C. Vahlehinz et al., AMINO-ACIDS MODIFY THALAMOCORTICAL RESPONSE TRANSFORMATION EXPRESSED BY NEURONS OF THE VENTROBASAL COMPLEX, Brain research, 637(1-2), 1994, pp. 139-155
The hypothesis has been tested that inhibitory mechanisms, active spat
ially and temporally between the input and the output of thalamic neur
ons, determine the nature of the information transmitted to the cerebr
al cortex. To enable this assessment, in barbiturate-anesthetized cats
and urethane-anesthetized rats juxtacellular recordings were performe
d together with microiontophoretic ejection of transmitter agonists an
d antagonists. The effects of these drugs were studied on responses ev
oked by mechanical stimulation of cutaneous receptive fields (RFs) of
neurons in the thalamic ventrobasal complex (VB). Neurons from differe
nt parts of the VB were investigated: 29 units were located medially,
in the ventral posteromedial nucleus (VPM; facial RFs), and 11 units w
ere located laterally, in the ventral posterolateral nucleus (VPL; for
epaw and body RFs). A further eleven VB units had no detectable RF. Tw
enty-six neurons were tested with electrical stimulation of the somato
sensory cortex (SI), 17 of these being identified as thalamo-cortical
relay neurons and 5 being classified as presumed interneurons; the rem
aining 4 could not be activated. Four additional recordings were from
trigemino-thalamic or thalamo-cortical fibers. For the quantitative as
sessment of the neurons' input and output, neuronal activity was induc
ed by feedback-controlled, mechanical trapezoidal and/or sinusoidal st
imuli applied to sinus hairs, fur or skin and the numbers of prepotent
ials and soma spikes were compared in peristimulus time histograms (PS
THs) generated simultaneously for both types of signal from 'DC' recor
dings. Iontophoretic administration of excitatory amino acids (EAAs) o
r bicuculline methiodide (BMI) increased output-input ratios in 87% of
the cases tested, due to a higher rate of conversion of prepotentials
into soma spikes taking place. In cases of neurons exhibiting a susta
ined-to-transient response pattern, changes to sustained-to-sustained
patterns were demonstrated. Tests with gammaaminobutyric acid (GABA) p
roduced decreased output-input ratios in 90% of the neurons, due to a
lower conversion rate of prepotentials into soma spikes taking place.
In cases of neurons exhibiting high output-input ratios (sustained-to-
sustained type), the responses changed to the sustained-to-transient p
attern. For cortically evoked antidromic spikes of VB neurons, GABA pr
oduced a failure of the initial segment (IS-) spike to invade the soma
, whereas BMI and glutamate (Glu) facilitated soma depolarization. Whe
n ejected with relatively higher currents than those needed to alter o
utput-input ratios, EAAs decreased prepotential amplitudes while GABA
produced increases in 16 of 18 neurons. Concurrent administration of b
oth types (excitatory and inhibitory) of amino acid yielded enhanced s
oma spike activity due to Glu, concomitant with the enlarged prepotent
ial amplitude caused by GABA. Tetrodotoxin (TTX) reversibly abolished
soma spikes in 9 of 11 cases (but not fiber spikes). EAA antagonists e
xerted no effect upon output-input ratios or upon synaptic transmissio
n. Glu and BMI both shortened the conversion time between prepotential
and soma spike and increased the spike discharge rate. Whereas BMI di
d so in a stimulus- and input-related manner, high doses of Glu caused
a continuous ongoing discharge until all spike activity stopped due t
o depolarization block. The results suggest that the output of thalami
c VB neurons is controlled by GABA-mediated inhibitory processes, like
ly operating at the initial segment of the axon. This holds for thalam
o-cortical relay neurons and presumed thalamic interneurons. Two proce
sses appear to be in action: an intrinsic mechanism that operates toni
cally in VB to generally constrain the output of naturally-driven neur
ons, and a second mechanism that influences the strength of this GABA-
mediated inhibition, thereby generating changes in the response repert
oire of the neurons. This process appears to be to a large extent unde
r the control of inputs from the neurons' peripheral receptive field.