8 research outputs found
Pharmacological characterization of presynaptic calcium currents underlying glutamatergic transmission in the avian auditory brainstem
We used whole-cell patch-clamp techniques on presynaptic terminals and postsynaptic neurons of the glutamatergic magnocellularis synapse in the chick auditory brainstem to study the effects of N, P, and L-type calcium channel blockers directly on presynaptic calcium currents and transmitter release. Presynaptic calcium currents and transmitter release were unaffected by nifedipine, blocked partially by omega- agatoxin IVA and completely by omega-conotoxin GVIA. The presynaptic calcium current is a low voltage-activated, noninactivating current and its block by omega-agatoxin IVA was not reversed by repeated depolarization of the presynaptic terminal. Thus, the presynaptic calcium current that underlies transmitter release at the chick magnocellularis synapse differs in some respects from N and P-type calcium currents described in vertebrate neuronal cell bodies
Pharmacological characterization of presynaptic calcium currents underlying glutamatergic transmission in the avian auditory brainstem
We used whole-cell patch-clamp techniques on presynaptic terminals and postsynaptic neurons of the glutamatergic magnocellularis synapse in the chick auditory brainstem to study the effects of N, P, and L-type calcium channel blockers directly on presynaptic calcium currents and transmitter release. Presynaptic calcium currents and transmitter release were unaffected by nifedipine, blocked partially by omega- agatoxin IVA and completely by omega-conotoxin GVIA. The presynaptic calcium current is a low voltage-activated, noninactivating current and its block by omega-agatoxin IVA was not reversed by repeated depolarization of the presynaptic terminal. Thus, the presynaptic calcium current that underlies transmitter release at the chick magnocellularis synapse differs in some respects from N and P-type calcium currents described in vertebrate neuronal cell bodies
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Presynaptic facilitation at the crayfish neuromuscular junction: Role of calcium-activated potassium conductance
Membrane potential was recorded intracellularly near presynaptic
terminals of the excitor axon of the crayfish opener neuromuscular junction (NMJ),
while transmitter release was recorded postsynaptically. This study focused on the
effects of a presynaptic calcium-activated potassium conductance, gK(Ca), on the
transmitter release evoked by single and paired depolarizing current pulses.
Blocking gK(Ca) by adding tetraethylammonium ion (TEA; 5-20 mM) to a solution
containing tetrodotoxin and aminopyridines caused the relation between presynaptic
potential and transmitter release to steepen and shift to less depolarized
potentials. When two depolarizing current pulses were applied at 20-ms intervals
with gK(Ca) not blocked, the presynaptic voltage change to the second (test) pulse was
inversely related to the amplitude of the first (conditioning) pulse. This effect of the
conditioning prepulse on the response to the test pulse was eliminated by 20 mM
TEA and by solutions containing 0 mM Ca2+/1 mM EGTA, suggesting that the
reduction in the amplitude of the test pulse was due to activation of gK(Ca) by calcium
remaining from the conditioning pulse. In the absence of TEA, facilitation of
transmitter release evoked by a test pulse increased as the conditioning pulse grew
from -40 to -20 mV, but then decreased with further increase in the conditioning
depolarization. A similar nonmonotonic relationship between facilitation and the
amplitude of the conditioning depolarization was reported in previous studies using
extracellular recording, and interpreted as supporting an additional voltagedependent
step in the activation of transmitter release. We suggest that this result
was due instead to activation of a gK(Ca) by the conditioning depolarization, since
facilitation of transmitter release increased monotonically with the amplitude of the
conditioning depolarization, and the early time course of the decay of facilitation
was prolonged when gK(Ca) was blocked. The different time courses for decay of the
presynaptic potential (20 ms) and facilitation (> 50 ms) suggest either that residual free calcium does not account for facilitation at the crayfish NMJ or that the
transmitter release mechanism has a markedly higher affinity or stoichiometry for
