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PubMed1997

Loss of dopamine terminals in the medial prefrontal cortex increased the ratio of DOPAC to DA in tissue of the nucleus accumbens shell: role of stress.

We examined whether dopamine depletion in the medial prefrontal cortex of the rat differentially affects basal and evoked dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) content in the subareas of the neostriatum and nucleus accumbens. Loss of approximately 80% of tissue dopamine content in the medial prefrontal cortex did not significantly alter basal tissue concentrations of dopamine or DOPAC or the DOPAC:dopamine ratio in either the nucleus accumbens core or shell or the medial or lateral neostriatum. However, tail pressure stress significantly increased the DOPAC:dopamine ratio in the nucleus accumbens shell of lesioned rats. Because dorsal and ventral areas of the medial prefrontal cortex preferentially innervate the core and shell, respectively, we sought to determine whether the selective effect of lesions on dopamine terminals in the shell of the nucleus accumbens are paralleled by greater dopamine loss in the ventral medial prefrontal cortex. 6-Hydroxydopamine decreased tissue concentrations of dopamine in both the dorsal (-74%) and ventral medial prefrontal cortex (-68%). In lesioned rats, few tyrosine hydroxylase-immunoreactive fibers remained in the dorsal medial prefrontal cortex whereas a dense innervation remained in the ventralmost area. The present data suggest that the influence of mesocortical dopamine neurons on the dopamine projection to the nucleus accumbens shell is expressed only under conditions of stress. Furthermore, lesion-induced alterations in dopamine neurons projecting to the nucleus accumbens shell are not due to a more extensive loss of dopamine terminals in the ventral than in the dorsal medial prefrontal cortex.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1986

Critical concentration of cadmium in kidney cortex of humans exposed to environmental cadmium.

Cadmium (Cd) was determined in kidney cortex and liver of 173 autopsied Japanese. Subjects consisted of 51 persons from Cd-polluted areas ages between 61-94 years and 122 controls ages between 3-90 years. The mean Cd concentrations for the Cd-polluted group were 35.2 micrograms/g wet wt for kidney cortex and 66.7 micrograms/g wet wt for liver. Corresponding values for the control group aged over 60 were 90.1 and 10.7, respectively. Both liver and kidney cortex Cd were analyzed for 127 subjects (41 Cd-polluted and 86 control subjects). The kidney cortex concentration tended to increase linearly with increasing liver concentrations up to approximately 20 micrograms/g of liver Cd; above this value there was no further increase in kidney cortex level. Only three persons showed kidney cortex Cd levels above 200 micrograms/g. The lowest liver Cd levels of the Cd-polluted subjects with renal damage were around 30 micrograms/g. The critical level of kidney cortex Cd may exist below 200 micrograms/g in humans exposed to environmental Cd. The corresponding value for the liver may be below 30 micrograms/g wet wt.

Adolescent↗

PubMed2003

Bilateral lesions of the entorhinal cortex differentially modify haloperidol- and olanzapine-induced c-fos mRNA expression in the rat forebrain.

Lesions of the entorhinal cortex are now an accepted model for mimicking some of the neuropathological aspects of schizophrenia, since evidence has accumulated for the presence of cytoarchitectonic abnormalities within this cortex in schizophrenic patients. The present study was undertaken to address the functional consequences of bilateral entorhinal cortex lesions on antipsychotic-induced c-fos expression. After a 15-day recovery period, the effect of a typical antipsychotic, haloperidol (1 mg/kg), on c-fos mRNA expression was compared with that of an atypical one, olanzapine (10 mg/kg), in both sham-lesioned and entorhinal cortex-lesioned rats. In sham-lesioned rats, both haloperidol and olanzapine induced c-fos expression in the caudal cingulate cortex, dorsomedial and dorsolateral caudate-putamen, nucleus accumbens core and shell and lateral septum. In addition, olanzapine, but not haloperidol, increased c-fos expression within the central amygdala. In entorhinal cortex-lesioned rats, haloperidol-induced c-fos expression was markedly reduced in most areas. In contrast, the olanzapine-induced c-fos expression was not altered in the nucleus accumbens shell and lateral septum of the lesioned rats. These findings reveal that entorhinal cortex lesions affect c-fos expression in a compound- and regional-dependent manner. Our results further emphasize the importance of the exploration of the mechanisms of action of antipsychotic drugs in the context of an associated cortical pathology.

