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Custom VLSI Implementations of Neural Networks: Early Attempts
Custom VLSI Implementations of Neural Networks: Early Attempts
Early attempts
The idea of making custom analog VLSI implementations of neural networks
dates back to the late 80s - early 90s:
[Holler et al. 1989, Satyanarayana et al. 1992, Hammerstrom 1993, Vittoz 1996]
Giacomo Indiveri
Neuromorphic Cognitive Systems group
Institute of Neuroinformatics
University of Zurich and ETH Zurich
Full-custom analog
implementation
Communication - bandwidth
limited
Difficult to program
Current research
Technological progress
Application-specific focus
Power-dissipation/computational
power
G.Indiveri (NCS @ INI)
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Many VLSI models of spiking neurons have been developed in the past, and
many are still being actively investigated:
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Most designs can be traced back to one of two types of silicon neurons,
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Mixed analog/digital
Fully analog
Rate-based
Spiking
Real-time
Accelerated-time
Conductance-based
Integrate-and-Fire
Large-scale, event-based
networks
Small-scale, hard-wired
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MOSFETs in subthreshold
Vd
Ids
Vg
Vs
where
I0 denotes the nFET current-scaling parameter
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Vg
Vd
Ir
-3
-4
10
V
Vs
Ir
Qs
Ids =
Vd
Ids =
If
Qd
subthreshold
10
is equivalent to:
If
Vg
-2
10
I0 e
Ug UVs
T
If
I0 e
-5
U g Ud
T
10
T
-6
10
Ir
Ids (A)
Vs
above threshold
-7
10
-8
10
-9
10
-10
10
-11
10
-12
10
0.5
1.5
2.5
3.5
4.5
Vgs (V)
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Vd
Vs
Vg
Vg
I out
I in
Vin
Vb
Current-mirror
I out
M1
M2
Vd
Vd
Vs
Inverting amplifier
In traditional CMOS circuits, all n-FETs have the common bulk potential (Vb )
connected to Ground (Gnd), and all p-FETs have a common bulk potential
(typically) connected to the power supply rail (Vdd ).
The corresponding (complementary) equation for the p-FET is
Differential pair
I1
V1
Vin
I2
M2
Vout
Vbn
Ids = I0 e
p (Vdd Vg )/UT
(Vdd Vs )/UT
(Vdd Vd )/UT
I2 = I0 e
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I1
V1 Vs
V1
V2 Vs
M2
UT
Ib
Vbn
Vs
V2
M3
Vdd
Vdd
M4
M5
M1
V1
V2
x 10
e UT + e UT
V1
I2
M1
I1
M2
I1, I2 (A)
V1
e UT
V2
V1
UT
+e
V2
UT
V2
2UT
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0.2
0.1
0
V1V2 (V)
0.1
0.2
(V1 V2 )
Ib
2UT
is a tunable conductance.
0.3
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where
0.4
0
0.3
e UT + e UT
G.Indiveri (NCS @ INI)
Iout gm (V1 V2 )
0.2
e UT
V1
M3
Iout V
out
gm =
V1
I2 = Ib
Vb
Ib
0.6
V1
Iout = Ib tanh
Vout
I2
Vs
V2
0.8
I1 = Ib
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Vb
Iout
I1
I0
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I2
UT
Vb
UVs
M1
Ib = I1 + I2 = I0 e UT
e
V2
The differential-pair
I1 = I0 e
M3
Vs
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What is a synapse?
Electrical | Chemical
Excitatory | Inhibitory
Vmem
Depressing | Facilitating
Gl
Cmem
AMPA | NMDA
GABA
...
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Synaptic transmission
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FIG .
2.
