scholarly journals Distinct Temporal Filters In Mitral Cells And External Tufted Cells Of The Olfactory Bulb

2017 ◽  
Author(s):  
Christopher E. Vaaga ◽  
Gary L. Westbrook
Keyword(s):  
Olfactory Bulb ◽  
High Frequency ◽  
Synaptic Depression ◽  
High Frequency Stimulation ◽  
Mitral Cells ◽  
Release Probability ◽  
High Release ◽  
Frequency Stimulation ◽  
Tufted Cells ◽  
Synaptic Dynamics

Short-term synaptic plasticity is a critical regulator of neural circuits, and largely determines how information is temporally processed. In the olfactory bulb, afferent olfactory receptor neurons respond to increasing concentrations of odorants with barrages of action potentials, and their terminals have an extraordinarily high release probability (Sicard, 1986; Murphy et al., 2004). These features suggest that during naturalistic stimuli, afferent input to the olfactory bulb is subject to strong synaptic depression, presumably truncating the postsynaptic response to afferent stimuli. To examine this issue, we used single glomerular stimulation in mouse olfactory bulb slices to measure the synaptic dynamics of afferent-evoked input at physiological stimulus frequencies. In cell-attached recordings, mitral cells responded to high frequency stimulation with sustained responses, whereas external tufted cells responded transiently. Consistent with previous reports (Murphy et al., 2004), olfactory nerve terminals onto both cell types had a high release probability (0.7), from a single pool of slowly recycling vesicles, indicating that the distinct responses of mitral and external tufted cells to high frequency stimulation did not originate presyaptically. Rather, distinct temporal response profiles in mitral cells and external tufted cells could be attributed to slow dendrodendritic responses in mitral cells, as blocking this slow current in mitral cells converted mitral cell responses to a transient response profile, typical of external tufted cells. Our results suggest that despite strong axodendritic synaptic depression, the balance of axodendritic and dendrodendritic circuitry in external tufted cells and mitral cells, respectively, tunes the postsynaptic responses to high frequency, naturalistic stimulation.

scholarly journals Persistent synaptic inhibition of the subthalamic nucleus by high frequency stimulation

2021 ◽  
Author(s):  
Leon A Steiner ◽  
Andrea A Kuehn ◽  
Joerg RP Geiger ◽  
Henrik Alle ◽  
Milos Popovic ◽  
...  
Keyword(s):  
Subthalamic Nucleus ◽  
High Frequency ◽  
Symptomatic Relief ◽  
Neuronal Firing ◽  
High Frequency Stimulation ◽  
Inhibitory Input ◽  
Frequency Specificity ◽  
Evoked Field Potentials ◽  
Frequency Stimulation ◽  
Synaptic Dynamics

Background: Deep brain stimulation (DBS) provides symptomatic relief in a growing number of neurological indications, but local synaptic dynamics in response to electrical stimulation that may relate to its mechanism of action have not been fully characterized. Objective: The objectives of this study were to (1) study local synaptic dynamics during high frequency extracellular stimulation of the subthalamic nucleus (STN), and (2) compare STN synaptic dynamics with those of the neighboring substantia nigra pars reticulata (SNr). Methods: Two microelectrodes were advanced into the STN and SNr of patients undergoing DBS surgery for PD. Neuronal firing and evoked field potentials (fEPs) were recorded with one microelectrode during stimulation from an adjacent microelectrode. Results: Excitatory and inhibitory fEPs could be discerned within the STN and their amplitudes predicted bidirectional effects on neuronal firing (p = .007). There were no differences between STN and SNr inhibitory fEP dynamics at low stimulation frequencies (p > .999). However, inhibitory neuronal responses were sustained over time in STN during high frequency stimulation, but not SNr (p < .001) where depression of inhibitory input was coupled with a return of neuronal firing (p = .003). Interpretation: Persistent inhibitory input to the STN suggests a local synaptic mechanism for the suppression of subthalamic firing during high frequency stimulation. Moreover, differences in the resiliency versus vulnerability of inhibitory inputs to the STN and SNr suggest a projection source- and frequency-specificity for this mechanism. The feasibility of targeting electrophysiologically-identified neural structures may provide insight into how DBS achieves frequency-specific modulation of neuronal projections.