Animals↗

PubMed1999

Ventromedial prefrontal cortex mediates guessing.

Guessing is an important component of everyday cognition. The present study examined the neural substrates of guessing using a simple card-playing task in conjunction with functional magnetic resonance imaging (fMRI). Subjects were scanned under four conditions. In two, they were shown images of the back of a playing card and had to guess either the colour or the suit of the card. In the other two they were shown the face of a card and had to report either the colour or the suit. Guessing compared to reporting was associated with significant activations in lateral prefrontal cortex (right more than left), right orbitofrontal cortex, anterior cingulate, bilateral inferior parietal cortex and right thalamus. Increasing the guessing demands by manipulating the number of alternative outcomes was associated with activation of the left lateral and medial orbitofrontal cortex. These data suggest that while simple two choice guessing depends on an extensive neural system including regions of the right lateral prefrontal cortex, activation of orbitofrontal cortex increases as the probabilistic contingencies become more complex. Guessing thus involves not only systems implicated in working memory processes but also depends upon orbitofrontal cortex. This region is not typically activated in working memory tasks and its activation may reflect additional requirements of dealing with uncertainty.

Adult↗

PubMed2002

Spatial working memory in human extrastriate cortex.

The performance of spatial working memory tasks is known to evoke activity in a set of higher-order association areas, including the prefrontal cortex, posterior parietal cortex and the frontal and supplementary eye fields. Recent physiological studies in monkey have shown that memory-related activity also is found in extrastriate cortex [J. Neurophysiol. 84 (2000) 677]. We conducted functional magnetic resonance imaging studies to determine whether human extrastriate cortex contributes to the on-line maintenance of spatial information in an eye movement task. We found that performance of memory-guided saccades, as compared to visually guided saccades, elicited significant activation in two areas of extrastriate cortex: the posterior superior temporal sulcus (PST) and lateral occipitotemporal cortex (LOT). Both areas also were activated during the basic sensorimotor task of visually guided saccades as compared to fixation. We further determined that area LOT is close to but distinct from motion-sensitive area MT+. These findings demonstrate that areas PST and LOT, along with higher-level association cortex, help to encode and maintain spatial representations.

Adult↗

PubMed2003

An MRI study of subgenual prefrontal cortex in patients with familial and non-familial bipolar I disorder.

BACKGROUND: Over the past few years there has been an interest in the use of magnetic resonance imaging (MRI) to study specific brain regions in bipolar disorder. The present study compared the grey matter volume in the subgenual prefrontal cortex in patients with familial and non-familial bipolar disorder and normal control subjects. METHODS: MRI brain scans were performed on 12 patients with bipolar I disorder including six patients with a positive family history of bipolar disorder as well as eight control subjects. RESULTS: There was a significant reduction in the grey matter volume in the right subgenual prefrontal cortex, but not in the left subgenual prefrontal cortex. A family history x sex interaction with right prefrontal cortex volume was also observed as a trend. For females, a positive family history was associated with reduced right prefrontal cortex volumes; for males, a positive family history was associated with increased right prefrontal cortex volumes. LIMITATIONS: Small sample size, reduced statistical power. CONCLUSION: These data add to the emerging literature on structural changes in the subgenual prefrontal cortex in bipolar disorder, especially in patients with a positive family history.

Adult↗

PubMed2003

Visual deprivation effects on the s100beta positive astrocytic population in the developing rat visual cortex: a quantitative study.

