Postnatal development of a persistent Na+ current in pyramidal neurons from rat sensorimotor cortex

1993 ◽  
Vol 69 (1) ◽  
pp. 290-292 ◽  
Author(s):  
C. Alzheimer ◽  
P. C. Schwindt ◽  
W. E. Crill
Keyword(s):  
Postnatal Development ◽  
Sensorimotor Cortex ◽  
Pyramidal Neurons ◽  
Direct Evidence ◽  
Fold Increase ◽  
Na Current ◽  
Early Postnatal Development ◽  
Neocortical Neurons ◽  
Voltage Dependent ◽  
Whole Cell Recordings

1. Whole-cell recordings were performed on acutely isolated pyramidal neurons from rat sensorimotor cortex 2 to 21 days postnatal to study the expression of a tetrodotoxin (TTX) sensitive, voltage dependent, persistent Na+ current (INaP) during different stages of postnatal development. 2. INaP was activated positive to about -60 mV and attained its peak amplitude between -40 and -35 mV. Activation of INaP did not require preceding activation of the transient Na+ current. 3. Peak INaP amplitudes showed a three-fold increase over the first three postnatal weeks, starting from 60.7 +/- 7.5 (SE) pA (n = 6) at postnatal day (P) 2-P5 and reaching 189.1 +/- 20.4 pA (n = 13) at P17–P21. 4. Measurements of peak INaP density, which took concomitant cell growth into account, revealed that a considerable current density already existed in very young neurons (P2–P5: 4.3 +/- 1.0 microA/cm2, n = 6) when compared with INaP density in early adult neurons (P17 - P21: 8.9 +/- 0.8 microA/cm2, n = 5). 5. Our data provide the first direct evidence for the presence of a significant INaP density during early postnatal development of neocortical neurons indicating that this current should play a role in the control of intrinsic excitability at this age.

scholarly journals Distinct AMPA-Type Glutamatergic Synapses in Developing Rat CA1 Hippocampus

2010 ◽  
Vol 104 (4) ◽  
pp. 1899-1912 ◽  
Author(s):  
Elizabeth A. Stubblefield ◽  
Tim A. Benke
Keyword(s):  
Pyramidal Neurons ◽  
Age Groups ◽  
Inward Rectification ◽  
Decay Kinetics ◽  
Glutamatergic Synapses ◽  
Early Postnatal Development ◽  
Paired Pulse ◽  
Age Related ◽  
Hippocampal Ca1 ◽  
Voltage Dependent

We assessed synaptic α-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptor (AMPAR) properties during synaptogenesis to describe the development of individual glutamatergic synapses on rat hippocampal CA1 principal neurons. Pharmacologically isolated AMPAR-mediated glutamatergic synaptic currents [evoked by stimulation of the Schaffer Collateral pathway, excitatory postsynaptic currents (EPSCs)], had significantly greater inward-rectification at ages P5–7 compared with P8–18. These inward rectifying EPSCs demonstrated paired-pulse dependent unblocking at positive holding potentials, consistent with voltage-dependent internal polyamine block. Measurements of paired-pulse facilitation did not support altered presynaptic properties associated with inward rectification. Using asynchronous EPSCs (aEPSCs) to analyze populations of individual synapses, we found that quantal amplitudes ( Q) increased across early postnatal development (P5-P18) and were directly modulated by increases in the number of activated receptors. Quantal AMPAR decay kinetics (aEPSC τdecays) exhibited the highest coefficient of variation (CV) from P5 to 7 and became markedly less variable at P8–18. At P5–7, faster quantal kinetics coexisted with much slower kinetics; only slower quantal kinetics were found at P8–18. This supports diverse quantal synaptic properties limited to P5–7. Multivariate cluster analysis of Q, CVτdecay, and median τdecay supported a segregation of neurons into two distinct age groups of P5–7 and P8–18, similar to the age-related segregation suggested by inward rectification. Taken together, these findings support synaptic, calcium permeable AMPARs at a subset of synapses onto CA1 pyramidal neurons exclusively at P5–7. These distinct synapses coexist with those sharing the properties of more mature synapses. These synapses disappear after P7 as activated receptor numbers increase with age.

scholarly journals GABAB Receptor-Mediated Regulation of Dendro-Somatic Synergy in Layer 5 Pyramidal Neurons

