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Modulatory Influence of Auditory Cortex on the Activity of Medial Geniculate Body Neurons in Rat
R. Moucha1, J. Poeplar2, D. Suta2, M.P. Kilgard1, J. Syka2
1 School of Behavioral and Brain Sciences, University of Texas at Dallas, USA
2 Institute of Experimental Medicine ASCR, Prague, Czech Republic
ABSTRACT
Cortico-thalamic feedback projections greatly outnumber the ascending thalamo-cortical input
fibers, yet there is little understanding of the functional role of these connections. The purpose
of this study was to investigate cortico-thalamic modulation in the rat (Long-Evans strain)
auditory system. We examined the effects of electrical activation of the deep layers of the
auditory cortex on the responses of neurons located in the medial geniculate body (MGB).
Extracellular multiunit recordings were collected in the MGB with 16 channel multielectrodes
during simultaneous electrical stimulation of the auditory cortex (short train of monophasic
pulses, 12.5-200µA). Neuronal responses were evaluated and compared during acoustic
stimulation (AS) with broadband noise, electrical stimulation (ES) and paired acoustic and
electrical activation (AS+ES). Broadband noise evoked excitatory sustained activation with an
increased onset in the majority of MGB sites. This response was mostly suppressed after
AS+ES pairing when the delay between ES and AS was between 10 and 30ms and the
suppression declined at longer intervals. In most cases the suppression affected the late part of
the response.
ES alone evoked short latency excitation within 5ms and a longer lasting suppression of
spontaneous activity. In some neurons the suppression of spontaneous activity decreased over
repetitions of stimulation. At some MGB sites ES triggered late excitatory responses at
approximately 200 ms. The relationship between the location of electrical stimulation and its
effect on different parts of the MGB are also being examined.
This research was supported by GACR grant 309/04/1074.
AIM OF THE STUDY
To investigate the modulatory effects of
cortico-thalamic feedback projections
+
IV
V
VI
+
+
_
+
MGB receives extensive feedback from
cortical layer VI
These projection greatly outnumber the
ascending fibers from thalamus to the
cortex.
RTN
MGB
Direct cortical feedback projections to
MGB are excitatory.
An important question to answer is how this feedback
participates in the specific processing of sensory information
METHODS
Recording
electrode
ES
AS
||||
0
15
||||
30
80
//
800
time (ms)
delay
1-2 Tungsten stimulating electrode in A1
Michigan 16 ch recording electrode in MGB
Acoustic stimulus = Broadband Noise 50ms duration (AS)
Electrical stimulus = 4 monophasic pulses .33ms width, 500Hz (ES)
Stimulation = AS alone, AS+ES, ES alone
Current = 12.5, 25, 50, 100A , monopolar
Delay = 10, 30, 60, 90, 120, 180, 240ms
Peristimulus Recording = 400 ms
1set = 100 repeats of one stimulation per 800ms (0.8 Hz)
Tracts between 5-6 mm post to Bregma,  A1, @ 4000-5000 depth
Excitatory Effect of Cortical ES on Thalamic Responses
during ES alone (dotted) and ES+AS (solid)
Position of stimulating electrode in A1,
and MGB recording sites @ 4000  depths
p
D
V
A
ES+AS
ES
Time (ms)
el.
Excit. to
pulse
ES
Excit. to
AS
Recordings of thalamus action potentials
||||
ES
AS
30ms
ES elicits short latency (~3-4ms) excitatory responses in MGB
In 60% of the units recorded
MGB
Effect of Electrical Stimulation
Total recordings:
N = 10 rats, under ketamine anesthesia
Sites = 384 multiunit recordings from auditory responsive thalamic sites
Tracts = 24 (16 tracts in MGv, 5 tracts in MGd, 3 tracts in VPM)
Yield = 3-16 channels on each tract
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
Effect of Cortical BF of Stimulated Site
1.
Suppression in ch 1-12, BF’s < 7 kHz (cortical BF = 7 kHz)
2.
Less/no suppression in ch 13-16, BF’s > 7 kHz
3.
All channels are suppressed by ES alone
Ch/CF: 1/?, 2/?, 3/4, 4/3, 5/4, 6/5, 7/4, 8/5, 9/4, 10/6, 11/7, 12/6,
13/9, 14/12, 15/14, 16/15
Immediate Recovery from Suppression
Ch 9
Ch 13
Effect of Stimulating Current Intensity
AS
AS+ES_12.5 A
AS+ES_25 A
AS+ES_50 A
N = 48 sites
Late evoked excitation, “rebound” from strong inhibition
AS
AS+ES_25 A
AS+ES_50 A
In some units stronger ES currents in addition to increasing
suppression also evoked a late excitatory response
@ 200 ms from ES onset
Effect of Delay between ES and AS : 30, 90, 180 ms
180 ms
N = 64 sites
30ms
90ms
Responses to AS at increasing delays between AS and ES
Mean response of 16 channels from one MGB tract
Difference in mean spikes evoked over 70 ms from the response onset
Delay –30 ms indicates reversed order between ES and AS
(i.e. AS precedes ES by 30ms)
Types of MGB responses to AS, in 3 units from the same tract
Onset only (37%)
On + Off (15%)
Onset & sustained (48%
Stability over time: dotted line is response to AS (broadband noise 50ms) after 30 min, shifted
Raster plots of Responses from 3 units to 100 reps of AS, and AS+ES
PSTH’s of the Responses presented above during AS and AS+ES
Effect of Cortical Blockade by Muscimol on MGB Responses
Pre Musc
AS
AS+ES
Post 30 min
AS
AS+ES
No effect of ES during cortical inactivation
(i.e. no suppression of AS response during cortical stimulation under Muscimol)
•Late responses are abolished
•Response latency is increased
Pre Muscimol
Post 10 min
Post 30 min
Post 1hr
Post 2 hrs
CONCLUSIONS
• Electrical activation of A1 suppresses the response of
MGB neurons to subsequent acoustic stimuli delivered
within 30 ms after ES, and facilitates the responses at
delays greater than 90 ms.
• The magnitude of suppression increases with the
intensity of stimulating current
(more suppression if more current).
• There is no lasting effect of electrical stimulation,
MGB responses recover to baseline immediately after A1
stimulation stops.