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Cholecystokinin octapeptide (CCK-8) and vasoactive intestinal peptide (VIP) have been shown to be antagonistic in various parameters in the rat in our previous studies. In the present investigation the effects of CCK-8 and VIP on spontaneous motility and rearing activity were observed in sham-operated and neofrontal decorticated rats. The results indicate that VIP antagonizes the effects of CCK-8 on spontaneous motility and rearing, and the effects are more apparent in the decorticated rats. It was suggested that CCK-8 affects presynaptic dopaminergic systems, while VIP is likely to stimulate post-synaptic dopaminergic mechanisms.
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Striatal and cortical extracellular acetylcholine (ACh) and choline (Ch) levels were determined in samples collected under in vivo conditions using microdialysis in normal (naive) and decorticated rats treated with saline or the monoganglioside GM1. ACh and Ch were assayed using a sensitive high performance liquid chromatography technique coupled to a postcolumn reactor with immobilized enzymes. Picomole amounts of ACh could be measured in the presence of an acetylcholinesterase inhibitor (neostigmine) in the microdialysis perfusion medium (striatal ACh = 0.2-0.4 microM; cortical ACh = 0.03-0.04 microM). Ch was detected both in the presence and in the absence of neostigmine (striatal Ch = 0.5-0.6 microM; cortical Ch = 0.6-2 microM). ACh, but not Ch, was strongly stimulated by 100 mM of KCl included in the perfusion medium. Decortication produced by devascularization did not significantly modify the cortical or striatal basal levels of ACh. However, in the cortex, KCl produced a higher ACh stimulation in the GM1-treated than in the saline-treated decorticated or naive rats. The present results indicate that GM1-treatment increases the ability of cortical cholinergic terminals to release ACh and support the idea that trophic factors such as monoganglioside GM1 can promote recovery following injuries of the central nervous system.
Sexually experienced or naive male rats, subjected to neocortex removal or neocortex plus hippocampus removal, were paired with female rats for up to 180 days and compared with control rats with respect to success and latency to impregnate the female. All of the control rats and half of the brain-damaged rats successfully impregnated female rats at least once. Success was not correlated with lesion type or presurgical experience. The brain-damaged rats took longer to impregnate the females than control rats. Since the ablations were extensive, more than 95% of the neocortex in many rats, the study shows that decorticate rats can copulate. Presumably the intact subcortical structures are sufficient for male copulation, but cortical structures in some way facilitate rapid female impregnation.
The present study shows a novel administration form of the monoganglioside GM1, which following microencapsulation in human serum albumin was topically applied on cortical regions damaged by devascularization in rats. The effects of microencapsulated GM1 on extracellular levels of acetylcholine, choline and dopamine in the cortex and in the striatum were analyzed using in vivo microdialysis. Cholinergic neurons in the nucleus basalis magnocellularis were studied immunohistochemically using monoclonal antibodies raised against choline acetyltransferase (ChAT). It was found that cortical devascularizing lesions produced a decrease in extracellular levels of cortical acetylcholine and choline, and retrograde morphological changes in cholinergic neurons in the nucleus basalis magnocellularis. GM1 promoted (1) recovery of the retrograde morphological changes produced by the decortication in the nucleus basalis magnocellularis and (2) a parallel increase in cortical acetylcholine release. No changes were observed in the striatum, nor on cortical or striatal dopamine levels simultaneously measured in the same perfusates.
Normal rats and rats with 98.8% (S.D. +/- 1.4) of neocortex surgically removed were trained in a two-choice discrimination apparatus for food reward. The animals were first trained to run the apparatus with identical non-patterned goal box doors followed by discrimination and reversal training using horizontal and vertical striped panels attached to the doors. These patterned stimuli were matched for total luminous flux and contour length and control procedures were included for unintended discriminative cues from other sensory modalities. The two groups did not differ in the number of trials taken to complete preliminary training but the decorticates were significantly faster at running the apparatus than the normals. All animals solved the visual discrimination and were able to reverse it. There were no significant differences between the groups in trials taken to acquire the visual discrimination except at the very highest criterion levels employed, though reversal of the discrimination was more difficult for the lesioned group. The preliminary training data are taken as further evidence that total decortication does not necessarily impair instrumental performance for food reward and that this lesion does not introduce any limiting sensory or motor deficit in the alleyway situation. It would also appear that neocortex is not essential for the solution of a horizontal/vertical stripe problem. It is not clear, however, that such a solution necessarily depends on a true pattern discrimination, and both lesioned and normal animals may have been employing strategies based on local cues within the two patterned stimuli. The appropriateness of the total decorticate preparation for a resolution of the problem of cortical vs subcortical substrates of residual vision following visual cortex lesions is discussed. The possibility that undamaged neocortical tissue remaining after visual cortex lesions may inhibit the full expression of residual subcortical function is raised by these data.
