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PubMed1983

Effect of specific serotonergic lesions on cholinergic neurons in the hippocampus, cortex and striatum.

Local injection of 5,7-dihydroxytryptamine into the median raphe nucleus of rats pretreated with desipramine decreases the serotonin content of the hippocampus and cortex. The turnover of acetylcholine, as measured by the rate of decline of acetylcholine content after hemicholinium-3, is not affected in the hippocampus or the striatum, but is increased in the cortex by such treatment. Local injection of 5,7-dihydroxytryptamine into the dorsal raphe nucleus of desipramine-treated rats decreases the serotonin content of the hippocampus, cortex, and striatum. The turnover of acetylcholine is increased in the hippocampus and cortex, but not affected in the striatum. Thus, serotonergic neurons from the median raphe nucleus appear to tonically inhibit cholinergic neurons in the cortex, and serotonergic neurons from the dorsal raphe nucleus appear to tonically inhibit cholinergic neurons in the hippocampus and cortex. These serotonergic neurons do not appear to act tonically on striatal cholinergic neurons.

5,6-Dihydroxytryptamine↗

PubMed1991

Single doses of methamphetamine cause changes in the density of dendritic spines in the prefrontal cortex of gerbils (Meriones unguiculatus).

Single doses of methamphetamine (25 mg/kg) were administered to adult gerbils. All detectable spines were counted along defined segments of basal, apical and lateral dendrites of Golgi-impregnated pyramidal cells in the medial prefrontal cortex (layers III and V) and the parietal cortex (layer V). These two areas were selected because previous investigations had shown methamphetamine-induced neurotoxicity in prefrontal cortex but not in parietal cortex. The frequencies of dendritic spines in methamphetamine-treated gerbils were found to be significantly increased in the prefrontal cortex, while no significant change was found in the parietal cortex.

Animals↗

PubMed1994

Item and order dissociation in humans with prefrontal cortex damage.

Subjects with bilateral, right or left prefrontal cortex damage and age matched controls were tested for item and order recognition memory for spatial location, word, abstract picture and hand position information. Prefrontal cortex damaged subjects showed, in general, no deficits on item recognition tests relative to controls with the exception of a deficit for hand positions. In contrast, prefrontal cortex damaged groups had severe deficits on all order recognition tests relative to controls. With respect to lateralization, order recognition memory deficits occurred for right, bilateral, but not left prefrontal cortex damaged subjects for spatial location information, but for both right and left prefrontal cortex damaged subjects for words, abstract pictures, and hand position. The data suggest that the prefrontal cortex mediates temporal order information for all modalities tested as well as item recognition memory for egocentric spatial information.

Adult↗

PubMed1976

Feedback training of 36 - 44 HZ EEG activity in the visual cortex and hippocampus of cats: evidence for sensory and motor involvement.

Milk reinforcement was contingent on the occurrence of 36 -44 (40) Hz EEG activity in the left visual cortex (VC) of one group of cats and in the right hippocampus (H) of a second group. Both groups learned to increase 40 Hz activity, and acquisition of reinforcement was associated with immobility. A third group (behavioral controls - BC) was trained by the method of successive approximation to behave in a similar manner to VC and H cats. Training significantly increased 40 Hz activity in all of the following structures, except the hippocampi of VC cats and between the right and left visual cortex of H and BC cats: posterior primary visual cortex (bilateral), anterior primary visual cortex (left), primary motor cortex (bilateral), dorsal hippocampus (bilateral), and midbrain reticular formation (bilateral). Since the behavioral and EEG changes of H and BC animals were similar, immobility appears to be important for increased hippocampal 40 Hz activity produced by feedback training. Testing in darkness enhanced 40 Hz activity in the trained area of VC cats but had no effect on H or BC animals. These results, in conjunction with the observation that VC cats appeared to visually fixate, suggest that VC cats may have learned to increase 40 Hz activity in the visual cortex by altering visual processing.

Animals↗

PubMed1990

Effects of dorsal and medial cortex lesions on reversals in turtles.