2/
Na
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sion. Autoreceptors were proposed to control evoked transmitter release (see Starke et al. 1989, for a review). The
evidence for a physiological role in the ganglion seems to
R E S U L G.Indiveri
TS
greatest for the muscarinic autoreceptors, which are pos(NCS @ INI)
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tulated to mediate a negative feedback loop that reduces
Synaptic current at the sympathetic ganglionic neuron
transmitter mobilization (Koelle 1961; Koketsu and Yamada
I1
Iin2
I2
Ib
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IWi
Vi =
Vmem
IWi
Cmem
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Cmem
Vdd
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Vdd
Wi
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Vg
Vdd
Id
Vg(t)
Vc
Id =
d
C dt
Vc
Id (t ) = I0 e UT
(Vdd Vg (t ))
Id(t)
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Iw = I0 e
M
Csyn
I
Vw
Vsyn
I = I0 e
Msyn
Mw
Ic = C
Isyn
Iw
Vw
UT
, c ,
(Vdd V )
d
dt
UT
Isyn (t ) =
Csyn UT
Iw = I0 e UT
Csyn UT
, d ,
M
I
I
Vw
(Vdd Vsyn )
Isyn = I0 e
Mpre
Csyn
I = I0 e
Vsyn
Msyn
Mw
UT
Mpre
(t t )
I e+ ci
dt
(charge phase)
syn
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d
dt
d
Vsyn
Msyn
Iin
Vthr
Mthr
Isyn
Min
I = I0 e
Ic = C
UT
(Vdd V )
d
dt
(Vdd Vsyn )
Isyn = I0 e
d
dt
d
dt
Isyn + Isyn
+e
UT
Vthr
Iout (ti +t ) =
UT
(Vdd Vsyn )
Isyn =
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(Vw Vdd )
UT
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Iout
I 1 +
dt
Iout + Iout
Ig
Iin ,
Iout
Ig
Iin
if Iout Ig , Iw I
Isyn
d
dt
ti ti 1
t
t
Ig Iin
1 e + Iout (ti )e , Iout (ti ) = Iout (ti 1 +t )e
I
Ig Iin
t
e
e ( )d
Iout (t ) =
I
0
UT
UT
Vsyn
Iw Igain
:
Mean response to spike train of mean frequency
< Iout >=
Vsyn
UT
Vsyn
Iw
Mpre
UT dt
Csyn UT
, Iw0 = I0 e
UT
Iin = Iw
Mw
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Vw
Vsyn
Vw
I0 Iw0
UT
Isyn Iw
Isyn + Isyn =
Isyn + Isyn =
(Vdd Vsyn )
DPI equations
Iw = I0 e
Csyn
(Vdd Vsyn )
Isyn = Isyn
(t t + )
+ di
I e
dt
dt
Isyn = I0 e
(discharge phase)
n
c +d )
c
1
c f ct (
t
d
Isyn (t ) = I0 e
, with f =
, f<
t
c + d t
UT
Isyn
Iw
(Vdd Vsyn )
syn
(Vdd V )
Ic = C
(Vsyn Vw )
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Ig Iin
I
t , =
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t + ISI
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300
200
400
Vw=300mV
Vw=440mV
350
Vw=320mV
Vw=460mV
300
Vw=340mV
EPSC (nA)
150
100
250
200
150
100
50
50
0
0
0.05
0.1
Time (s)
0.15
0
0
0.5
1.5
2
2.5
Time (s)
3.5
100
80
60
40
20
0
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50
100
150
Input Frequency (Hz)
200
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Short-term depression
Va
Vgain
Va
Vw
M6
M1
M7
0.35
Id
Slow recovery
C2
Vx
0.3
M5
Ir
Vd
Ir
Cd
Vd
M2
C
Vpre
Vd=0.26 V
0.25 Update
Isyn
Vx (V)
EPSC (nA)
250
Vw=420mV
450
l
e
e
f
e
h
M4
Vd=0.28 V
Fast recovery
0.2
Vd=0.3 V
0.15
Vpre
e
n
M3
0.1
0.04
(a)
P,
V =1.30V
w
V =1.33V
w
V =1.35V
120
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0.06
0.08
0.1
0.12
Time (s)
0.14
0.16
(b)
Figure 1: Schematic for a depressing synapse circuit and responses to a regular input spike
(M. Boegerhausen, P. Suter, and S.-C. Liu 2003)
train. (a) Depressing synapse circuit. The voltage @A determines
the synaptic conductance
D
;
C
E
while the synaptic term
or B
is exponential in the voltage, @GF . The subcircuit
DC;E . The presynaptic
5 ( , 5IH , and 5K
J , control
consisting
of transistors,
G.Indiveri
(NCS @ INI)
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Tutorial the dynamics of B
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5
J
input goes to the gate terminal of
which acts like a switch. When there is a presynaptic
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Neurons . . . in a nutshell
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A quick tutorial
Complexity
Real Neurons
Conductance based models
Integrate and fire models
Rate based models
I
I
Sigmoidal units
Linear threshold units
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Equivalent Circuit
ENa
Glutammate
gNa
Vmem
Vmem
Gl
Cmem
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Cmem
EK
If excitatory input currents are relatively small, the neuron behaves exactly like
a first order low-pass filter.
Gl
gK
GABA
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Spike properties
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Refractory
Period
Refractory Period
Pulse Width
Iin=I2 > I1
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The first artificial neuron model was proposed in the 1943 by McCulloch and
Pitts. Hardware implementations of this model date almost back to the same
period.
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Sodium
Vdd
Vdd
Sodium Current
1V
Vm
+
VNa
Vthr
INaoff
+
GNaoff
[Ca]
INa
INaon
Vthr
ENa
Passive Leak
GNaon
Vm
[Ca]
Vmem
Vdd
Eleak
Vdd
Vmem
Gleak
Passive
+
VK
Potassium
Vthr
Cmem
IK
Vm
IK
GK
[Ca]
Potassium Current
EK
EK
I
50 ms
G.Indiveri (NCS @ INI)
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Positive Feedback
Input current
Membrane voltage
Vmem
Vmem
Vout
Vout
Vmem
Vout
Output voltage
Vout
time
Vpw
Reset
Slope = A
Vpw
Vmem
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Capacitive Divider
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Positive Feedback
C2
Q
Q = C1 V1 + C2 (V1 V2 ) = constant
C1 V1 + C2 (V1 V2 ) = 0
C2
C1 + C2
V1
Vmem
A
C1
V2
time
V2
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Vout
Vmem
Vout
Cm
Vpw
voltage
Cfb
V1 =
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Positive Feedback
Cfb
Vmem =
V
Cm + Cfb dd
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Cfb
Iin
Vmem
Gain
Vmem
Vout
Vout
Cm
tH
tL
time
Ir
Vpw
tL =
Cfb + Cm
Iin
Vmem =
Frequency Iin
G.Indiveri (NCS @ INI)
Cfb
Iin
Vdd
tH =
Cfb + Cm
Ir Iin
Vmem =
Cfb
Ir Iin
Vdd
Power Dissipation
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Conductance-based models
Integrate and Fire vs Hodgkin-Huxley
BUT
it has a major drawback: power consumption
During the time when an inverter switches, a large amount
of current flows from Vdd to Gnd.