Regulation of Synaptic Depression Rates in the Cricket Cercal Sensory System

1998 ◽  
Vol 79 (3) ◽  
pp. 1277-1285 ◽  
Author(s):  
Andrew A. V. Hill ◽  
Ping Jin
Keyword(s):  
Sensory Neuron ◽  
Sensory Neurons ◽  
High Frequency ◽  
Sensory System ◽  
Synaptic Depression ◽  
High Frequency Stimulation ◽  
Excitatory Postsynaptic Potential ◽  
Short Term ◽  
Frequency Stimulation ◽  
Postsynaptic Target

Hill, Andrew A. V. and Ping Jin. Regulation of synaptic depression rates in the cricket cercal sensory system. J. Neurophysiol. 79: 1277–1285, 1998. To assess the roles of pre- and postsynaptic mechanisms in the regulation of depression, short-term synaptic depression was characterized at the synapses between sensory neurons and two interneurons in the cricket cercal sensory system. Changes in excitatory postsynaptic potential (EPSP) amplitude with repetitive stimulation at 5 and 20 Hz were quantified and fitted to the depletion model of transmitter release. The depression rates of different sensory neuron synapses on a single interneuron varied with the age of the sensory neurons such that old sensory neuron synapses depressed faster than young synapses. Although all synapses showed depression, short-term facilitation was selectively expressed only at sensory neuron synapses on one interneuron, the medial giant interneuron (MGI). These synapses showed concurrent facilitation and depression with high-frequency stimulation (100 Hz), whereas the synapses on another interneuron, 10-3, showed only depression at all stimulus frequencies. A previous study showed that the ability of a synapse to facilitate is correlated with the identity of the postsynaptic neuron. The present results indicate that depression and facilitation are regulated independently. Depression is regulated presynaptically in a manner related to sensory neuron age; whereas, facilitation is regulated by the postsynaptic target.

scholarly journals Tissue-specific dynamin-1 deletion at the calyx of Held decreases short-term depression through a mechanism distinct from vesicle resupply

2016 ◽  
Vol 113 (22) ◽  
pp. E3150-E3158 ◽  
Author(s):  
Satyajit Mahapatra ◽  
Fan Fan ◽  
Xuelin Lou
Keyword(s):  
Steady State ◽  
Synaptic Vesicle ◽  
High Frequency ◽  
Synaptic Depression ◽  
Conditional Knockout ◽  
High Frequency Stimulation ◽  
Latrunculin B ◽  
Short Term ◽  
Tissue Specific ◽  
Frequency Stimulation

Dynamin is a large GTPase with a crucial role in synaptic vesicle regeneration. Acute dynamin inhibition impairs neurotransmitter release, in agreement with the protein’s established role in vesicle resupply. Here, using tissue-specific dynamin-1 knockout [conditional knockout (cKO)] mice at a fast central synapse that releases neurotransmitter at high rates, we report that dynamin-1 deletion unexpectedly leads to enhanced steady-state neurotransmission and consequently less synaptic depression during brief periods of high-frequency stimulation. These changes are also accompanied by increased transmission failures. Interestingly, synaptic vesicle resupply and several other synaptic properties remain intact, including basal neurotransmission, presynaptic Ca2+ influx, initial release probability, and postsynaptic receptor saturation and desensitization. However, acute application of Latrunculin B, a reagent known to induce actin depolymerization and impair bulk and ultrafast endocytosis, has a stronger effect on steady-state depression in cKO than in control and brings the depression down to a control level. The slow phase of presynaptic capacitance decay following strong stimulation is impaired in cKO; the rapid capacitance changes immediately after strong depolarization are also different between control and cKO and sensitive to Latrunculin B. These data raise the possibility that, in addition to its established function in regenerating synaptic vesicles, the endocytosis protein dynamin-1 may have an impact on short-term synaptic depression. This role comes into play primarily during brief high-frequency stimulation.

Depression of postsynaptic potentials by high-frequency stimulation in embryonic motoneurons grown in spinal cord slice cultures

1992 ◽  
Vol 68 (5) ◽  
pp. 1793-1803 ◽  
Author(s):  
J. Streit ◽  
C. Luscher ◽  
H. R. Luscher
Keyword(s):  
Spinal Cord ◽  
Dorsal Root Ganglia ◽  
High Frequency ◽  
Dorsal Root ◽  
Input Resistance ◽  
Synaptic Depression ◽  
High Frequency Stimulation ◽  
Postsynaptic Potentials ◽  
Wide Range ◽  
Frequency Stimulation

1. In embryonic cocultures of spinal cord, dorsal root ganglia, and muscle, excitatory postsynaptic potentials (EPSPs) were recorded in motoneurons during focal electrical stimulation of the dorsal root ganglia or the spinal cord. 2. EPSPs were depressed in amplitude at high-frequency stimulation relative to a control frequency of 0.5 Hz by 47 and 75% at 5 and 10 Hz, respectively. This was true for composite EPSPs and unitary EPSPs. 3. The depression showed a wide range of variability between individual experiments. The degree of depression at 5 Hz was negatively correlated to the rate of spontaneous excitatory input the motoneurons received. There was no correlation to the soma size, the average amplitude of the EPSPs, the rheobase, or the input resistance of the motoneurons. 4. An increase in latency of EPSPs was observed concomitant with or preceding the synaptic depression in most experiments. Total transmission failures, which were absent at low-frequency stimulation, appeared during depression. 5. Large incremental steps in amplitude could be seen during depression, suggesting that several release sites were switched off and on together. 6. Decreasing the extracellular calcium concentration from 5 to 1 mM led to a decrease in the frequency sensitivity of the synaptic efficacy and to a decrease of the EPSP amplitude and latency. 7. Measurements of the antidromic conduction of action potentials evoked in the axons and recorded in the somata of dorsal root ganglion cells revealed an increase in latency and the appearance of conduction failures at stimulation frequencies of 1-10 Hz. The frequency modulation of conduction was decreased in 1 mM compared with 5 mM external calcium. 8. Together these findings suggest that conduction failures in the presynaptic axons contribute to the synaptic depression of EPSPs in embryonic motoneurons.

