Regional brain activity during shape recognition impaired by a scopolamine challenge to encoding.

In the present positron emission tomography (PET) study, we examine the effect of a scopolamine-induced challenge to encoding upon the pattern of regional cerebral blood flow during recognition of a list of abstract visual shapes 3 days after encoding of these shapes. This study was conducted to test hypotheses concerning the fusiform and thalamic contributions to object recognition arising from a previous imaging study of impaired recognition. In that study, we demonstrated that activity in the fusiform cortex and the thalamus during shape recognition was modulated by memory challenges. These memory challenges included, on one hand, impaired storage as a consequence of diazepam administration during encoding, and, on the other hand, impaired retrieval caused by a perceptual challenge. Activation in the fusiform cortex decreased during impaired recognition, irrespective of the type of challenge. In contrast, thalamic activation increased only when the recognition deficit resulted from impaired memory storage. Based on these results, we hypothesized that fusiform activation during recognition reflects the matching of an incoming stimulus with a stored one, whereas thalamic activation reflects retrieval attempts. These hypotheses would receive considerable support if scopolamine, which also impairs memory storage, induced similar modulations of fusiform and thalamic activation. In the present study, we observed that a scopolamine challenge to encoding does indeed modulate the activity in the very same regions that were previously modulated by a diazepam challenge. Hence, a similar memory deficit, although primarily effected through different neurochemical pathways, was paralleled by a similar modulation of activity in the same set of nodes in the shape recognition network. In the fusiform cortex, scopolamine decreased recognition-related activity, as did the sensory challenge of retrieval. Furthermore, covariate analysis demonstrated that the level of fusiform activity linearly correlates with behavioural performance. In the thalamus, activation increased following impaired encoding. This is in accordance with the idea that enhanced thalamic activity reflects increased effort expended in retrieval. In addition, in the intraparietal sulcus, differential activation also increased following impaired memory storage, possibly reflecting enhanced visuospatial attention in an effort to compensate for impaired performance.

The kinetic occipital region in human visual cortex.

In the present study we showed that the kinetic occipital (KO) region, located laterally in occipital cortex approximately 20 mm behind human MT/V5, can be strongly and bilaterally activated under passive viewing conditions. We used continuous, randomly changing visual stimulation to compare kinetic gratings to uniform motion and kinetic gratings to luminance defined gratings. The KO activations under these passive conditions are stronger than those observed when the two types of gratings are compared under active conditions, i.e. while subjects perform a task (counting gratings of a given orientation). Region KO was shown to process both shape and motion information, the conjunction of which is typically present in kinetic contours. Area MT/V5 also processes these two aspects of visual stimulation but favors motion signals. Clear segregation of shape and motion processing was observed only in occipitotemporal and parietal regions respectively. Although neurons with properties similar to those derived from the conditions activating the KO region have been documented in the macaque monkey, their location seems inappropriate for them to correspond to the KO activation observed in humans.

Effect of sensory deafferentation on immunoreactivity of GABAergic cells and on GABA receptors in the adult cat visual cortex.

To investigate the effects of sensory deafferentation on the cortical GABAergic circuitry in adult cats, glutamic acid decarboxylase (GAD) and gamma-aminobutyric acid (GABA) immunoreactivity and GABA receptor binding were studied in the visual cortex of normal cats and compared with cats that had received restricted binocular central lesions of the retina and had survived for 2 weeks postlesion in a normal visual environment. In the visual cortex of lesioned cats, two changes were observed in the number of GAD-immunoreactive elements in the regions affected by the retinal lesions: the number of GAD-positive puncta decreased, whereas that of GAD-immunoreactive somata increased. In contrast, no detectable changes were measured in the number of GABA-immunopositive somata or puncta. At the receptor level, we observed no differences in either the laminar distribution or the affinity of cortical GABAA and GABAB receptors labeled with [3H]-muscimol and [3H]-baclofen, respectively, in the lesioned versus normal cats. We present the hypothesis that sensory deafferentation in these adult cats (1) leads to a reduction of cortical GABAergic inhibition in the deafferented region, and (2) that this decreased inhibition may permit changes in efficiency of synapses and (3) that these changes may represent a first stage of events underlying the retinotopic reorganization preceeding the structural changes.

Laminar distribution of NMDA receptors in cat and monkey visual cortex visualized by [3H]-MK-801 binding.