After birth, exposure to visual inputs modulates cortical development, inducing numerous changes of all components of the visual cortex. Most of the cortical changes thus induced occur during what is called the critical period. Astrocytes play an important role in the development, maintenance and plasticity of the cortex, as well as in the structure and function of the vascular network. Dark-reared Sprague-Dawley rats and age-matched controls sampled at 14, 21, 28, 35, 42, 49, 56 and 63 days postnatal (dpn) were studied in order to elucidate quantitative differences in the number of positive cells in the striate cortex. The astrocytic population was estimated by immunohistochemistry for S-100beta protein. The same quantification was also performed in a nonsensory area, the retrosplenial granular cortex. S-100beta positive cells had adult morphology in the visual cortex at 14 dpn and their numbers were not significantly different in light-exposed and nonexposed rats up to 35 dpn, and were even higher in dark-reared rats at 21 dpn. However, significant quantitative changes were recorded after the beginning of the critical period. The main finding of the present study was the significantly lower astroglial density estimated in the visual cortex of dark-reared rats over 35 dpn as well as the lack of difference at previous ages. Our results also showed that there were no differences when comparing the measurements from a nonsensory area between both groups. This led us to postulate that the astrocytic population in the visual cortex is downregulated by the lack of visual experience.

Animals↗

PubMed1997

Neonatal androgen manipulation differentially affects the development of monoamine systems in rat cerebral cortex, amygdala and hypothalamus.

Neural tissue during perinatal life is sufficiently plastic to respond to the presence of testicular androgens. Here we studied the effect of neonatal androgen manipulation (castration of male and androgenization of female rats) on monoamine neurotransmitter systems in the cerebral cortex and sexually dimorphic regions of brain (hypothalamus and amygdala). Norepinephrine (NE) and dopamine (DA) concentrations in cortex, amygdala and hypothalamus of rats were assayed by HPLC at days 25, 60, 120, 180, 240 and 300. Results show that NE levels in all groups of rats at day 25 were higher in the hypothalamus (5-9 ng/mg protein) compared to the amygdala (0.5-3 ng/mg protein) and the cortex (0.5-1 ng/mg protein). Levels of DA at day 25 in the hypothalamus and the amygdala were comparable (up to 3.5 ng/mg) but higher than in the cortex (1.25-1.75 ng/mg protein). NE and DA concentrations in sham-castrated male and androgen-treated females were higher at day 25 compared to castrated male and control females in both amygdala and hypothalamus; however, levels of NE and DA remained unchanged in the cortex. Pattern of NE concentrations started reversing with increase in age, i.e., NE levels in control females and castrated males increased almost 4-fold in amygdala and 2-fold in hypothalamus by day 300, but there was no significant change in the cortex. Compared to that, NE levels decreased in sham-castrated male (2-fold) and androgen-treated females (3-fold) in amygdala as well as in the hypothalamus (2-fold) in both these groups. A similar pattern of reversal of DA levels was found in both amygdala and hypothalamus, however, at day 300 DA levels were comparable in all the four groups. These studies suggest that androgen manipulation (castration or androgen administration) induces age-dependent short- and long-term effects on the development of noradrenergic and dopaminergic systems in the sexually dimorphic regions of brain, amygdala and hypothalamus, without a significant change in the cerebral cortex.

Amygdala↗

PubMed1997

Short-term memory for food reward magnitude: the role of the prefrontal cortex.

Memory for magnitude of reinforcement was assessed in rats using a go/no-go short-term memory paradigm. During the task's study phase rats were given a piece of cereal comprised of either 25 or 50% sugar. For all trials, one of the cereal types was designated positive, the other negative. On the ensuing test phase the rat was presented with an object which covered a food well. If a positive food reward was given during the study phase, a second food reward was placed beneath the object. No food reward was placed under the object if the study phase consisted of a negative food reward. Latency to object displacement was used as the measure of performance. Following the establishment of a significant difference between latency to approach the object with reward compared to latency to approach the object without reward, rats were given either agranular insular cortex, anterior cingulate cortex, pre- and infralimbic cortex or control lesions. Agranular insular cortex lesioned animals demonstrated a mild post-surgery impairment. Trials consisting of 10 and 20 s delays between the study and test phases were then introduced. Delays exacerbated the previous deficit of the agranular insular cortex lesion group, but had little effect on the other lesion groups. All animals transferred to a new set of cereals containing 25 and 50% sugar and exhibited taste preferences to sugar solutions of different concentrations. These results indicate that the agranular insular cortex may play an important role in the processing of affect-laden information within a prefrontal cortex short-term or working memory system.