The brain weights, cross-sectional areas of subcortical structures, gross morphology, and retrograde degeneration in the thalamus and basal ganglia were compared in rats with neonatal (1 or 5 days of age) or adult ablation of all of the neocortex. Neonatal decorticate and control rats also were given injections of fluorescent retrograde tracers. True blue or Nuclear yellow into the striatum, hippocampus, or subiculum in order to identify afferent pathways to these structures. Neonatal decortication resulted in morphological changes that included a dramatically shrunken and misshapen thalamus, a shrunken brainstem, distortion of the hippocampal structure and abnormal growth of the subiculum, none of which were observed following adult decortication. There was a complete absence of gliosis and calcification in the 1-day decorticates that was present in 5-day and adult decorticates. Although most striatal and hippocampal afferents from subcortical structures were present, label was not found in the ventral tegmental area or thalamus after True blue injections into the striatum and hippocampus, respectively. Acetylcholinesterase staining showed the normal striatal patchy organization. The absence of evidence for the development of new pathways or the reorganization of existing pathways is consistent with previous behavioral studies showing little sparing of function after neonatal decortication. The results suggest that the cortex plays little role in programming pattern formation and connections in subcortical structures and that cortical and subcortical structures provide unique contributions to the control of behavior.
Rabbits were trained on a Pavlovian conditioned inhibition (CI) task using light as the reinforced conditional stimulus (CS) and the same light compounded with a tone as the non-reinforced CS. The conditional response was the nictitating membrane response (NMR). The subjects then received an extensive neocortical lesion or a sham operation. After 9 weeks postoperative recovery, the animals were retrained on the CI task. Sham operated control animals showed immediate and high levels of CI retention but the decorticates showed a profound initial loss, showing that there is a cortical influence in CI. Reacquisition of CI by the decorticates was rapid and showed considerable savings over de novo acquisition. This supports our earlier finding that the neocortex is not essential for the acquisition of CI.
The study shows that although many features of copulation in decorticate male rats are normal, copulatory success is importantly dependent upon the control of approaches exerted by the normal female rat. Copulation by neonatally decorticated adult rats and normal adult rats was studied in cohabitation and videotaped tests. Seven of 10 decorticate rats and 6 of 6 normal rats sired pups in the cohabitation test. When initially paired with ovariectomized and primed female rats, in the videotaped tests, all normal rats, but only one decorticated rat, copulated. All decorticate rats made movements indicative of sexual interest including: treading on the female's back, passing over the female, and sniffing the female's genitals. After activating stimulation, 5 of 6 remaining decorticated males copulated. After one successful mount the remaining copulatory patterns proceeded relatively normally. Numbers of mounts, intromissions, ejaculations, postejaculatory songs, and the intromission and ejaculatory patterns were like those of control rats, although the decorticate rats had fewer mount bouts and showed abnormalities in the execution of movements. Precopulatory movements were notated, using the Eshkol-Wachmann system, and compared with copulatory movements. Non-copulatory and copulatory approaches were similar, except that clasping appeared to be the key movement involved in the transition of an approach movement into a copulatory movement. The analysis also showed that the females' movements of hopping, turning, and kicking were important for regulating the males' approaches, and were instrumental in the success achieved by the decorticated males. The study shows that although the cortex, insofar as it facilitates the appearance of certain movements and contributes to their efficiency, is involved in male sexual activity, in its absence well organized sexual activity is possible, although this is dependent, in part, upon the behaviour of the female.
The effects of substantia nigra (SN) stimulation on the activity of the nucleus ventralis lateralis of the thalamus (VL) have been studied. The VL cells were identified as relay or non-relay cells among the cerebellothalamocortical pathway on the basis of orthodromical activation from the cerebellum and antidromical activation from the cortex. Certain experiments were performed after wide pericruciate decortication in order to eliminate the response due to unavoidable activation of corticofugal fibers. These results show that nigrothalamic neurons exert an inhibitory effect on VL cells. This inhibition was observed on the relay as well as on non-relay cells and was strong enought to suppress the cerebellar monosynaptic excitatory input. Thus the SN can modulate the information running along the cerebellothalamocortical pathway. The topographic localization of inhibited cells suggests that the SN controls the activity of the thalamic neurons which interfere with axial and proximal musculature.
With the onset of puberty, play fighting in rats decreases in frequency and the tactics of attack and defense that are used are rougher. Previous studies have shown that the changes in the frequency of play and in the use of defensive tactics arise independently of social experience. Furthermore, while the former involves subcortical regulation, the latter depends on cortical mechanisms. In this study, the possible mechanisms regulating the developmental changes in the tactics of attack were examined. Two experiments were conducted using male rats. In the first study, rats reared in isolation from weaning were compared to rats reared in pairs, and were tested in the juvenile and early post-pubertal phases (30 and 60 days postnatally). In the second experiment, rats with their cortex removed shortly after birth were compared to sham-treated controls, and were tested in pairs at both the juvenile and early adult phases (30 and 90 days). Two measures of 'roughness,' derived from previous studies, were measured. Results showed that isolation-reared rats had the typical age-related changes in roughness of attack, whereas decorticated rats failed to show this age-related modulation, maintaining, or even exaggerating, the juvenile-typical pattern of attack. These findings suggest that social experience is not needed for this developmental change to occur, and that an intact cortex is needed to regulate this change in behavior.
