this mechanism we injected EGTA intracellularly and found that it decreased the duration of both PTP and the Ca2+ -activated K+ current.

Action Potentials↗