Abstract
The information from whiskers is processed in layer IV of the cortex by groups of
neurones arranged in discrete functional units known as barrels. Each barrel
processes input obtained from a single whisker. The barrel cortex can be
differentiated into the cytochrome rich barrel centres and the septal cells surrounding
the barrels. Previous work in the laboratory had established two cortical inputs to
striatum from the barrel cortex. One of these arises from septal cells and is bilateral
and composed of thin calibre fibres. The other route involves the barrel centres, is
only unilaterally represented and is composed of topographically arranged, thick
fibres. Based on these morphological differences, the postsynaptic targets of the two
pathways with reference to the two output pathways of the striatum were examined.
A method was also developed to examine the physiological consequences of
stimulation of the two pathways upon the striatal output cells of the anaesthetised rat
in both normal and dopamine-depleted animals. An anatomical study of the cortical
input to the GABAergic intemeurones was also undertaken as these cells strongly
modulate the output of striatal neurones.
The pathways differ in their connectivity, with the bilateral pathway
contacting the neurones of the striatopallidal pathway more often than the fibres of
the topographic system. The stimulation of the two pathways can depolarise striatal
cells and give rise to EPSPs, which can be differentiated based on their rise times.
EPSPs in response to whisker pad stimulation have a rapid rise time, while the
contralateral cortically derived EPSPs are slower to rise and the spike initiation
latency more variable. Both pathways interacted at the level of a single striatal cell
and gave rise to a summation of EPSPs at a time interval of 10ms, followed by a
period of inhibition, the extent of which was dependent on the order and source of
the stimuli. This pattern ofinteraction was not seen in cortical neurones. In dopamine
depleted animals both stimuli were also able to depolarise the spiny neurones to their
firing threshold. However the EPSPs to whisker pad stimulation were significantly
slower to rise compared to control animals and were similar to the rise times of
EPSPs in response to contralateral cortical stimulation. The interaction of the two
pathways was also affected by the loss of dopamine and the summation of EPSP
amplitude observed when stimuli were delivered 1 Oms apart in control animals was
no longer present. The anatomical study revealed that GABAergic intemeurones
receive convergent cortical input from both motor and sensory cortices and that their
pattern of innervation is different from the cortical innervation of striatal output
neurones
The results of this thesis suggest that the two inputs from the barrel cortex
differ in their physiological influence on striatal neurones, and that they might
convey different aspects of somatosensory information to the striatum. The changes
observed in dopamine-lesioned animals indicate that the topographic, ipsilateral
pathway is selectively affected by the loss of dopamine suggesting that dopaminedepletion does not have a generalized action that is independent of presynaptic or
postsynaptic origins. Rather its effects are specific to the neuronal subtype affected
as well to the origin of the synapses. The complex pattern of innervation of striatal
intemeurones suggests that these cells play a very important role in striatal
physiology and that their modulation by dopamine may serve as a possible
explanation for the effects seen after lesion in this study