Two experiments were performed to investigate the effect of cortical lesions on the acquisition and reversal of simultaneous discriminations in turtles. The first experiment examined the effect of cortical lesions on the acquisition and reversal of a spatial discrimination. The results of the first experiment revealed that lesions of the dorsal cortex produced a deficit in spatial learning. The results of the first experiment also revealed that when damage to the dorsal cortex was accompanied by substantial damage to the medial cortex, no deficit was manifest. The second experiment examined the effects of cortical lesions on the acquisition and reversal of a brightness discrimination. The results of the second experiment revealed that damage to neither the dorsal cortex nor the medial cortex produced a deficit. It was suggested that brightness is not represented in the thalamofugal visual pathway but is instead represented in the tectofugal visual pathway in reptiles. It was also suggested that the medial cortex, which is the evolutionary precursor to the mammalian hippocampal formation, functions differently from the mammalian hippocampus.

Animals↗

PubMed1993

Lithium increases accumulation of second messenger inositol 1,4,5-trisphosphate in brain cortex slices in species ranging from mouse to monkey.

Historical aspects of the phosphoinositide field are briefly reviewed. The effects of the anti-manic depressive drug, lithium, on inositol 1,4,5-trisphosphate accumulation in brain cortex slices in species ranging from mouse to monkey are presented. In the guinea pig, lithium, in the presence of acetylcholine, increases the accumulation of inositol 1,4,5-trisphosphate and inositol 1,3,4,5-tetrakisphosphate, but at therapeutic concentrations of lithium 1 mM inositol is required to see a statistically significant effect. In previous studies in rat brain cortex slices, lithium inhibited accumulation of inositol 1,4,5-trisphosphate by 15-20%. We have confirmed this and found a similar effect in mouse brain cortex slices. However, if we added 20-30 mM inositol we observed lithium-stimulated accumulations of inositol 1,4,5-trisphosphate and inositol 1,3,4,5-tetrakisphosphate in these two latter species. These observations in rat and mouse appear to relate to the following facts: (1) brain cortices of mouse and rat contain in vivo concentrations of inositol half that of guinea pig, (2) incubated rat brain cortex slices are depleted of inositol by 80% and (3) the slices require 10 mM inositol supplementation to restore in vivo concentrations. More recently, we have shown that in monkey brain cortex slices, therapeutic concentrations of Li+ increase accumulation of inositol 1,4,5-trisphosphate. Inositol 1,3,4,5-tetrakisphosphate is not increased. Neither inositol, nor an agonist, is required. The same effects are seen whether inositol 1,4,5-trisphosphate is measured by the [3H]inositol-prelabelling technique or by mass assay, although mass includes a pool of inositol 1,4,5-trisphosphate which is metabolically inactive. Thus, in a therapeutically relevant model for man, Li+ increases Ins(1,4,5)P3 in brain cortex slices, as was previously seen in lower mammals at nonrate-limiting concentrations of inositol.

Animals↗

PubMed1984

Differential interactions of GABA agonists, depressant and convulsant drugs with [35S]-t-butylbicyclophosphorothionate binding sites in cortex and cerebellum.

Effects of three GABA agonists, four GABA antagonists and convulsants (picrotoxinin, alpha-dihydropicrotoxinin [DHP], pentamethylenetetrazole [PTZ] and isopropylbicyclophosphate ester) and three depressant drugs (pentobarbital, (+)etomidate and etazolate) were investigated on [35S]t-butylbicyclophosphorothionate (TBPT) in cortex and cerebellum. All the convulsants tested were equipotent in inhibiting [35S]TBPT binding in cortex and cerebellum. Convulsants like picrotoxinin inhibited [35S]-TBPT binding competitively in both cortex and cerebellum. In contrast, gamma-aminobutyric acid (GABA) agonists (muscimol, GABA and 4,5,6,7-tetrahydroisoxazol[5,4-C]pyridine-3-ol [THIP]), and depressants like etazolate, (+)etomidate and pentobarbital were more potent inhibitors of [35S]TBPT binding in cerebellum than in cortex. GABA inhibition of [35S]TBPT binding appears to be mediated through a low-affinity site. GABA and pentobarbital inhibited [35S]TBPT binding in cortex and cerebellum noncompetitively. Depressants like pentobarbital appear to interact with the TBPT sites allosterically. These results suggest that depressant and convulsant drugs that modulate GABAergic transmission interact differently with the TBPT binding sites in cortex and cerebellum.

Animals↗

PubMed1983

The anterior cingulate cortex and the phonatory control in monkey and man.

