SEARCH · PubMed Health

Results for “cortex”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,639 records · Page 91Linked to original sources

PubMed1992

Excitotoxic lesions of rat basal forebrain: differential effects on choline acetyltransferase in the cortex and amygdala.

Previous studies have shown that basal forebrain lesions using different excitotoxins produce similar decreases in cortical choline acetyltransferase, but differential effects on memory. However, basal forebrain cholinergic neurons send efferents to the amygdala and cortex. The present studies compared the effects of several excitotoxins on choline acetyltransferase levels in both of these structures. Lesions of the basal forebrain were made in rats by infusing different doses of either alpha-amine-3-hydroxy-5-methyl-4-isoxazole propionic acid, ibotenic acid, quisqualic acid, quinolinic acid or N-methyl-D-aspartic acid and measuring choline acetyltransferase seven days later. All of the excitotoxins exerted a differential response on cholinergic neurons of the basal forebrain projecting to the cortex or amygdala. Quinolinic acid was a more potent neurotoxin to cholinergic neurons innervating the amygdala than those projecting to the cortex. In contrast, quisqualic acid and alpha-amine-3-hydroxy-5-methyl-4-isoxazole were more potent neurotoxins to the cortical projection. alpha-Amine-3-hydroxy-5-methyl-4-isoxazole propionic acid was the most potent excitotoxin for destroying cholinergic neurons innervating either the cortex or amygdala. A parallel neurotoxic response was obtained in the cortex and amygdala following infusion of ibotenic acid or N-methyl-D-aspartic acid with little selectivity for choline acetyltransferase depletion in the cortex or amygdala. Histological analysis of the injection site revealed that acetylcholinesterase-positive neurons were destroyed by the excitotoxins in a dose-dependent manner. Excitotoxins (ibotenic acid, quinolinic acid, N-methyl-D-aspartic acid) that produce the greatest impairments in memory were found to produce the greatest depletion of choline acetyltransferase in the amygdala.(ABSTRACT TRUNCATED AT 250 WORDS)

Amygdala↗

PubMed1992

Influences from different areas of the cerebral cortex on preoptic neurons: morphological and electrophysiological data.

Spatial organization of neurons in the prefrontal and cingulate cortex, cortex of the piriform lobe and the hippocampus which project axons to the preoptic region, has been studied in cats using horseradish peroxidase tracing. Cortical areas were selected taking into consideration their phylogenetical distinctions. The prefrontal cortex was found to send a major portion of fibres to the preoptic region, while the density of units forming such connections was maximal in the cingulate cortex. Field potentials and neuronal reactions of the medial and lateral divisions of the preoptic region and the adjacent hypothalamic zones were studied in ketamine-anaesthetized cats. The most pronounced field potentials were recorded in the preoptic region upon stimulation of the cortex of the piriform lobe and cingulate cortex. There was a close correlation between the responses of single neurons and components of the field potentials. The majority of neurons responding to cortical stimuli were located mainly in the lateral preoptic region, where the larger amount of primary excitatory reactions were recorded. The medial preoptic region contained a smaller number of responsive neurons prevailingly generating the primary inhibitory reactions. For the lateral preoptic region the inhibition/excitation ratio was 0.6:1 at all cortical stimulations, but for the medial region it was 5.8:1. In the preoptic division adjoining the bed nucleus of the stria terminalis, the primary inhibitory reactions considerably prevailed over the primary excitatory; on the other hand, in the supraoptic nucleus the primary excitatory reactions prevailed weakly (ratios of 4.9:1 and 0.7:1, respectively). The preoptic region was found to be a zone of wide convergence of cortical inputs to single cells, where three-quarters of neurons responded to the stimulation of two, three or even four cortical areas.

Animals↗

PubMed1993

Reversal of paw preference after ablation of the preferred forelimb primary motor cortex representation of the rat depends on the size of the forelimb representation.

