As mentioned above, it may not be possible to explain the P3b in tenns of one particular psychological process but an explanation in tenns of a more general physiological process, which is necessary or involved in a number of different psychological processes, may be required (e.g. Pineda et al., 1989). This latter suggestion is supported by reports of P300-like potentials, recordable with similar latency, in a number of different areas of human and animal brains, e.g. the cingulate gyms (Gabriel et al., 1983), suprasylvian and marginal gyri (O’Connor and Starr, 1985), hippocampus and amygdala (Halgren et al., 1980) and thalamus (Yingling and Hosobuchi, 1984). It is possible that a widely distributed neuronal system which synchronously acts on a number of areas of the brain may be involved in the generation or modulation of the P300 complex (this is consistent with the suggestion of Donchin and Coles (1988) that the P3b may be an index of information processing which may occur in a number of different stmctures concurrently).
One system showing the necessary anatomical, physiological and functional properties for the generation or modulation of the P300 complex appears to be that part of the noradrenergic system arising from the locus coemleus (see Foote et al., 1983 for review). The diversity of projections of the dorsal noradrenergic bundle arising from the locus coemleus suggests that it could have a modulatory effect on many different processes occurring at its tenninal regions. Stimulation of this part of the noradrenergic system has been found to decrease background activity relative to stimulus elicited activity in neurons of the auditory, visual and somatosensory cortex and has similar effects on hippocampal cells. Noradrenaline (NA) is therefore thought to increase the ’signal-to-noise ratio’ of infonnation entering the
46 respective brain region and so facilitate processing. It has been suggested that the
release of NA from the locus coemleus modulates the responsiveness of the ’ organism to biologically relevant events whilst in a waking state and particularly
whilst in a state of increased attentiveness (Aston-Jones et al., 1984; Foote and Morrison, 1987).
Pineda et al. (1989) found that lesioning of the locus coemleus and ascending noradrenergic pathways in the monkey led to a reduction in the amplitude of a scalp- recorded P300-like potential to rare tones (presented with a probability of 0.1 among
frequent tones of probability of 0.9) but had little effect on other components in the | wavefonn. This finding suggested that the integrity of the locus coemleus-
noradienergic system was necessary for the elicitation of the monkey P300-like potential. Lesioning of the locus coemleus and dorsal noradrenergic bundle would have also caused damage to other brain regions and systems making unequivocal interpretation of the results difficult. A subsequent study (Pineda et al., 1991)
provided further support for the role of the locus coemleus-noradrenergic system in ï generating P300-like potentials. Monkeys received injections of saline or clonidine 4 i (an alpha-2 adrenergic agonist which was thought to suppress locus coemleus ■ § activity at the 3 doses used). The P300-like potential elicited in the auditory oddball
task described above showed a dose-related decrease in amplitude in the clonidine
condition. Amplitude of the P300-like potential returned to normal levels in a post- î dmg testing session.
The results of the studies reported by Pineda suggest a critical role for the locus coemleus-noradrenergic system in the generation of P300-like potentials in the monkey but whether these results are generalisable to human P300 potentials is yet to be seen. A study on humans conducted by Clark et al. (1989) suggested that
noradrenaline and dopamine were involved in facilitation of the disengagement of attention which, as will be seen in section 1.28, bears similarities to the proposed functional significance of the P3a component in humans.
It is probably more realistic to think of NA as one of several neurotransmitters whose release is necessary for the occurrence of processing reflected by P300-like potentials. An example is provided by the study of Harrison et al. (1988) in which bilateral lesions of the septal nuclei in cats caused P300-like potentials to disappear. These lesions produced a marked depletion of acetylcholine (AChE) in the hippocampus. The results of the study suggested that the integrity of the septo- hippocampal cholinergic system was critical for the modulation of these potentials. Another study suggested the role of the serotonergic system in P300 generation (Ito et al., 1990). Ito et al, (1990) measured cerebral spinal fluid concentrations of the serotonin metabolite 5-hydroxyindoleacetic acid 5-HIAA and the dopamine metabolite homovanillic acid HVA in patients with Alzheimers dementia (DAT). ERPs were also recorded in the patients during a two stimulus auditory oddball task. The amplitude of the P300 elicited by the targets in the oddball task was significantly reduced and the latency prolonged in the patients compared with healthy age matched controls. P300 amplitude was significantly correlated with 5- HIAA concentration but not HVA concentration which led the authors to suggest that the serotonergic system was modulating the P300 component in these patients.
In summary, present knowledge does not give a clear indication of the role of neurotransmitter systems in the generation or modulation of the P300 complex. However, studies in animals suggest that the integrity of these systems appears necessary for the generation of P300-like potentials. This leaves open the possibility
48 that the P300 complex (or components of it) may be reflecting a facilitation of processing in certain brain regions rather than a specific psychological process.