2021 ◽  
Vol 15 ◽  
Author(s):  
Jan M. Schulz ◽  
Jim W. Kay ◽  
Josef Bischofberger ◽  
Matthew E. Larkum
Keyword(s):  
Pyramidal Neurons ◽  
Partial Information ◽  
Gabab Receptor ◽  
Fold Increase ◽  
Substantial Contribution ◽  
Transfer Resistance ◽  
Girk Channels ◽  
Synergistic Interactions ◽  
Voltage Dependent

Synergistic interactions between independent synaptic input streams may fundamentally change the action potential (AP) output. Using partial information decomposition, we demonstrate here a substantial contribution of synergy between somatic and apical dendritic inputs to the information in the AP output of L5b pyramidal neurons. Activation of dendritic GABAB receptors (GABABRs), known to decrease APs in vivo, potently decreased synergy and increased somatic control of AP output. Synergy was the result of the voltage-dependence of the transfer resistance between dendrite and soma, which showed a two-fold increase per 28.7 mV dendritic depolarization. GIRK channels activated by dendritic GABABRs decreased voltage-dependent transfer resistances and AP output. In contrast, inhibition of dendritic L-type Ca2+ channels prevented high-frequency bursts of APs, but did not affect dendro-somatic synergy. Finally, we show that NDNF-positive neurogliaform cells effectively control somatic AP via synaptic activation of dendritic GIRK channels. These results uncover a novel inhibitory mechanism that powerfully gates cellular information flow in the cortex.

scholarly journals Functional CB1 Receptors Are Broadly Expressed in Neocortical GABAergic and Glutamatergic Neurons

2007 ◽  
Vol 97 (4) ◽  
pp. 2580-2589 ◽  
Author(s):  
Elisa L. Hill ◽  
Thierry Gallopin ◽  
Isabelle Férézou ◽  
Bruno Cauli ◽  
Jean Rossier ◽  
...  
Keyword(s):  
Pyramidal Neurons ◽  
Cannabinoid Receptor ◽  
Physiological Data ◽  
Glutamatergic Neurons ◽  
Neuronal Populations ◽  
Postsynaptic Currents ◽  
Neocortical Neurons ◽  
Neuronal Types ◽  
Cb1 Antagonist ◽  
Whole Cell Recordings

The cannabinoid receptor CB1 is found in abundance in brain neurons, whereas CB2 is essentially expressed outside the brain. In the neocortex, CB1 is observed predominantly on large cholecystokinin (CCK)-expressing interneurons. However, physiological evidence suggests that functional CB1 are present on other neocortical neuronal types. We investigated the expression of CB1 and CB2 in identified neurons of rat neocortical slices using single-cell RT-PCR. We found that 63% of somatostatin (SST)-expressing and 69% of vasoactive intestinal polypeptide (VIP)-expressing interneurons co-expressed CB1. As much as 49% of pyramidal neurons expressed CB1. In contrast, CB2 was observed in a small proportion of neocortical neurons. We performed whole cell recordings of pyramidal neurons to corroborate our molecular findings. Inhibitory postsynaptic currents (IPSCs) induced by a mixed muscarinic/nicotinic cholinergic agonist showed depolarization-induced suppression of inhibition and were decreased by the CB1 agonist WIN-55212-2 (WIN-2), suggesting that interneurons excited by cholinergic agonists (mainly SST and VIP neurons) possess CB1. IPSCs elicited by a nicotinic receptor agonist were also reduced in the presence of WIN-2, suggesting that neurons excited by nicotinic agonists (mainly VIP neurons) indeed possess CB1. WIN-2 largely decreased excitatory postsynaptic currents evoked by intracortical electrical stimulation, pointing at the presence of CB1 on glutamatergic pyramidal neurons. All WIN-2 effects were strongly reduced by the CB1 antagonist AM 251. We conclude that CB1 is expressed in various neocortical neuronal populations, including glutamatergic neurons. Our combined molecular and physiological data suggest that CB1 widely mediates endocannabinoid effects on glutamatergic and GABAergic transmission to modulate cortical networks.