Glutamate is the major excitatory neurotransmitter of the mammalian central nervous system. Two major classes of glutamate receptors have been reported. The actions of glutamate on its N-methyl-D-aspartate (NMDA)-type receptor may underlie developmental and adult plasticity as well as neurotoxicity. The NMDA-type of glutamate receptor in cat and monkey visual cortex was visualized by means of in vitro receptor autoradiography with the noncompetitive NMDA-receptor antagonist [3H]-MK-801. The kinetics, performed on tissue sections, revealed an apparently single, saturable site with an approximate dissociation constant (KD) of 18.5 nM in cat and 15.9 nM in monkey visual cortex. Autoradiography, performed on frontal sections of cat and monkey visual cortex, revealed a heterogeneous laminar distribution of NMDA receptors. Cat areas 17, 18, 19, and the lateral suprasylvian areas exhibited a similar NMDA-receptor distribution. In these areas, NMDA receptors were most prominent in layer II and the upper part of layer III. In monkey striate cortex, NMDA receptors were primarily concentrated in layers II, upper III, IVc, V, and VI. In monkey secondary visual cortex, [3H]-MK-801 labeling was most prominent in layers II, V, and VI; whereas in the temporal visual areas included in this study layer II displayed the heaviest receptor labeling. In neither cat nor monkey could we observe significant differences in NMDA-receptor distribution between different retinotopic subdivisions within a single visual area. Neither did we detect any periodic changes in NMDA-receptor distribution that would correspond to the compartments defined by cytochrome-oxidase in monkey V1 and V2.

Distribution of somatostatin receptors in the cat and monkey visual cortex demonstrated by in vitro receptor autoradiography.

Somatostatin (SRIF, S14) receptors in the cat and monkey visual cortex were visualized by means of in vitro autoradiography with an iodinated agonist of SRIF, [125I-Tyr0,DTrp8]S14. The kinetics, performed on tissue sections, revealed an apparently single, saturable site (KD = 3.92 +/- 0.31 10(-10) M for the cat, and 3.82 +/- 0.28 10(-10) M for the monkey visual cortex) with pharmacological specificity for S14 and [DTrp]-substituted S14. Autoradiography, performed on frontal sections of the cat and monkey visual cortex, revealed a heterogeneous regional and laminar distribution of SRIF receptors. In cat areas 17, 18, and 19, SRIF receptors occur mainly in the supragranular layers, although small interareal and intra-areal differences are observed. The infragranular layers (V-VI) in area 19 contain a significantly higher proportion of SRIF receptors compared to both areas 17 and 18. In the antero- (AMLS) and posteromedial lateral suprasylvian area (PMLS), layers V and VI contain the highest proportion of SRIF receptors. This latter pattern is also observed in the area prostriata medially adjoining area 17 in the splenial sulcus. In the monkey visual cortex, areas 17 and 18 exhibit similar distribution patterns, SRIF receptors being primarily concentrated in layers V and VI. Neither in the cat nor the monkey visual cortex could we observe significant differences in SRIF receptor distribution between different retinotopic subdivisions within one area.

Laminar and regional distribution of galanin binding sites in cat and monkey visual cortex determined by in vitro receptor autoradiography.

The distribution of galanin (GAL) binding sites in the visual cortex of cat and monkey was determined by autoradiographic visualization of [125I]-GAL binding to tissue sections. Binding conditions were optimized and, as a result, the binding was saturable and specific. In cat visual cortex, GAL binding sites were concentrated in layers I, IVc, V, and VI. Areas 17, 18, and 19 exhibited a similar distribution pattern. In monkey primary visual cortex, the highest density of GAL binding sites was observed in layers II/III, lower IVc, and upper V. Layers IVA and VI contained moderate numbers of GAL binding sites, while layer I and the remaining parts of layer IV displayed the lowest density. In monkey secondary visual cortex, GAL binding sites were mainly concentrated in layers V-VI. Layer IV exhibited a moderate density, while the supragranular layers contained the lowest proportion of GAL binding sites. In both cat and monkey, we found little difference between regions subserving central and those subserving peripheral vision. Similarities in the distribution of GAL and acetylcholine binding sites are discussed.

Regional distribution of binding sites for neuropeptide Y in cat and monkey visual cortex determined by in vitro receptor autoradiography.

The goal of this study was to elucidate the precise regional and laminar distribution of neuropeptide Y (NPY) binding sites in feline and primate visual cortex. By means of in vitro receptor autoradiography, NPY binding sites in primate and feline visual cortex were specifically labeled with 3H-NPY. In cat area 17, the highest density of NPY-binding sites was present in lamina I and the upper half of lamina II. The density then gradually decreased towards lamina VI. Areas 18 and 19 exhibited a similar binding site-density profile. The decrease in density from superficial to deep layers was more gradual in area 18 than in areas 17 and 19. In monkey primary visual cortex (V1), layer IVc presented a high concentration of NPY binding sites, in addition to a dense zone of binding sites in layer I. Monkey secondary visual cortex (V2) displays a similar dense zone in layer I, but lacks such high density of NPY binding sites in layer IV. Therefore, the border between primary and secondary visual cortex coincides with the abrupt disappearance of this latter high density in layer IV. In cat as well as in monkey visual cortex, no significant differences were found between regions representing central vision and those representing the peripheral parts of the visual field. Comparison of our results for NPY binding sites with the distribution of alpha 1-adrenergic receptors, as recently described by Rakic et al. (J. Neurosci. 8(10):3670-3690, 1988) for primate and Parkinson et al. (Brain Res. 457:70-78, 1988) for feline visual cortex, revealed that those two patterns are very similar.