Short- and long-term synaptic depression in rat neostriatum

1993 ◽  
Vol 70 (5) ◽  
pp. 1937-1949 ◽  
Author(s):  
D. M. Lovinger ◽  
E. C. Tyler ◽  
A. Merritt
Keyword(s):  
High Frequency ◽  
Time Course ◽  
Glutamate Release ◽  
Synaptic Depression ◽  
High Frequency Stimulation ◽  
Glutamatergic Synapses ◽  
Glutamatergic Synaptic Transmission ◽  
Frequency Stimulation ◽  
Short And Long Term

1. We have examined plasticity at glutamatergic synapses on neurons in slices of neostriatum, a forebrain area involved in movement and cognitive function. 2. High-frequency stimulation of afferent inputs to neostriatal neurons induced depression of glutamatergic synaptic transmission. Depression could be induced using either prolonged trains or short repetitive bursts of high-frequency stimulation. Depression developed within seconds after such stimulation. Responses recovered to baseline levels within 10 min in most slices but persisted for up to 60 min in others. 3. Postsynaptic passive electrical properties and the ability to elicit action potentials by postsynaptic depolarization were not altered during depression. 4. The magnitude and time course of depression was similar whether postsynaptic responses were mediated by alpha amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) or N-methyl-D-aspartate (NMDA) type glutamate receptors. Depression was not altered by antagonism of AMPA or NMDA receptors or potentiation of AMPA receptor function with aniracetam. 5. Depression was blocked by treatments that increase transmitter release including increased extracellular Ca2+, application of 4-aminopyridine, or application of phorbol ester. 6. Our findings indicate that glutamatergic synapses in neostriatum are capable of expressing a form of synaptic depression that may involve decreased glutamate release.

Synaptic depression in frog neuromuscular junction

1987 ◽  
Vol 58 (1) ◽  
pp. 230-246 ◽  
Author(s):  
M. I. Glavinovic
Keyword(s):  
Nerve Stimulation ◽  
High Frequency ◽  
Synaptic Depression ◽  
High Frequency Stimulation ◽  
Frog Neuromuscular Junction ◽  
Choline Uptake ◽  
Uptake System ◽  
End Plate ◽  
Quantal Size ◽  
Frequency Stimulation

1. The amplitudes of end-plate currents (EPCs) evoked by stimulating the nerve with frequencies ranging from 1 to 5 Hz and the amplitudes of miniature end-plate currents (MEPCs) gradually diminish if choline uptake is blocked by hemicholinium-3 (HC-3, 20 microM). This reduction of EPC amplitudes is predominantly of presynaptic origin, although an observed decrease in MEPC amplitudes suggests that some postsynaptic changes [due to direct action of HC-3 on acetylcholine (ACh) receptors or on open ACh channels] also occurs. 2. Shortening of both EPCs and MEPCs is observed during high-frequency stimulation (5 Hz) in the presence of cholinesterase inhibitor after impairment of ACh synthesis. Shortening of MEPCs probably results from a direct blocking action of HC-3 on open ACh channels, as well as from reduction in quantal size. Shortening of EPCs is more pronounced (EPCs eventually have shorter time courses than MEPCs) and usually does not result from a gradual reduction in the spatial overlap of quantal events (because of reduced quantal content) or from a diminished 'lingering ACh' (ACh that remains in the synaptic cleft between nerve impulses), but rather from a much reduced quantal size of nerve-evoked quanta. 3. It therefore appears that the quanta that are released by nerve stimulation are preferentially filled with newly synthesized ACh. In its absence nerve stimulation leads to secretion of only partially filled quanta. This occurs simultaneously with spontaneous secretion of almost normally filled quanta. Hence it seems that the quantal discharge is not strongly dependent, if at all, on its ACh content. Moreover, the correspondence between the quantal sizes of nerve-evoked and spontaneously released quanta does not remain valid during high-frequency prolonged stimulation. 4. Even with the choline uptake system intact, prolonged high-frequency stimulation leads to a gradual shortening of EPCs and, to a small extent, MEPCs. Shortening of EPCs appears to be mainly a result of a reduction of their quantal size. 5. It is estimated from the shortening of EPCs and the known EPC versus MEPC relationship that the reduction of the quantal sizes of nerve-evoked quanta probably contributes very significantly to synaptic depression that occurs during prolonged high-frequency nerve stimulation.(ABSTRACT TRUNCATED AT 400 WORDS)

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