Electrical stimulation of the anterior cingulate cortex yields vocalization in the monkey. The elicited vocalizations seem to represent primary stimulus responses. Monkeys are not able to perform a vocal conditioning task after ablation of the anterior cingulate cortex. However, they can carry out a lever-pressing conditioning task following destruction of this area. It is hypothesized that the anterior cingulate cortex exerts the volitional control of species-specific vocalizations in monkey. The non-verbal emotional vocal utterances are considered to be the human homologue of monkey's vocalizations. Therefore, bilateral lesion of the anterior cingulate cortex in man should hamper the volitional control of emotional vocal utterances in man as it does in monkeys. One personal observation is reported where after a bilateral infarction of the anterior cingulate cortex the patient's voice showed a permanent lack of emotional expression. The anterior cingulate cortex seems to play the decisive role in the volitional verbalization of emotions.

Animals↗

PubMed1981

Development of receptive field properties in the visual cortex of rabbits subjected to early epileptiform cortical discharges.

We examined the effects of early epileptiform activity on development of visuocortical receptive fields in the rabbit. Aqueous penicillin was injected twice a day into a cannula implanted over the monocular area of one visual cortex. Drug administration was begun on postnatal day 8-9 and continued until postnatal day 24-30. Concomitant with the penicillin injections a mixture of penicillin and penicillinase was similarly applied to the monocular area of the contralateral control cortex. Interictal discharges were routinely observed only from the penicillin-treated or epileptic cortex. Single-unit recordings made on postnatal day 25-31 revealed that in the neuronal population adjacent to the cortical penicillin focus percentages of receptive field types were severely altered relative to control cortex percentages. Epileptic cortex showed an abnormally high percentage of no response type cells together with an abnormally low percentage of complex and oriented-directional type cells. These abnormalities were greater closer to the penicillin focus than further from it. Epileptic visual cortex receptive field percentages are compared with those for the neonatal rabbit and the rabbit subjected to early monocular deprivation. One interpretation of our results is that development of complex and oriented-directional type cells is impeded by epileptogenic disruption of organized geniculostriate activity.

Aging↗

PubMed1982

Postnatal development of monoamine content and synthesis in the cerebral cortex of rhesus monkeys.

The concentration and rates of synthesis of norepinephrine, dopamine and serotonin were determined by spectrophotofluorometric methods in various cytoarchitectonic areas of the cerebral cortex in 54 rhesus monkeys ranging in age from 1 day to 36 months. For most regions studied, norepinephrine levels exhibit steady increases from birth through 36 months while over the same period changes in dopamine concentration are more complex and variable, particularly in the frontal lobe. Among the 3 monoamines examined, endogenous serotonin content shows the least dramatic and most rapid development, reaching adult values between 2 and 5 months of age in most cortical regions. As a consequence of these developmental shifts, the relationship of monoamine levels in various cortical areas also changes with age. At maturity, however, norepinephrine concentration exceeds that of dopamine and serotonin in the cortex of the frontal and parietal lobes whereas serotonin levels are higher than norepinephrine in the occipital cortex. Changes in rates of synthesis of the catecholamines and serotonin generally parallel developmental changes in concentrations. The greatest increments in catecholamine synthesis occur in prefrontal and posterior association cortices. Smaller but significant increases in serotonin metabolism were measured in the parietal and visual cortex between birth and 36 months while in other areas of the cortex, age-related changes in serotonin synthesis were negligible. A consistent finding at all ages is that the distribution of catecholaminergic synthesis varies inversely with that of serotonergic synthesis, indicating substantial interaction in the regulation of the two cortical systems. The present findings demonstrate that in the rhesus monkey development of monoaminergic storage capacity and synthetic processes: (1) continues over a period of months and years; (2) is generally more rapid for serotonin than for catecholamines; and (3) varies greatly in different cytoarchitectonic regions of the cerebral cortex.

Aging↗

PubMed1983

The effects of unilateral neonatal removal of visual cortex on transmitter parameters in the adult superior colliculus and lateral geniculate body.

High affinity glutamate uptake was reduced in the ipsilateral lateral geniculate body by 75% and in the ipsilateral superior colliculus by 50% one week after ablation of the visual cortex in the adult rat. Six days after neonatal removal of visual cortex, there were no effects on the high affinity glutamate uptake in these regions indicating that there were few functionally corticofugal fibres established at birth. Seventy-five days after unilateral neonatal ablation of visual cortex, the glutamate uptake in both ipsi- and contralateral superior colliculus was reduced 50% compared to unoperated controls. The glutamate uptake in the lateral geniculate body was reduced 55% ipsilateral to and 38% contralateral to the lesion. The neonatal lesion had therefore affected the development of glutamate nerve terminals bilaterally in these target regions. Destruction of the visual cortex on the unoperated side caused in these adults an additional bilateral decrease of the glutamate uptake in the superior colliculus, showing the presence of aberrant glutamatergic fibres crossing from the unoperated visual cortex. In the lateral geniculate body, a similar lesion was accompanied only by a reduction in glutamate uptake on the ipsilateral side. The neonatal ablation of visual cortex also induced small changes in glutamate decarboxylase and GABA uptake in superior colliculus 75 days after the operation.

