paul at phy.ucsf.edu (Paul Bush) wrote:
>I don't have a good understanding of how the basal ganglia
>work. Basically, though, the striatum appears to be a lateral
>inhibitory network designed for filtering out input patterns
>(compromised in Huntinton's).
Maybe. The evidence for an effect of one spiny neuron on its
neighbors is lacking despite a good bit of effort to find it (see
Jaeger and Wilson in J. Neurophysiol last year). Many modellers have
incorporated the notion of lateral inhibition into their models of the
basal ganglia. In fact, a paper from my lab argued that this
circuitry gives rise to a form of working memory (Woodward et al. in
the Houk book). The best evidence for this to date comes from studies
of striatal interneurons (see stuff by Kita, Kawaguchi, Plenz).
Still, the jury's out on this one ...
>A projection from the dopaminergic
>midbrain perhaps provides a lower brain 'go' signal to inititate a
>process in frontal cortex (compromised in Parkinson's).
Probably not. Schultz has shown that da neurons fire to trigger
stimuli in simple tasks but when sensory events (conditional stimuli)
are added before the trigger cue, the da cells shift to the earlier
events. The exaxt role of the da signal is yet to be clarified.
Also, it should be pointed out that the standard bit about da and the
striatum is based on the rat. In primates, da neurons innervate all
areas of cortex (see paper from Kaas' lab last year in JCN).
>There is probably a role for the two separate patch and matrix
>systems. Interestingly, they receive input from different depths of
>cortical layer 5. This would correspond to different stages of
>prediction of the future in each cortical module.
This really only holds for the prefrontal cortex and its neighbors.
The inputs to patches by neurons in deep layers of other areas have
been shown to innervate the patches (Tony Kincaid had a great poster
on this two years ago at the SFN meeting), but, as I recall it, the
density of these projections and the extent of the source neurons are
considerably less than in, say, the prelimbic cortex in the rat.
Also, work in monkeys (from Graybiel's lab) has typically _not_ shown
any input to patches from somatosensory areas, e.g.,
Finally, once you learn the dorsal striatal anatomy and then move to
consider the ventral striatum everything becomes confused. The inputs
from the deep layers of the prelimbic area target appear to target
opposite regions in ventral striatum (_within_ calbindin compartments)
(see the work of Berendse and Groenewegen 1990-1992). At the same
time, the deep layer projections from infralimbic target other
patch-like structures in ventral striatum that I recently described
with 5'-nucleotidase histochemistry (in JCN), which, BTW, also stains
the patches in dorsal striatum. These points, I think, argue against
there being any simple patch/matrix partition that will hold for the
str as a whole.
(Things may have changed of late; the bg literature changes faster
than I can sometimes keep up with it. But this view was valid as of
>The basal ganglia assign processes to high level frontal cortex (attention)
>which has reciprocal relationships with the limbic cortex, which as
>described previously is the model the brain makes of itself -
>consciousness. In this way consciousness is integrated with perceptual state.
The best evidence for the role of the bg in the control of behavior
comes from studies of reaction-time performance. The effect of str
lesions of da depletions is to eliminate a process known as motor
readiness, responding faster with more time to prepare a response.
Carli et al. (1989) showed that the interpretation of a role of the bg
in motor preparation, and not attention, is valid. This has been
corroborated by Verity Brown and Trevor Robbins in several more recent
Just thought I'd put in my two cents worth.
Dept. of Physiology & Pharmacology
Bowman Gray School of Medicine
Wake Forest University
Winston-Salem, NC 27157
laubach at biogfx.neuro.wfu.edu