Animals were tested for forelimb preference in a grasp or in a force task before microstimulation mapping of the primary motor cortex contralateral to the preferred forelimb. The size and location of the preferred forelimb primary motor cortex representation was determined and ablated. Seven days later, forelimb preference was again evaluated. Reversal of the initial preference after cortical ablation depended on the size of the preferred forelimb primary motor cortex representation. The mean size of the forelimb representation of the animals that immediately reversed forelimb preference after the cortical ablation was significantly smaller than the mean size of the representation of the animals that did not reverse forelimb preference in three consecutive tests seven days after the lesion. In another experiment, the size, location, and threshold currents of the forelimb representations were evaluated bilaterally before the forelimb preference test. The mean size of the preferred representations did not differ from the mean size of the non-preferred representations. However, when the primary motor cortex representation of the preferred forelimb was ablated, reversal of the initial preference depended, as in the previous experiment, on the size of the forelimb representation. In conclusion, reversal of forelimb preference after ablation of the preferred forelimb primary motor cortex representation depends on the size of the forelimb representation. Moreover, forelimb preference in a behavioral task is not associated with a larger forelimb representation in the contralateral primary motor cortex.

Animals↗

PubMed1994

The induction of serotonin3-like receptor supersensitivity and dopamine receptor subsensitivity in the rat medial prefrontal cortex after the intraventricular administration of the neurotoxin 5,7-dihydroxytryptamine: a microiontophoretic study.

This study examines the effect of intraventricular administration of the neurotoxin 5,7-dihydroxytryptamine on serotonin1A, serotonin2 and serotonin3 receptors in the rat medial prefrontal cortex using in vivo extracellular single cell recording and iontophoresis. Iontophoresis of the serotonin1A, serotonin1C,2 and serotonin3 receptor agonists (+-)-8-hydroxy-(di-n-propyl)aminotetralin, (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane and 2-methylserotonin, respectively, produces a current-dependent (5-80 nA) suppression of the basal firing rate of medial prefrontal cortical cells in sham- and 5,7-dihydroxytryptamine-lesioned rats. The suppression produced by 2-methylserotonin and serotonin was significantly greater in 5,7-dihydroxytryptamine-lesioned rats than in control rats. No significant difference in the spontaneous activity of medial prefrontal cortex cells was observed between experimental and control rats after iontophoresis of (+-)-8-hydroxy-(di-n-propyl)aminotetralin or (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane. There was no significant difference between the groups regarding the response of medial prefrontal cortex cells to the iontophoresis of GABA, whereas the response of medial prefrontal cortex cells to the iontophoresis of dopamine was significantly attenuated in animals pretreated with 5,7-dihydroxytryptamine compared to controls. Our results indicate that 5,7-dihydroxytryptamine-induced denervation selectively enhances the sensitivity of serotonin3-like receptors in the medial prefrontal cortex, which could, at least partially, account for the serotonin denervation supersensitivity. Moreover, the finding that the response of medial prefrontal cortical cells to the iontophoresis of dopamine is attenuated in 5,7-dihydroxytryptamine pretreated rats is consistent with the view that the inhibitory action of dopamine in the medial prefrontal cortex is dependent upon serotonin tone.

5,7-Dihydroxytryptamine↗

PubMed1996

Prefrontal cortex inputs of the nucleus accumbens-nigro-thalamic circuit.

The functional organization of the cortico-nucleus accumbens-substantia nigra pars reticulata circuit was investigated in the rat using combined anatomical and electrophysiological approaches. The nucleus accumbens neurons which project to the substantia nigra pars reticulata are located in a circumscribed region of the core immediately adjacent and extending dorsally to the anterior commissure. As shown by retrograde and anterograde transports of wheatgerm agglutinin conjugated to horseradish peroxidase, the region of the nucleus accumbens related to the substantia nigra was found to receive bilateral inputs from restricted areas of the medial and lateral prefrontal cortex, i.e., prelimbic/medial orbital and dorsal agranular insular areas. The electrical stimulation of these medial and lateral prefrontal cortical areas induced excitatory responses in nucleus accumbens neurons projecting to the dorsomedial substantia nigra pars reticulata. Interestingly, an important proportion (61%) of the nucleus accumbens-nigral cells responding to the stimulation of the lateral prefrontal cortex were also excited by the stimulation of the medial prefrontal cortex, demonstrating the existence of a convergent influence of these cortical areas on single nucleus accumbens cells. Furthermore, the present data also show that the stimulation of the medial prefrontal cortex results in a powerful inhibition of the tonic firing of the substantia nigra pars reticulata neurons. In conclusion, this study reveals the existence of a functional link between the prefrontal cortex (prelimbic/medial orbital and agranular insular areas) and the nucleus accumbens neurons which innervate the dorsomedial region of the substantia nigra pars reticulata. Since the dorsomedial region of substantia nigra pars reticulata is known to project to subfields of the mediodorsal and ventromedial thalamic nuclei related to the prefrontal cortex, the present data further demonstrate the existence of a prefrontal-nucleus accumbens-thalamo-cortical circuit involving the substantia nigra pars reticulata.