Animals↗

PubMed1985

Transplantation of fetal postmitotic neurons to rat cortex: survival, early pathway choices and long-term projections of outgrowing axons.

A system for studying growth and development of transplanted subpopulations of postmitotic cerebral cortical neurons is described. The cytotoxic drug methylazoxymethanol (MAM) was given to pregnant rats on the fourteenth day of gestation to destroy precursor cells of layers II-IV of the fetal cerebral cortex. Layer V and VI precursor cells which had completed their final division before MAM treatment and were unaffected by it, were labeled by a prior injection of [3H]thymidine. This strategy provides a donor cerebral cortex containing mainly neurons destined to form layers V and VI of the adult cerebral cortex; these cells are postmitotic. Pieces of donor cerebral cortex were transplanted to the cerebral hemispheres of normal newborn hosts at one day, two days, or 6 days after MAM treatment; survival was assessed 1-12 weeks after transplantation by autoradiography of histological sections. Radiolabeled graft cells survived in 89% of recipients and many of these grew axons into the host, as indicated by retrograde labeling with horseradish peroxidase. Significant numbers of graft cells could also be stained immunocytochemically for glutamic acid decarboxylase or for the peptides, somatostatin, vasoactive intestinal polypeptide or cholecystokinin. A second group of experiments examined the routes of early axon outgrowth from normal and postmitotic fetal grafts. When the donor cortex had been incubated in a mixture of [3H]proline and [3H]leucine for 20 min prior to transplantation, the earliest axons growing out of the graft into normal newborn hosts could be assessed by autoradiography of axoplasmic transport after survivals in the host of 7 days. Normal and postmitotic grafts taken at E15 or E20 were capable of outgrowth, though the axons of E20 postmitotic cells did not grow far. The location of the transplant was the major determinant of where graft cells' axons grew and growth was mainly into existing axonal pathways of the host. In a third group of experiments, long term axonal projections from normal and postmitotic fetal transplants to 4 regions of the host brain--thalamus, contralateral cortex, striatum, and hippocampus--were examined with retrograde tracers 2-4 months after transplantation. Projections from grafts to the 4 host sites were highly dependent on the presence of nearby host axons connecting with those sites. Neurons in all types of graft projected to one or other of the 4 sites, but generally in small numbers. Higher proportions of cells in grafts from E15 MAM-treated donors projected to the host thalamus.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1988

Ontogeny of dopaminergic function in the rat midbrain tegmentum, corpus striatum and frontal cortex.

Ontogenic development of the dopaminergic system in rat brain was investigated. This was accomplished by monitoring changes in postsynaptic dopamine receptor formation and presynaptic dopamine content in the midbrain tegmentum, frontal cortex and corpus striatum from the 18th day of gestation through adulthood. The dopamine antagonist spiperone was used as the binding ligand to quantitate receptor number while dopamine content was measured chromatographically. [3H]Spiperone binding kinetics in adult animals revealed that the maximum number of receptor sites (Bmax) was 160, 900 and 597 fmol/mg protein in midbrain tegmentum, frontal cortex and corpus striatum, respectively, while the corresponding equilibrium constant (Kd) values were 0.15, 0.52 and 0.15 nM. During the course of development, the affinity for spiperone binding in corpus striatum and frontal cortex did not change significantly, while in midbrain tegmentum the binding affinity in younger animals was significantly lower. Results from competitive inhibition experiments using various serotonergic and dopaminergic antagonists suggested that at all ages dopamine D2-receptors were responsible for spiperone binding in corpus striatum and midbrain tegmentum. In frontal cortex, binding properties consistent with D2-receptors were observed in non-adult animals; by the time adulthood was reached, however, spiperone binding characteristics were altered and appeared to correspond to serotonin sites. The developmental patterns of the dopaminergic markers were different in all 3 tissues. Adult receptor levels were achieved very early in midbrain tegmentum, while increases in receptor number continued in corpus striatum and frontal cortex, at different rates, throughout the postnatal period. A marked increase in dopamine in corpus striatum occurred during the second and third postnatal weeks and the transmitter content remained relatively constant after this time. Transient fluctuations in endogenous dopamine during the postnatal period were observed in midbrain tegmentum and frontal cortex. A general feature of the ontogenic pattern in all tissues appeared to be increases in dopamine receptor preceding increases in dopamine synthesis. A hypothesis on the developmental regulation of dopamine neurons was derived.