Animals↗

PubMed2001

Neuronal mechanisms of executive control by the prefrontal cortex.

Executive function is considered to be a product of the coordinated operation of various processes to accomplish a particular goal in a flexible manner. The mechanism or system responsible for the coordinated operation of various processes is called executive control. Impairments caused by damage to the prefrontal cortex are often called dysexecutive syndromes. Therefore, the prefrontal cortex is considered to play a significant role in executive control. Prefrontal participation to executive control can be partly explained by working memory that includes mechanisms for temporary active storage of information and processing stored information. For the prefrontal cortex to exert executive control, neuronal mechanisms for temporary storage of information and dynamic and flexible interactions among them are necessary. In this article, we present the presence of dynamic and flexible changes in the strength of functional interaction and extensive functional interactions among temporal information-storage processes in the prefrontal cortex. In addition, recent imaging studies show dynamic changes in functional connectivity between the prefrontal cortex and other cortical and subcortical structures depending upon the characteristics or the temporal context of the task. These observations indicate that the examination of dynamic and flexible modulation in neuronal interaction among prefrontal neurons as well as between the prefrontal cortex and other cortical and subcortical areas is important for explaining how the prefrontal cortex exerts executive control.

Animals↗

PubMed2000

Cholinergic modulation of synaptic transmission and plasticity in entorhinal cortex and hippocampus of the rat.

Effects of cholinergic agents on synaptic transmission and plasticity were examined in entorhinal cortex and hippocampus. Bath application of carbachol (0.25-0.75 microM) induced transient depression of field potential responses in all cases tested (24/24 in layer III of medial entorhinal cortex slices and 24/24 in CA1 of hippocampal slices; 11.0+/-1.9% and 7.8+/-2.5%, respectively) and long-lasting potentiation in some cases (4/24 in entorhinal cortex and 12/24 in hippocampus; 33.7+/-3.7% and 32.1+/-9.9%, respectively, in successful cases). Carbachol (0.5 microM) induced transient depression, but not long-lasting potentiation, of N-methyl-D-aspartate receptor-mediated responses in entorhinal cortex. At 5 microM, carbachol induced transient depression only (55. 9+/-4.7% in entorhinal cortex and 41.4+/-2.9% in hippocampus), which was blocked by atropine. Paired-pulse facilitation was not altered during carbachol-induced potentiation but enhanced during carbachol-induced depression. These results suggest that the underlying mechanisms of carbachol-induced depression and potentiation are decreased transmitter release and selective enhancement of non-N-methyl-D-aspartate receptor-mediated responses, respectively. Long-term potentiation could be induced in the presence of 10 microM atropine by theta burst stimulation. The magnitude was significantly lower (15.2+/-5.2%, n=9) compared with control (37.2+/-6.1%, n=8) in entorhinal cortex, however. These results demonstrate similar, but not identical, cholinergic modulation of synaptic transmission and plasticity in entorhinal cortex and hippocampus.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed2000

Nitrergic neurons make synapses on dual-input dendritic spines of neurons in the cerebral cortex and the striatum of the rat: implication for a postsynaptic action of nitric oxide.