Using immunohistochemical techniques we have analysed the occurrence of cholecystokinin-like immunoreactivity (CCK-LI) in the cortex and striatum of the rat. In the cortex few CCK-immunoreactive cell bodies, mainly interneurons, could be visualized in normal brains, and a moderately dense network of CCK fibres was also observed. Injections of colchicine into the striatum led to an accumulation, in the surrounding cortex, of CCK-LI in the initial segment of the axon of numerous cells. In addition, with an antibody to pro-CCK several cell bodies, many of which with pyramidal shape, could be visualized. Furthermore, retrograde staining of cortical cells after unilateral injection of wheat germ agglutinin into the striatum revealed bilaterally in the cortex a number of labelled cells that also contained pro-CCK-LI. In the striatum CCK-LI was diffusely distributed in fine fibres as well as in patches of fibres located in the medial aspects. After decortication followed by callosotomy these patches disappeared on the side ipsilateral to the lesion, while the pattern of immunoreactivity of several other peptides in the striatum was unaffected. No change was observed on the contralateral side. Decortication or callosotomy alone did not affect the pattern of CCK-LI. At the ultrastructural level several CCK-immunoreactive terminals could be observed, mostly with clear, densely packed vesicles and straight asymmetric synaptic contacts with small spines, characteristic for terminals of cortical origin. The results are consistent with the presence of a major, partly crossed, CCK-containing cortico-striatal pathway.
In mice, prior destruction of striatal 5-hydroxytryptamine (5-HT) neurons by intrastriatal or intraventricular injections of 5,7-dihydroxytryptamine did not abolish or attenuate DA depletions produced in striatum by 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP). This suggests that although they contain monoamine oxidase type B, the oxidative conversion of MPTP to 1-methyl-4-phenyl-pyridinium ion (MPP+) does not take place in 5-HT neurons. Likewise, decortication and kainic acid lesions did not prevent or enhance striatal MPTP-induced DA decrements suggesting that corticostriatal projections and striatal neurons are not involved in the mechanisms of MPTP neurotoxicity.
Experiments were conducted to determine whether rats having unilateral or bilateral ablation of either the neocortex or telencephalon can learn to escape from a tank of water by climbing a platform. Hemi- or bilaterally decorticated rats were able to learn the swimming escape task, the same being observed for hemidetelencephalated rats. Fully detelencephalated rats, however, did not exhibit this capability. These results show that integrity of one of the cerebral hemispheres is necessary in order to allow swimming escape learning.
Rabbits with substantial neocortical lesions were given trace conditioning of the nictitating membrane response over a range of interstimulus intervals (ISIs). Unlike hippocampal lesioned animals, which show deficits in such conditioning, the decorticates were not impaired and they gave greater numbers of conditioned responses at longer ISIs than did sham-operated controls. These results suggest that a neocortical-entorhinal input to the hippocampus may not be crucial for trace conditioning.
Extracellularly recorded field potentials, evoked by stimulation of cortico-nucleus accumbens border, were recorded in the nucleus accumbens (NAcc) in horizontal slices of rat ventral forebrain. The field excitatory postsynaptic potential (EPSP) event (N2) was calcium dependent, blocked by tetrodotoxin (1 microM), and reduced by over 70% by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) (10 microM), the antagonist of AMPA-type glutamate receptors. The EPSP amplitude was enhanced by either of the GABA(A) receptor antagonists, picrotoxin (10 microM; by 252+/-33%, n=18) and bicuculline methiodide (20 microM; by 216+/-34%, n=4). Additionally, picrotoxin (3-50 microM) and bicuculline methiodide (20 microM) promoted epileptiform activity within the NAcc, manifest as the emergence of additional late components, N3, N4 and N5, in the evoked synaptic waveform. In slices with the frontal cortex removed, picrotoxin (10-50 microM) and bicuculline methiodide (20 microM) were unable to promote epileptiform activity within the NAcc, although a smaller increase in the peak amplitude of the field EPSP (163+/-18%, n=6) was observed at the highest concentrations of picrotoxin (50 microM). Histological examination of the slice demonstrated that in such decorticated slices, the piriform cortex (PC) had been removed. We propose that stimulation of the cortico-NAcc border not only evokes an orthodromic EPSP in the NAcc, but also causes antidromic activation of cortical tissue. Disinhibition by GABA(A) antagonists of circuits intrinsic to the cortex, possibly the piriform cortex, is the principal cause of the facilitation of the EPSP and of regenerative epileptiform activity in NAcc evoked by stimulation of cortical input.