P/Q type voltage dependent Ca2+ channel is crucial for early postnatal development of climbing fiber to Purkinje cell synapse

2010 ◽  
Vol 68 ◽  
pp. e37-e38
Author(s):  
Kouichi Hashimoto ◽  
Mika Tsujita ◽  
Kazuo Kitamura ◽  
Taisuke Miyazaki ◽  
Maya Yamazaki ◽  
...  
Keyword(s):  
Purkinje Cell ◽  
Postnatal Development ◽  
Climbing Fiber ◽  
Early Postnatal Development ◽  
Voltage Dependent ◽  
Cell Synapse

Characterization of pharmacologically identified voltage-gated calcium channel currents in acutely isolated rat neocortical neurons. II. Postnatal development

1995 ◽  
Vol 73 (4) ◽  
pp. 1443-1451 ◽  
Author(s):  
N. M. Lorenzon ◽  
R. C. Foehring
Keyword(s):  
Calcium Channel ◽  
Pyramidal Neurons ◽  
Companion Paper ◽  
Whole Cell ◽  
Time To Peak ◽  
Neocortical Neurons ◽  
P Type ◽  
Channel Currents ◽  
Whole Cell Recordings

1. Whole cell recordings were obtained from pyramidal neurons acutely dissociated from the sensorimotor cortex of adult (from Lorenzon and Foehring, companion paper) and immature rats postnatal day 1 (P1) to adult. 2. Whole cell calcium channel currents were similar in appearance at all ages. Current amplitudes and estimated densities were initially low (approximately 16 pA/pF at ages < P6) and increased gradually, attaining adult values at approximately 4-5 wk postnatally (approximately 100 pA/pF). 3. L-type current was operationally defined as that blocked by 5 microM nifedipine, N-type current as that blocked by 1 microM omega-conotoxin GVIA, and P-type current as that blocked by 100 nM omega-agatoxin IVA. A resistant current remained in the presence of the combination of these three blockers. The proportions of these four current types did not change during ontogeny. 4. Few biophysical differences were found between the pharmacologically defined current components in adult or 1-wk-old cells. At both ages the resistant current had a more rapid time-to-peak and inactivated more completely and rapidly than the other three types. Resistant currents also activated at more negative potentials. N-, L-, and P-type currents activated at more positive potentials in 1-wk-old cells than in adult cells. For the resistant current, the voltage dependence of activation was not significantly different between the two ages.

Amplification of synaptic current by persistent sodium conductance in apical dendrite of neocortical neurons

1995 ◽  
Vol 74 (5) ◽  
pp. 2220-2224 ◽  
Author(s):  
P. C. Schwindt ◽  
W. E. Crill
Keyword(s):  
Pyramidal Neurons ◽  
Apical Dendrite ◽  
Synaptic Current ◽  
Neocortical Neurons ◽  
Excitatory Synaptic Input ◽  
Voltage Dependent ◽  
Nmda Glutamate Receptors ◽  
Nmda Channels ◽  
Voltage Gated Channels ◽  
Effective Transmission

1. Evidence for amplification of synaptic current by voltage-gated channels in dendrites of neocortical pyramidal neurons was demonstrated by examining the effect of specific channel blocking agents on the current arriving at the soma during iontophoresis of glutamate at a distal site on the apical dendrite. 2. Dendritic noninactivating Na+ channels were implicated in this voltage-dependent amplification of the transmitted current because it was maintained for > 1 s and because tetrodotoxin (TTX) eliminated much of this amplification. 3. Specific blockers of N-methyl-D-aspartate (NMDA) glutamate receptors reduced the amplitude of the glutamate-evoked current at all potentials and also reduced the non-TTX-sensitive component of voltage-dependent augmentation. The effects of TTX were identical whether or not NMDA channels were blocked. 4. We conclude that a persistent Na+ conductance exists in the apical dendrite of neocortical neurons. Together with the NMDA conductance at the synaptic site it provides a mechanism for the graded, voltage-dependent amplification of tonic, excitatory synaptic input. This amplification results in much more effective transmission of tonic excitatory current to the soma than would occur in a passive dendrite.

scholarly journals Early postnatal development of pyramidal neurons across layers of the mouse medial prefrontal cortex

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Tim Kroon ◽  
Eline van Hugte ◽  
Lola van Linge ◽  
Huibert D. Mansvelder ◽  
Rhiannon M. Meredith
Keyword(s):  
Prefrontal Cortex ◽  
Postnatal Development ◽  
Medial Prefrontal Cortex ◽  
Pyramidal Neurons ◽  
Early Postnatal Development
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