The availability of implantable subdural electrode arrays has made systematic studies of electrocorticographic (ECoG) coherence possible. Studies of coherence patterns recorded directly from human cortex are reviewed along with the presentation of original human clinical data, which reveal reliable and characteristic patterns of coherence. A data-driven technique for discriminating between reliable and unreliable coherence and phase values is described and used to reveal the relationship between coherence and cortical anatomy, such as in the region of the central sulcus, where low phase coherence declines and high phase-shifted coherence increases. Analysis of coherence magnitude and phase makes it possible to determine which signals likely arise from the cortical surface, and which arise from the depths of a sulcus. Alterations in coherence patterns caused by tumors or epilepsy are described and may be used to identify normal and pathological functional relationships between distant cortical areas. Some electrophysiologic/pathologic correlations indicate at least two types of epileptic abnormality, implying a sequence in breakdown of epileptic tissue. The relationship between coherence patterns and behavior and cognition is introduced and compared to similar studies of single-unit binding in animals.

The compartmental organization of visual cortical neurons was examined across species of primates by directly comparing the pattern of immunoreactivity for the 28-kD vitamin D-dependent calcium-binding protein (calbindin) in area 17 of squirrel monkeys, macaques, and neurologically normal adult humans. Area 17 of macaques and squirrel monkeys was similar in that somata and processes intensely immunoreactive for calbindin were present in the same layers (II-III, IVB, and V) and in both species formed a well-stained matrix that surrounded the CO-rich puffs in layer III. These intensely calbindin-immunoreactive neurons were identified as subpopulations of GABA-immunoreactive neurons. Among the most obvious differences in the two monkey species was the distribution of calbindin-positive elements outside of layer III: a dense immunostained matrix surrounded the puffs in layers II, IVB, V, and VI of squirrel monkeys but the immunostained neurons adopted no regular pattern outside layer III in macaques. In addition, although somata lightly immunoreactive for calbindin were present in both species, they were much more abundant in squirrel monkeys than macaques. The pattern of calbindin immunostaining in human area 17 resembled that of macaques in forming an intense matrix that surrounded puffs only in layer III, yet also resembled that of squirrel monkeys by including large numbers of lightly immunoreactive somata. These lightly immunostained somata included a very dense population forming a prominent band in layer IVA of human visual cortex. We conclude that for layer III of primary visual cortex, a similar pattern of neuronal chemistry exists across species of primates which is related to this layer's compartmental organization. Yet for other layers, the expression of calbindin immunoreactivity varies from one species to the next, perhaps reflecting variations in other neuronal properties.

Monospecific antibodies to glutamate were used to characterize the organization of excitatory neurons and the plasticity of glutamate expression in the macaque striate cortex. Somata and processes immunoreactive for glutamate were densely and unevenly distributed in layers II-III, IVA, IVC. In tangential sections through layers II and III, patches of intense glutamate immunostaining were observed and were found to coincide with regions of the cytochrome oxidase (CO)-rich puffs. By contrast, clusters of intense immunostaining were surrounded by the lightly immunostained but intensely CO-stained lattice in layer IVA. Similarly, in layer IVC, focal aggregates of intense glutamate immunoreactivity were interspersed among regions of light immunostaining but intense CO staining. Glutamate immunoreactivity was also intense in layer VI but was much lighter in layers I, IVB, and V. Throughout the striate cortex, neurons resembling pyramidal cells and spiny stellate cells and processes that included dendrites and axons were immunostained. None of the glutamate-positive neurons was GABA immunoreactive. Following monocular deprivation of adult monkeys by intravitreal injections of TTX into one eye, glutamate immunoreactivity in layers IVC was distributed in alternating intensely and lightly stained stripes. The stripes of reduced immunostaining, which contained an abnormally low concentration of glutamate neurons and pale neuropil, corresponded to columns dominated by the TTX-injected eye. Similar stripes of alternating intense and light immunoreactivity were seen in layers II-III, where they corresponded to rows of puffs at the centers of intact-eye and deprived-eye columns, respectively. These findings demonstrate that glutamate-immunoreactive neurons and terminals in monkey striate cortex are densely concentrated in layers receiving direct geniculocortical innervation. In addition, the glutamate neurons and terminals form discrete units, which in layers II and III coincide precisely with regions receiving geniculocortical terminations but in layers IVA are segregated from these terminations. The findings also indicate that glutamate immunoreactivity is regulated by visually driven activity, and suggest that monocular deprivation in adulthood leads to a reduction in the major excitatory neurotransmitter in visual cortex as well as previously indicated reductions in GABA, the major inhibitory neurotransmitter.

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Monocular deprivation produces an imbalance in visual drive from the two eyes, which in adult macaque V1 leads to marked changes in the neurochemistry of GABA interneurons. Such changes were further examined by studying immunoreactivity for calbindin, calretinin, and parvalbumin, three calcium-binding proteins that mark distinct subpopulations of GABA neurons, in macaques that had been monocularly deprived by intravitreal injection of tetrodotoxin. Deprivation for 5 d or longer produced a reversal in the normal pattern of calbindin immunostaining in layer III, from one in which intense neuronal immunostaining surrounded the cytochrome oxidase-rich puffs to one in which it occupied the puffs. Over the same period, calbindin immunostaining in other layers was reduced across the entire width of deprived-eye columns or extended into flanking regions of normal-eye columns. In contrast, reduction in parvalbumin immunostaining occurred only in deprived-eye columns and included only terminals with short periods of deprivation (up to 17 d) but both terminals and somata with longer periods. No change in calretinin immunoreactivity was observed. These findings demonstrate that GABA neurons of macaque V1 vary in their response to monocular deprivation according to their neurochemistry and position, suggesting that the weight of inputs from the two eyes and the intrinsic characteristics of each GABA population determine how a neuron responds to a change in visual input.