Pre-embedding electron microscopic immunocytochemistry was used to examine the ultrastructure of neurons containing nitric oxide synthase and to evaluate their synaptic relationships with target neurons in the striatum and sensorimotor cerebral cortex. Intense nitric oxide synthase immunoreactivity was found by light and electron microscopy in a type of aspiny neuron scattered in these two regions. The intensity of the labeling was uniform in the soma, dendrites and axon terminals of these neurons. In both forebrain regions, nitric oxide synthase-immunoreactive neurons received synaptic contacts from unlabeled terminals, which were mostly apposed to small-caliber dendrites. The unlabeled symmetric contacts were generally about four times as abundant as the unlabeled asymmetric contacts on the nitric oxide synthase-immunoreactive neurons. Terminals labeled for nitric oxide synthase were filled with synaptic vesicles and were observed to contact unlabeled neurons. Only 54% (in the cerebral cortex) and 44.3% (in the striatum) of the nitric oxide synthase-immunoreactive terminals making apposition with the target structures were observed to form synaptic membrane specializations within the plane of the randomly sampled sections. The most common targets of nitric oxide synthase-immunoreactive terminals were thin dendritic shafts (54% of the immunoreactive terminals in the cortex and 75.7% of the immunoreactive terminals in the striatum), while dendritic spines were a common secondary target (42% of the immunoreactive terminals in the cortex and 20.6% of the immunoreactive terminals in the striatum). The spines contacted by nitric oxide synthase-immunoreactive terminals typically also received an asymmetric synaptic contact from an unlabeled axon terminal. These findings suggest that: (i) nitric oxide synthase-immunoreactive neurons in the cortex and striatum preponderantly receive inhibitory input; (ii) nitric oxide synthase-containing terminals commonly make synaptic contact with target structures in the cortex and striatum; (iii) spines targeted by nitric oxide synthase-containing terminals in the cortex and striatum commonly receive an asymmetric contact as well, which may provide a basis for a synaptic interaction of nitric oxide with excitatory input to individual spines.

Animals↗

PubMed2002

Effects of gonadectomy on immunoreactivity for choline acetyltransferase in the cortex, hippocampus, and basal forebrain of adult male rats.

Androgens are known to affect cognitive and mnemonic aspects of spatial processing. The cholinergic system is thought to play an important role in cognition and memory, but little is known about the interaction between androgen and cholinergic neurons. The present study focused on the effects of testosterone on the cholinergic neurons in the anterior cingulate cortex, the posterior parietal cortex, the hippocampus, and the basal forebrain including the medial septum, i.e., regions related to spatial processing. We examined choline acetyltransferase (ChAT) immunoreactivity in three groups of adult male rats: sham-operated (Sham), 28-day gonadectomized (GDX), and 28-day gonadectomized with immediate implantation of testosterone propionate (GDX+TP). Comparison of the Sham and GDX+TP groups demonstrated that the GDX group had significantly decreased cell counts of ChAT-immunoreactive neurons in anterior cingulate cortex layer II/III, posterior parietal cortex layer II/III, and the medial septum, but not in the other basal forebrain subregions examined (the horizontal part of the diagonal band of Broca and the substantia innominata). The GDX group also had significantly reduced hippocampal ChAT-immunoreactive fiber pixel density. The GDX+TP group maintained ChAT-immunoreactive cell counts in the anterior cingulate cortex, posterior parietal cortex, and medial septum equivalent to those in the Sham group. Less than 1% of identified cells showed colocalization of immunoreactivity for ChAT and androgen receptor in the cell bodies of the cortex and basal forebrain. Our observations demonstrate that the presence or absence of testosterone for 4 weeks influenced the cholinergic population region-specifically in the adult rat brain.

Acetylcholine↗

PubMed2002

Regulation of medial prefrontal cortex dopamine by alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate/kainate receptors.