Animals↗

PubMed1986

Visual cortex controls retinal output in the rat.

The first objective of the present investigation was to shed more light on corticofugal influences on the retina by providing an analysis of the type and proportion of retinal ganglion cells that are affected by cooling the visual cortex in rats. The second question was to determine if the pretectum participates in functional cortico-retinal relationships. In urethane-anesthetized and paralyzed hooded rats, axonal activity of retinal ganglion cells was recorded with glass micropipettes at optic chiasm level. Units were classified as ON, OFF, suppressed-by-light and concentric. The visual cortex was inactivated by cooling its surface with a 4 mm2 steel probe using the Peltier effect. The pretectum was blocked with microinjections of 50 to 100 nanoliters of cobalt ions, lidocaine hydrochloride or KCl. The inactivations and recoveries at both sites were monitored by simultaneously recording evoked field potentials. Interrupting corticofugal impulses caused modifications of the evoked discharge pattern in all types of cells. The concentric type was the group least affected by cortical cooling. A common trend emerged suggesting that cooling of the visual cortex led to an enhancement of the initial evoked excitation. This was often followed by an enhanced post-excitatory inhibition. The Pearson coefficient allowed us to measure the degree of similarity between two histograms. When all data were pooled, a weak correlation between control and test histograms (r = 0.29, N = 56) was found, while the control and recovery patterns averaged a correlation of more than twice that size (r = 0.68). In a second series of experiments, the pretectum and visual cortex (VC) were simultaneously inactivated. It is shown that both sites summed their influence and acted synergistically upon the pattern of ganglion cell responses. The results strongly suggest that the visual cortex exerts a major control over the response pattern of thirty percent of retinal ganglion cells, and that the pretectum participates in the functional relationships between visual cortex and retina in rats.

Animals↗

PubMed1987

Reciprocal functional connections of the olfactory bulbs and other olfactory related areas with the prefrontal cortex.

Reciprocal putative connections of the prefrontal cortex (PFC) (agranular insular, ventral and lateral orbital region) with the ipsi and contralateral main olfactory bulb (IOB; COB), the mediodorsal thalamic nucleus (MD), the basolateral amygdaloid nucleus (BLA) and the piriform cortex (PC) were investigated with electrophysiological techniques. Evoked field responses and orthodromic unit driving, generated in PFC following electrical stimulation of the above mentioned structures, were abolished following topical application of KCl, except for COB evoked mass potentials. Thus, locally generated activity was elicited in agranular insular cortex following IOB activation, the same region where recently, the taste cortex in the rat was localized. Since gustatory-visceral afferent information reaches insular cortex via 2-3 synaptic relays, autonomic, olfactory and gustatory inputs may interact at this level, and, as suggested previously for the mouse, play a key integrative role in flavor perception. Antidromically invaded neurons, 47% of which were identified by the collision-extinction technique, were also found in PFC areas which overlapped to a considerable extent with those from which orthodromic unit responses were obtained. In particular, closely spaced neurons in ventrolateral orbital (VLO) and lateral orbital (LO) regions were antidromically invaded following IOB and PC shocks; some neurons antidromically discharged by IOB were also transsynaptically activated following PC stimulation. These findings are in agreement with recent neuroanatomical studies which demonstrate axonal projections from PFC neurons to the IOB and COB in the rat and South American armadillo. In addition, stimulation of PFC regions dorsal to the rhinal fissure mostly inhibited spontaneous unit discharges recorded at the mitral cell layer of the IOB, suggesting that this effect may be partially mediated by excitatory inputs of prefrontal axons onto granule cells. The conduction properties, antidromic thresholds and activity-dependent variations in conduction velocity (CV) of bulbopetal neurons in prefrontal cortex were found to be similar to those exhibited by cells projecting to the IOB from olfactory peduncle regions, but not to those present in bulbopetal neurons of the horizontal limb of diagonal band, indicating that the OB may be subjected to centrifugal control by at least two cell groups differing in both histochemical and electrophysiological properties.