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Conductance-based (R-C)
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Conductance-based models
Adaptation
But recently proposed models bridge the gap between the two:
M11
M5
Iin
Vahp
Vrest
Vthr
M1
DPI
M7
M12
M6
Ifb
M8
Cmem
Leak
M9
M15
M19
M16
M20
Vspk
Imem
M22
Iahp
Vtau
M18
Vmem
M3
M2
Vthr_ahp
M14
Cahp
M10
M4
M17
DPI
Vtau_ahp
Vrf
M21
M13
RefractoryPeriod
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Generalized Integrate and Fire models can account for a very large set of
DPI
neuron sub-threshold equations
d
M5
Vahp
dt
M11
Cmem
M12
+ F (umem )
M18
M2
Vthr_ahp
M1
M6
Vmem
M3
Cmem
Imem
Vtau
M9
M4
M15
M19
M16
M20
15
Vspk
Vthr=0.325 V
Vthr=0.350 V
Vthr=0.375 V
14
12
10
M22
Iahp
Leak
20
Ifb
M8
M7
DPI
Cahp
M10
Vrf
M17
Vtau_ahp
M21
Imem (A)
Vrest
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PositiveFeedback
in
M14
M13
10
Imem (A)
Iin
umem =
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SPICE simulations
8
6
4
RefractoryPeriod
d
dt
Imem + Imem
1
I
I0+1 , ,
Ig Iin
I
0
2
+ (Imem )
6
Time (ms)
10
20
40
60
Time (ms)
80
100
2 + 1
+1
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Experimental results
Experimental results
Single spike
Population activity
2.8
Vthr= 0.0V
V = 0.3V
Voltage (V)
2.7
Vthr= 0.6V
2.6
Vthr= 0.9V
Neurons
thr
2.5
30
30
25
25
20
20
15
15
10
10
0.5
1.5
0.5
1.5
0.5
1
Time (s)
1.5
2.4
2.3
Neurons
2.2
2.1
2
1.9
0.01
G.Indiveri (NCS @ INI)
0.02
0.03
Time (s)
0.04
0.05
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30
30
25
25
20
20
15
15
10
10
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0.5
1
Time (s)
1.5
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Vmem (V)
0.8
0.6
0.4
Encode
Decode
0.2
0
0
0.05
0.1
Time (s)
0.15
0.2
1
2
3
Inputs
1
2
3
12
Outputs
Source
Chip
Destination
Chip
Address-Event
representation of
action potential
Winner-Take-All architectures
Spike-based plasticity mechanisms
Action Potential
G.Indiveri (NCS @ INI)
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15
10
5
0
180
120
60
60
120
180
AMS 0.35 m
3.9mm 2.5mm
128
28 128
4 128
32 128 | . . . | 1 4096
Technology:
Size:
Neurons:
AER plastic synapses:
AER non-plastic synapses
Dendritic tree multiplexer:
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Summary
Vg
Ir
Ir
M11
M5
Vahp
Vrest
Vthr
M2
M1
DPI
Vthr_ahp
M7
M6
M9
M4
V4/PIT
V4
V1
V1
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769
http://ncs.ethz.ch/
Vd
If
Qd
M18
M15
Cmem
Leak
IT
Ifb
M8
Imem
M19
Vspk
M16
M20
M22
Iahp
Vtau
AIT
M14
M12
Vmem
M3
Ident.
PositiveFeedback
Adaptation
Iin
Qs
Categ.
If
Vg
Vs
AER INPUT Y
PFC
Vd
Vs
communication
AER OUTPUT
which several models have been suggested24; see also review in this
issue by Abbott and Regehr, page 796), since it depends only on
passive experience of the visual inputs. However, the weights of the
combination (see Fig. 3) depend on learning the task and require at
least some feedback (see Box 2).
Thus, generalization in the brain can emerge from the linear combination of neurons tuned to an optimal stimulus effectively
defined by multiple dimensions25,23,26. This is a powerful extension of
Analog
processing, asynchronous
digital
the older computation-through-memory
models of vision
and
motor control. The question now is whether the available evidence
supports the existence of a similar architecture underlying generalization in domains other than vision.
AER INPUT X
239
20
M17
DPI
Cahp
M10
Vtau_ahp
Vrf
M21
M13
RefractoryPeriod
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