In the medial prefrontal cortex, repeated cocaine produces tolerance of the extracellular dopamine response to subsequent cocaine injection. These studies characterized the influence of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate/kainate receptors on the medial prefrontal cortex dopamine response to acute cocaine, amphetamine and potassium chloride as a first step to assess whether these receptor subtypes may be candidates for mediating dopamine tolerance after repeated cocaine. Local infusion of 10 microM 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) produced an approximate 40% increase in dopamine levels in the medial prefrontal cortex, while a 30 microM dose did not alter basal levels infused over a 3-h period. Thus, 30 microM CNQX was chosen for the remaining experiments, and was infused for 1 h prior to and during all in vivo treatments. Local medial prefrontal cortex infusion of the 30 microM dose blocked the small increase in dopamine levels elicited by systemic saline injection (maximum of 26%), as well as the much larger increase in response to acute cocaine injection (maximum of 340%). Local infusion of D-amphetamine (3 and 30 microM) through the probe increased dopamine to 300 and 600% of basal levels, respectively. Co-infusion of CNQX partially blocked the response for the first 40 min, but dopamine levels recovered by 60 min later. Local infusion of 100 mM potassium chloride elicited a 600% increase in dopamine levels, which was attenuated approximately 50% by CNQX co-infusion. Potassium-stimulated release of dopamine was also measured in vitro in medial prefrontal cortical and striatal tissue. By 30 s after potassium addition, dopamine levels increased to 800% above baseline in the medial prefrontal cortex, and this increase was blocked by the presence of 30 microM CNQX. In contrast, potassium-stimulated dopamine release in striatal tissue was approximately 250% above basal levels, with no effect of CNQX on dopamine release. Locomotor behavior collected during dialysis experiments demonstrated that increased activity induced by local infusion of potassium chloride was severely attenuated by co-infusion of 30 microM CNQX, while no effects of this drug were found for cocaine-elicited behavior. These results suggest a potent influence of glutamate via alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate/kainate receptors on extracellular dopamine in the medial prefrontal cortex, and these receptors may regulate dopamine release through a presynaptic mechanism. The findings may help elucidate the role of medial prefrontal cortex dopamine-glutamate interactions in drug abuse and stress- and drug-precipitated psychosis.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed2003

Electrophysiological studies on the hippocampus and prefrontal cortex assessing the effects of amyloidosis in amyloid precursor protein 23 transgenic mice.

In vitro and in vivo electrophysiological studies were done to investigate the neuronal function of the hippocampus and prefrontal cortex in the amyloid precursor protein (APP) 23 transgenic mouse model for amyloidosis developed by Sturchler-Pierrat et al. [Proc Natl Acad Sci USA 94 (1997) 13287]. Brain slices were taken from 3, 6, 9, 12, 18 and 24 month old wildtype and hemizygous type APP23 mice. Extracellular field potentials were recorded from the CA1 region of the hippocampus while stimulating the Schaffer collaterals. In addition, extracellular field potentials were elicited from areas within layer V/VI of the prefrontal cortex by stimulating the same layer V/VI. Basic synaptic function in the hippocampus was reduced in hemizygous APP23 mice compared with their wildtype littermates at 12 and 18 months of age, whereas, it was unaltered within the prefrontal cortex. Long-term potentiation in the hippocampus and the prefrontal cortex of hemizygous APP23 mice was similar compared with their wildtype littermates. In vivo electrophysiological experiments were done in 3, 9, 18 and 24 month old wildtype and hemizygous APP23 mice. No differences were observed in the number of single spontaneously active units recorded within the prefrontal cortex of hemizygous APP23 mice compared with their wildtype littermates. Field potentials elicited during stimulation of cortico-cortical pathways to assess synaptic transmission and short-term synaptic plasticity were also unchanged in hemizygous APP23 mice. Furthermore, presumable antidromic field potentials recorded in the prefrontal cortex during stimulation of the striatum were similar between the hemizygous APP23 and wildtype mice at each age. The present study shows that amyloidosis impairs basic synaptic function but not long-term potentiation in the hippocampus, however, does not alter any of the neurophysiological functions measured within the prefrontal cortex. These findings suggest that amyloidosis may be involved in altering some neurophysiological functions within only certain brain structures. Although APP23 mice have impaired cognitive performance, long-term plasticity, a cellular model for memory, is not affected, raising the question on the relationship between these processes.

Action Potentials↗

PubMed1998

Neuronal damage after the injection of aminooxyacetic acid into the rat entorhinal cortex: a silver impregnation study.