Afferent Pathways↗

PubMed1989

Mode of [14C] 2-deoxy-D-glucose uptake into retrosplenial cortex and other memory-related structures of the monkey during a delayed response.

Physiological studies on the monkey retrosplenial (RS) cortex have been few, and its functional role remains to be investigated. In the present study, activity of the RS cortex was investigated using radioactive 2-DG while the monkey was performing a visual tracking task with a delay (a delayed-response task) for 45 minutes. A remarkable increase in 2-DG uptake was observed equally in the left as well as in the right RS cortex. The anterior nucleus of the thalamus also showed increased 2-DG uptake. In addition, other memory-related structures (prefrontal cortex, dorsomedial nucleus of the thalamus, amygdala and hippocampus) showed a similar increase in 2-DG uptake compared to control monkeys, though their respective absolute values were different from one another. Since the RS cortex receives afferents from the anterior nucleus of the thalamus, which is one of the main nuclei of the Papez circuit, it is assumed that the RS cortex is important in memory function. Therefore, the remarkable increase in 2-DG uptake in the present study could reflect some aspects of memory or learning processes required to perform the delayed response.

Animals↗

PubMed1991

Unilateral kindling of the inferior collicular cortex does not transfer to the contralateral seizure sensitive site or alter [3H]flunitrazepam and [35S]TBPS binding.

Acute electrical stimulation of a specific area in the inferior collicular cortex produced bilateral collicular afterdischarge and symmetrical wild running seizures. However, generalized seizures induced by kindling the inferior collicular cortex did not alter the kindling rate in the contralateral side. Furthermore, after both sides of the inferior collicular cortex have been kindled unilateral electrolytic lesions did not alter the seizure initiation or generalization elicited from the contralateral side. Since GABAergic function has been implicated in inferior collicular seizures, potential seizure-induced changes were measured for the chloride channel ([35S]TBPS) and the benzodiazepine receptor ([3H]flunitrazepam). Prior kindling did not alter [35S]TBPS or [3H]flunitrazepam binding in the central nucleus or cortex of the inferior colliculus, the medial geniculate, or the deep prepiriform cortex. Thus, the permanent neural change that subserves seizure generalization from the inferior collicular cortex is unilateral, but this change is not reflected by altered binding characteristics of the GABAA receptor complex.

Animals↗

PubMed1993

The binding of the adenosine A2 receptor selective agonist [3H]CGS 21680 to rat cortex differs from its binding to rat striatum.

The binding of the reportedly A2A selective agonist CGS 21680 (2-[p-(2-carboxyethyl)phenylethylamino]-5'N-ethylcarboxamidoadenos ine) to cortex and striatum was examined in parallel using quantitative receptor autoradiography. [3H]CGS 21680 bound to a single site in rat striatum with KD 2.3 nM and Bmax 320 fmol/mg grey matter. In addition [3H]CGS 21680 bound to a single site in the cerebral cortex with KD 47 nM and Bmax 100 fmol/mg grey matter. In cat cortex [3H]CGS 21680 (2 nM) binding was strong and particularly evident in the most superficial layers. The potency order for inhibition of 2 nM [3H]CGS 21680 binding to rat striatum was NECA (5'-N-ethylcarboxamidoadenosine; IC50 9.0 nM) > 2-CADO (2-chloroadenosine; 87 nM) > R-PIA (N6-(R)-phenylisopropyladenosine; 110 nM). The potency order for inhibition of 2 nM [3H]CGS 21680 binding to rat cortex was NECA (3.0 nM) > 2-CADO (14 nM) > or = R-PIA (16 nM). Gpp(NH)p (5'-guanylyl imidodiphosphate) inhibited [3H]CGS 21680 binding to both cortex and striatum, but more potently in cortex (IC50 100 nM vs. 470 nM). The present results show that there is a cortical binding site for [3H]CGS 21680 which appears to be different from the the striatal A2A receptor, the A2B receptor and the A1 receptor.