internal free calcium than does g K(Ca). Finally, our data suggest that the calcium
channels responsible for transmitter release at the crayfish NMJ are not of the L, N,
or T type.This work was partially supported by NIAAA grant AA0776 to G. D. Bittner.Neuroscienc
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Calcium-activated potassium conductance in presynaptic terminals at the crayfish neuromuscular junction
Membrane potential changes that typically evoke transmitter release
were studied by recording intracellularly from the excitor axon near presynaptic
terminals of the crayfish opener neuromuscular junction. Depolarization of the
presynaptic terminal with intracellular current pulses activated a conductance that
caused a decrease in depolarization during the constant current pulse. This
conductance was identified as a calcium-activated potassium conductance, g~c~), by
its disappearance in a zero-calcium/EGTA medium and its block by cadmium,
barium, tetraethylammonium ions, and charybdotoxin. In addition to gK~c,), a
delayed rectifier potassium conductance (gK) is present in or near the presynaptic
terminal. Both these potassium conductances are involved in the repolarization of
the membrane during a presynaptic action potential.This work was supported in part by NIAAA grant AA0776 to G. D. Bittner.Neuroscienc
Presynaptic facilitation at the crayfish neuromuscular junctions. Role of Calcium-activated potassium conductance
ABSTRACT Membrane potential was recorded intracellularly near presynaptic terminals of the excitor axon of the crayfish opener neuromuscular junction (NMJ), while transmitter release was recorded postsynaptically. This study focused on the effects of a presynaptic calcium-activated potassium conductance, gK~c~, on the transmitter release evoked by single and paired depolarizing current pulses. Blocking gK~c~) by adding tetraethylammonium ion (TEA; 5-20 mM) to a solution containing tetrodotoxin and aminopyridines caused the relation between presynaptic potential and transmitter release to steepen and shift to less depolarized potentials. When two depolarizing current pulses were applied at 20-ms intervals with g~c ~ not blocked, the presynaptic voltage change to the second (test) pulse was inversely related to the amplitude of the first (conditioning) pulse. This effect of the conditioning prepulse on the response to the test pulse was eliminated by 20 mM TEA and by solutions containing 0 mM Ca2+/1 mM EGTA, suggesting that the reduction in the amplitude of the test pulse was due to activation of gK~c ~ by calcium remaining from the conditioning pulse. In the absence of TEA, facilitation o
Neuronal Responses to Lemniscal Stimulation in Laminar Brain Slices of the Inferior Colliculus
The central nucleus of the inferior colliculus (ICC) receives inputs from all parts of the auditory brainstem and transmits the information to the forebrain. Fibrodendritic laminae of the ICC provide a structural basis for a tonotopic organization, and the interaction of inputs within a single layer is important for ICC processing. Transverse slice planes of the ICC sever the layers and many of the ascending axons that enter through the lateral lemniscus. Consequently, the activity initiated within a lamina by a pure lemniscal stimulus is not well characterized. Here, we use a slice plane that maintains the integrity of the laminae in ICC and allows the axons in the lateral lemniscus to be stimulated at a distance from the ICC. We examined both the postsynaptic currents and potentials of the same neurons to lemniscal stimuli in this laminar brain slice. Our main finding is that lemniscal stimulation evokes prolonged synaptic potentials in ICC neurons. Synaptic potential amplitudes and durations increase with lemniscal shock strength. In ∼50% of ICC neurons, the postsynaptic potential is equal in duration to the postsynaptic current, whereas in the remaining neurons it is three to four times longer. Synaptic responses to single shocks or shock trains exhibit plateau potentials that enable sustained firing in ICC neurons. Plateau potentials are evoked by N-methyl-d-aspartate (NMDA) receptor activation, and their amplitudes and durations are regulated by both NMDA-R and gamma-aminobutyric acid A (GABA(A))-R activation. These data suggest that in the intact laminae of the ICC, lemniscal inputs initiate sustained firing through monosynaptic and polysynaptic NMDA-mediated synapses regulated by GABA(A) synapses