In rats, most neurons in layer III of the medial entorhinal cortex are exquisitely vulnerable to prolonged seizure activity. These neurons have also been shown to die preferentially in the entorhinal cortex of patients with temporal lobe epilepsy. This lesion can be duplicated in rats by a focal injection of the indirect excitotoxin aminooxyacetic acid into the entorhinal cortex. The present study was designed to examine the neuropathological consequences of an intra-entorhinal aminooxyacetic acid injection at various time-points with a sensitive silver staining method for the visualization of damaged neurons. After 3 h, affected cells with prominently stained processes were readily observed in the transition zone of the hippocampal CA1 field and the subiculum, but no silver-stained neurons were seen in the entorhinal cortex. Less consistently, damaged neurons were observed in the presubiculum, in the temporal and perirhinal cortices and in the lateral amygdaloid nucleus. At 6 h after an aminooxyacetic acid injection, numerous silver-stained neurons, which were typically devoid of processes, were also seen in layer III of the medial entorhinal cortex. This pattern of neurodegeneration remained similar at 12 and 24 h following the aminooxyacetic acid injection, though many silver-stained neurons were noted in layer II of the lateral entorhinal cortex as well. Notably, at five days, silver-stained neurons had disappeared. Instead, dendritic arbors, debris of degenerated neurons and reactive glial cells were present in lesioned brain regions. These data demonstrate the chronology and the extent of neuronal damage following an intra-entorhinal injection of aminooxyacetic acid. The results suggest that a detailed examination of the temporal sequence of neuronal death in the entorhinal cortex and in extra-entorhinal areas is likely to benefit our understanding of the pathophysiology of temporal lobe epilepsy.

Aminooxyacetic Acid↗

PubMed1998

Ibotenic acid lesions of the dorsal prefrontal cortex disrupt the expression of behavioral sensitization to cocaine.

The present study determined the effect of bilateral lesions of specific cortical or thalamic nuclei that provide excitatory amino acid afferents to the nucleus accumbens (i.e. the dorsal prefrontal cortex, ventral prefrontal cortex, amygdala, hippocampus and periventricular thalamus) on the expression of cocaine-induced behavioral sensitization. Lesions of these nuclei were made during a three-week withdrawal period following repeated daily injections of cocaine or saline. The results indicate that dorsal prefrontal cortex lesions block the expression of behavioral sensitization to cocaine, while ventral prefrontal cortex, fimbria fornix, amygdala and thalamic lesions have no effect. A subsequent microdialysis experiment was performed in order to evaluate the effect of dorsal prefrontal cortex lesions on glutamate transmission in the nucleus accumbens core of cocaine- and saline-pretreated rats. The systemic injection of cocaine produced a significant increase in extracellular glutamate in the nucleus accumbens core among animals with a sham surgery; this effect was blocked by a bilateral lesion of the dorsal prefrontal cortex. Taken together, these results indicate that the dorsal prefrontal cortex, which provides excitatory amino acid input selectively to the core region of the nucleus accumbens, enhances the expression of behavioral sensitization to cocaine by increasing glutamate transmission in this subnucleus.

Animals↗

PubMed1998

Subthreshold membrane potential oscillations in neurons of deep layers of the entorhinal cortex.

Neuronal oscillations are important for information processing. The entorhinal cortex is one of the structures which is involved in generation of theta rhythm. The major role of the entorhinal cortex is to feed diverse sources of information both to and from the hippocampus. Far from simply being a funnel for this information it becomes clear that the entorhinal cortex has its own active properties that contribute to signal processing. Interestingly, stellate cells in layer II of the entorhinal cortex can intrinsically generate subthreshold, Na+-dependent membrane potential oscillations. Here, using intracellular and patch-clamp recordings, we report a similar phenomenon from neurons of the deep layers of the entorhinal cortex. In our in vitro slice preparation about two-thirds of recorded neurons were able to generate voltage-sensitive subthreshold membrane potential oscillations. At a membrane potential of about 50 mV the mean frequency of the voltage-oscillations was 8.1 Hz, whereby at slightly more positive potentials (-44 mV) the frequency of the membrane potential oscillations was 20 Hz and the oscillations became interrupted by clusters of non-adapting trains of spikes. Pharmacological experiments revealed that the oscillations were not affected by Cs+, but could be blocked by the fast Na+-channel blocker tetrodotoxin. We therefore conclude that voltage- and Na+-dependent subthreshold membrane potential oscillations are not only present in stellate cells of entorhinal cortex-layer II, but are also typical for neurons of the deep layers of the entorhinal cortex.

Animals↗