Dieter Jaeger Department of Biology Emory University djaeger@emory
42
description
How neurons integrate thousands of synaptic inputs each second. Dieter Jaeger Department of Biology Emory University [email protected]. The textbook view. KSJ 4th ed., Fig. 10-7. Kandel, 4 th edition. In vivo input levels. 100 m m. 100 m m. GP neuron surface area:17,700 m m 2 - PowerPoint PPT Presentation
Transcript of Dieter Jaeger Department of Biology Emory University djaeger@emory
KSJ 4th ed., Fig. 10-7
Kandel, 4th edition
100 m
100 m
GP neuron
• surface area: 17,700 m2
• number of synapses (ex/in): 1,200 / 6,800
• number of inputs / s 12,000 / 6,800
Ca3 pyramidal neuron
• surface area: 38,800 m2
• number of synapses (ex/in): 17,000 / 2,000
• number of inputs / s 170,000 / 20,000
In vivo input levels
In vivo recording from striatal medium spiny neuron
5,000 AMPA and 500 GABAA Synapses at 10 Hz
Ein = -70 mV
Eex = 0 mV
Isyn = Gin * (Vm - Ein) + Gex * (Vm - Eex)
Esyn = (Gin * Ein)+ (Gex * Eex) / (Gin+ Gex)
Isyn = (Gin + Gex) * (Vm - Esyn)
Isyn = (300 nS) * (60-50mV) = 3 nA
AxoClamp 2B
Isyn = Iex + Iin= Gex*(Vm-Eex)+ Gin*(Vm-Ein)
Vm
Isyn
Isyn Vm
dynamic current clamp
patchpipette
To apply in vivo like input
DCNneuron
slice, 32 C
Dynamic current clamping of GP neuron
current versus conductance source
100 msec
- 40 mV
0.2 nA
5 mV
0 nAoutward
inward
Vm
Esyn
Isyn
Iexp
spike triggering events
1.0
input synchronization:
10 groups100 groups
50 ms
Input frequency
Input conductance
50 ms0.1 nA
0 nAoutward
inward
Isyn
Iexp
Input current
Small conductance K[Ca] current (Sk)
The effect of Sk block on synaptic integration
Space! The next frontier
Shunting by somatic conductance
Shunting by distributed conductance
Functional Implications
• synaptic conductance stabilizes Vm through shunting
• spikes can only be triggered from transients
• spikes reflect inputs correlated on the order of 1-10 ms
• spike rate reflects correlation as well as input rate
• inhibition has equal access to the control of spiking
More complexity to come
• gap junctions
• short term plasticity (history dependence)
• calcium signaling
•dendritic spike initiation
Acknowledgements
Contributors:
Volker Gauck
Svetlana Gurvich
Lisa Kreiner
Mayuri Maddi
Kelly Suter
Other Lab Members:
Alfonso Delgado-Reyes
Jesse Hanson
Chris Roland
Simon Peron
Current models of basal ganglia function determine spike rates based on simple summing of synaptic inputs
Normal Parkinson’s Disease
(Obeso et. al., Trends Neurosci 23(10):S8-S19, 2000)
DCN
from Paxinos & Watson, "The rat brain', Academic Press
Cerebellar cortex
deepcerebellar
nuclei
cerebellar cortex
mossy fibersclimbing fibers
!?
cerebellar circuit
-50 mV
20 mV
200 msec
The effect of synchronization
200 msec
100 independent inputs 10 independent inputs
spike timing precision
gain factor
spike frequency
synchronization highintermediatenone
0.5 1 2 4 8 16
2.5
2.0
1.5
1.0
0.5
0.5 1 2 4 8 16
0
20
40
60[%]
precision & rate
[rel.]
gain factor
200 msec
20 mV
spiking in vitro and in vivo
in vivo, awake (from LeDoux et al. 1998, Neuroscience, 86(2):533)
in vitro
500 msec 10 msectime scale for coding:
rate code temporal code
30,100 UC’s/s
inhibitory unitary conductance
Constructing in-vivo like synaptic input
100 ms
0.5
10 mV
0
Gex
Gin: 1 nS at gain 1
Esyn
- 40 mV
gmax: 2.1 pS - 69 pS gain 0.5 - gain 16
Shink and Smith, J. Comp. Neurol. 358: 119-141 (1995)
~100 m
100 m
Purkinje cell
• surface area: 261,000 m2
• number of synapses (ex/in): 175,000 / 5,000
• number of inputs / s 350,000 / 10,000
DCN neuron
• surface area: 11,056 m2
• number of synapses (ex/in): 5,000 / 15,000
• number of inputs / s 25,000 / 750,000
100 m
Cerebellar Stellate cell
• surface area: 2,305 m2
• number of synapses (ex/in): 1,000 / 100
• number of inputs / s 2,000 / 200
-70 mV = Eleak