Aging↗

PubMed1988

Immunohistological localization of cell adhesion molecules L1, J1, N-CAM and their common carbohydrate L2 in the embryonic cortex of normal and reeler mice.

The expression of the cell adhesion molecules L1, J1 and N-CAM and their shared carbohydrate L2 was studied in the embryonic cerebral cortex of normal and reeler mutant mice using light and electron microscopic immunocytochemistry. Apart from a general delay in their appearance in the reeler cortex, the 4 antigens were present with a cellular distribution in both genotypes reflecting the anatomical characteristics of normal and mutant phenotypes. The cell surface glycoprotein L1 was exclusively expressed by neurons, particularly axons, but was never detected at sites of neuron-glia contact. L1 was accumulated in the marginal zone and subplate of the normal cortex and in the homologous layers of the reeler cortex. The secreted glycoprotein J1 was found on glia and neurons. Although initially present in regions of fiber outgrowth, J1 became characteristically excluded from the large fiber tracts at later stages. J1 mapped in the marginal zone and subcortical plate of the normal cortex and in the corresponding layers of the mutant cortex. N-CAM had a more ubiquitous distribution and was present in ventricular zones, particularly at early stages, as well as on glia and neurons and large fiber tracts at later developmental stages. The distribution of the L2 epitope was quite similar to that of the J1 molecule but remained present on large fiber tracts, like N-CAM and L1, also at later developmental stages. These comparative observations in normal and reeler mutant mice lend support to previous suggestions that L1, together with N-CAM, may play a role in the aggregation of neuronal cell bodies after migration and in the fasciculation of developing fiber bundles. They also point to a possible function of the extracellular matrix component J1 in the guidance or support of fiber outgrowth in large fiber tracts.

Animals↗

PubMed1990

Effect of the richness of the environment on neurons in cat visual cortex. I. Receptive field properties.

In a recent study, it was demonstrated that the number of synaptic contacts associated with flat vesicles (FS synapses) is higher in the visual cortex of cats raised in an enriched environmental condition (EC) compared to those reared in an impoverished condition (IC). Moreover, the size of the FS synaptic contacts is also affected by the richness of the animal's environment during development. Based on evidence that the vast majority of FS synapses are GABAergic (gamma-aminobutyric acid) and that many of the properties of visual cortex neurons are influenced by GABA-dependent mechanisms, it has been suggested that these morphological synaptic changes induced by the richness of the environment correlate with differences in cortical receptive field properties. In the present study, this has been explored by recording visual responses of area 17 cells in cats raised either in isolation (IC) or in a colony with ample environmental stimulation (EC). Enriched visual cortex contains a higher proportion of orientation selective cells and a lower proportion of orientation biased and unoriented cells. In addition, orientation tuning is significantly sharper in EC animals (mean bandwidth of responsive units is equal to 32 degrees) than in IC cats (mean bandwidth is equal to 38 degrees; P less than 0.001). This is mostly due to the greater incidence of orientation biased units in impoverished cortex (23% in EC and 41% in IC animals; P less than 0.01). Unit responsivity is significantly affected by the richness of the environment. We found that all units of the EC cortex were responsive to light stimuli. In contrast, 14% of the impoverished cells studied fail to increase their response to at least twice the standard deviation of the spontaneous activity and were judged as unresponsive. We suggest that the lower responsivity in IC visual units is related to the higher number of GABAergic synapses per IC neuron, while the broader selectivity in IC cortex might be due to a more diffuse distribution of the GABAergic inhibitory connections.

Animals↗

PubMed1991

Primary auditory cortex in the rat: transient expression of acetylcholinesterase activity in developing geniculocortical projections.