Adenosine↗

PubMed1995

Hypofrontality does not occur with 6-hydroxydopamine lesions of the medial prefrontal cortex in rat brain.

This study examined the effect of lesions of dopamine (DA) nerve terminals the medial prefrontal cortex on local cerebral glucose utilization (LCGU) and dopamine metabolism in the rat brain. Bilateral 6-hydroxydopamine lesions were stereotaxically placed in the medial prefrontal cortex. Twenty-eight days after the lesion, concentrations of DA and its metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), were determined in eight brain regions with a high-performance liquid chromatographic assay. LCGU was assessed by [14C]2-deoxy-D-glucose autoradiography. The lesion produced a striking reduction in DA (to 6% of the control value), and a moderate reduction in DOPAC and HVA in the medial prefrontal cortex. The ratio of DOPAC to DA in the medial prefrontal cortex was significantly elevated in the 6-OHDA lesioned animals. In contrast to DA depletion, LCGU in the medial prefrontal cortex of the lesioned rats was unaltered when compared with the control. These findings suggest that decreased energy metabolism in the frontal cortex, i.e., hypofrontality, does not occur with decreased DA innervation of that site.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1994

Intracellular progesterone receptors are differentially regulated by sex steroid hormones in the hypothalamus and the cerebral cortex of the rabbit.

The aim of this study was to examine the role of sex steroid hormones in the regulation of intracellular progesterone receptors (PR) in the rabbit central nervous system. We determined PR concentration in cytosol preparations from the hypothalamus, the frontal, tempo-parietal and occipital cortex, by using the specific binding of the synthetic progestin [3H]ORG 2058. PR concentration was higher in the hypothalamus of intact adult females than in that of adult males and prepubertal females, whereas no significant differences were observed in the cerebral cortex of these animals. PR concentration was similar in the three cortical regions analyzed, indicating a homogeneous distribution of PR in the cerebral cortex. The administration of estradiol to ovariectomized animals increased PR concentration in the hypothalamus but not in the cortex. The administration of progesterone to ovariectomized rabbits did not modify PR concentration in any region, however when progesterone was administered after estradiol, it induced a significant diminution in hypothalamic PR concentration without effects in the cortex. These findings suggest that in the rabbit, PR are estrogen regulated in the hypothalamus but not in the cerebral cortex. In the latter, PR are not regulated by progesterone, whereas in the former the estrogen-induced PR are down-regulated by progesterone. Interestingly, hypothalamic PR constitutively expressed in ovariectomized animals are progesterone-insensitive.

Animals↗

PubMed2006

Peripheral immune activation by lipopolysaccharide decreases neurotrophins in the cortex and hippocampus in rats.

Lipopolysaccharide (LPS), a cell wall component of Gram-negative bacteria, induces neuronal death, decreases neurogenesis, and impairs synaptic plasticity and memory, but the mechanisms for these effects are not well understood. We hypothesize that neurotrophin levels in the brain are influenced by LPS. To test this hypothesis, we determined effects of LPS on brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), and NT-3 levels in the brain after intraperitoneal injection of saline or LPS (0.1, 0.3 or 1.0mg/kg) in rats. LPS significantly decreased BDNF in the hippocampus (-20%), frontal cortex (-19%), parietal cortex (-63%), temporal cortex (-29%), and occipital cortex (-41%). LPS also significantly decreased NGF levels by 10-20% in the hippocampus and different cortical regions, except in the occipital cortex. Finally, LPS decreased NT-3 by 15-25% in the frontal cortex. These observations indicate that the neuroprotection mediated by neurotrophins in the brain are compromised by systemic immune activation induced by LPS.

Animals↗

PubMed2003

Dissociable aspects of performance on the 5-choice serial reaction time task following lesions of the dorsal anterior cingulate, infralimbic and orbitofrontal cortex in the rat: differential effects on selectivity, impulsivity and compulsivity.