A characteristic pattern of acetylcholinesterase (AChE) activity is expressed transiently in primary auditory cortex (cortical area 41) of developing laboratory rats during early postnatal life. This AChE activity occurs as a dense plexus in cortical layer IV and the deep part of layer III. This transient band of AChE activity is first detected by histochemical techniques on postnatal day (P) 3, reaches peak intensity at approximately P8-10, and declines to form the adult pattern by P23. The ventral nucleus of the medial geniculate body of the thalamus also displays prominent, and transient, staining for AChE. This intense staining for AChE, found within neuronal somata and neuropil, is detected at the time of birth, reaches peak intensity around P8, and declines to adult levels by P16. The areal and laminar patterns of the transient band of AChE activity in temporal cortex correspond to the patterns of anterograde transneuronal labeling of geniculocortical terminals following injection of wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP) into the inferior colliculus. Placement of lesions that include the medial geniculate nucleus or the geniculocortical axons results in a marked decrease in AChE staining in thalamorecipient layers of auditory cortex. Placement of lesions that include the medial globus pallidus reduce AChE staining of some axons in temporal cortex of developing rats, but the dense band of AChE in layers III and IV remains. Placement of lesions in the inferior colliculus in newborn animals results in marked decrease in AChE staining in cells of the ipsilateral ventral medial geniculate nucleus and in ipsilateral auditory cortex of developing pups. These data indicate that transiently expressed AChE activity is characteristic of geniculocortical neurons, including their somata in the medial geniculate body and their terminal axons in primary auditory cortex. This AChE activity is expressed early in postnatal development, probably during the time when thalamocortical axons are proliferating in cortical layer IV and forming synaptic contacts with cortical neurons.

Acetylcholinesterase↗

PubMed1992

Development of AChE-positive neuronal projections from basal forebrain to cerebral cortex in organotypic tissue slice cultures.

Development of the innervation of the cerebral cortex by acetylcholinesterase (AChE)-stained basal forebrain neurons was studied in vitro using the roller tube technique. Slice cultures were maintained from 3 days to 4 weeks either in serum based medium or in chemically defined medium, each supplemented in some cases with nerve growth factor (NGF). The distribution of AChE and choline acetyltransferase (CAT)-containing neurons was investigated using histo- and immunocytochemical techniques. Slice cultures of basal forebrain revealed the presence of large and medium sized AChE-positive neurons. Within one week of cultivation, numerous AChE-labeled fibers could be seen growing out from the basal forebrain toward the cortex. After entering cortical tissue most of the afferent basal forebrain fibers projected either radially or obliquely into the cortical layers. Many afferent axons initially also travelled tangentially within the white matter, and turned then to grow into the cortical layers. Cerebral cortex tissue maintained a coarse laminar organization. Ramifications of basal forebrain fibers were visible within the subplate region, the deep and superficial cortical layers, and within the marginal zone; greatest density occurred in the subplate region and in marginal zones. Many of these processes exhibited branching patterns markedly similar to those observed during cortical development in vivo. Cortex slices placed with the pial surface adjacent to the basal forebrain revealed AChE-stained fibers that entered the cortical tissue through the marginal surface and gave off ramifications within the superficial layers and, less frequently, the deeper cortical layers. CAT-immunostaining revealed labeled cell bodies and neurites only in the basal forebrain, not in the cortex tissue. Control experiments with co-cultures of basal forebrain and cerebellum slices showed no AChE-positive fiber ingrowth into the cerebellum tissue. The results of these studies demonstrate that basal forebrain projections to cerebral cortex in vitro appear similar to the projections that develop in vivo, and indicate that organotypic co-cultures provide a valuable model for studies of developing cortical afferents.

Acetylcholinesterase↗

PubMedDate not supplied

Autonomic responses are elicited by electrical stimulation of the medial but not lateral frontal cortex in rabbits.

Conscious rabbits received electrical stimulation of the anterior midline frontal cortex or lateral somatosensory and motor cortex, through chronically-implanted electrodes. Active sites for cardiovascular responses were found in the anterior midline cortex, but stimulation of the frontolateral sensory-motor cortex either did not elicit cardiovascular changes or elicited only small and variable changes when stimulated. The heart-rate response elicited was, in all cases, bradycardia. All blood pressure changes consisted of depressor responses. Stimulation of the lateral frontal cortex almost always resulted in increases in EMG activity, although many placements were observed in the medial frontal cortex that were unaccompanied by movement. In all cases in which depressor responses and bradycardia were elicited, increases in respiration rate and decreases in depth also occurred. The active area from which bradycardia and depressor responses were elicited forms the medial portion of the cortical projection area of the mediodorsal nucleus of the thalamus and thus may be involved in the autonomic accompaniments of the behavioral activities, i.e. learning and memory processes, associated with this nucleus.

Animals↗