It is becoming increasingly apparent that multiple functions of the frontal cortex such as inhibitory control and executive attention are likely sustained by its functionally distinct and interacting sub-regions but the precise localization of dissociable executive processes has proved difficult and controversial. In the present series of studies, we investigated the behavioural effects of bilateral excitotoxic lesions of different regions of the rat neocortex in the 5-choice serial reaction time task. Whereas lesions of the dorsal anterior cingulate cortex (ACC) impaired performance of the task as revealed by a reduction in discriminative accuracy, lesions made to distinct ventral regions of the frontal cortex showed selective deficits in inhibitory measures of control. Specifically, the infralimbic lesion produced increases in premature responding that was accompanied by fast response latencies. By comparison, the orbitofrontal lesion showed perseverative tendencies particularly when the inter-trial interval was made long and unpredictable, a challenge that would normally promote premature responding instead. These different behavioural effects following dorsal and ventral lesions of the rodent frontal cortex signifies the integrity of the frontal cortex in multiple executive mechanisms that work independently and complementarily by which performance is optimized. Furthermore, these data provide new insights into the functional organization of the rodent frontal cortex with a particular emphasis on localization of function.

Animals↗

PubMed2003

Inactivation of the infralimbic prefrontal cortex reinstates goal-directed responding in overtrained rats.

Over the course of extended training, instrumental responding in rats shows a transition from goal-dependent performance to goal-independent performance, as assessed by sensitivity to reward-devaluation induced by taste aversions or specific satiety. It has been suggested that this reflects the gradual dominance of reflexive, habit-based responding over voluntary, goal-directed actions. Previous research suggests that lesions of the medial prefrontal cortex disrupt this interaction between goal-directed and habitual responding. More specifically, whereas lesions of the prelimbic prefrontal cortex appear to disrupt normal goal-directed responding, lesions of the infralimbic prefrontal cortex cause animals to remain goal-directed even after substantial overtraining. The current experiment explored further the nature of this interaction between actions and habits. Rats were given extended training of an instrumental lever press response before bilateral intracerebral cannulae giving access to the infralimbic cortex were implanted. Following further reminder training all animals were given a test of goal sensitivity by specific-satiety devaluation of the instrumental outcome, or a matched reward, prior to extinction tests. Before these tests, half of the animals received bilateral infusions of muscimol into the infralimbic cortex, and the remainder, control vehicle infusions. As expected after extended instrumental training, control-infused animals showed habitual performance that was not selectively influenced by devaluation of the instrumental outcome. In contrast, animals receiving temporary inactivation of the infralimbic cortex by muscimol showed selective sensitivity to devaluation of the instrumental outcome, indicating a reinstatement of goal-directed responding in these animals. This suggests that the development of habitual responding reflects the active inhibition of goal-directed responses that are mediated by action-outcome associations.

Analysis of Variance↗

PubMed2006

Localization and developmental ontogeny of the pro-apoptotic Bnip3 mRNA in the postnatal rat cortex and hippocampus.

Naturally occurring cell death occurs during the first two postnatal weeks in the rat cortex and hippocampus. During this process, apoptosis is initiated by activating or altering expression of pro-apoptotic members of the Bcl-2 family. Bnip3 is a pro-apoptotic member of the Bcl-2 family that induces cell death by opening the mitochondrial permeability transition pore. To date, Bnip3 expression in the central nervous system has only been examined during hypoxia-mediated apoptosis in the adult rat brain. In this study, we investigated the localization and ontogeny of Bnip3 mRNA expression in the postnatal male and female rat brain. Bnip3 mRNA was localized by in situ hybridization in the neonatal cortex, hippocampus, habenula and thalamus. Using quantitative real-time RT-PCR, Bnip3 mRNA levels were found to be greatest at postnatal day 6.5 in the female anterior and posterior cingulate cortices and hippocampus. Bnip3 mRNA expression also increased in the male anterior cingulate cortex at postnatal day 6.5. However, a developmental change in Bnip3 levels did not occur in the male posterior cingulate cortex and hippocampus. In the anterior cingulate cortex on postnatal day 6.0 and adulthood, female rats had significantly greater levels of Bnip3 mRNA compared to that of males. Altering levels of testosterone in the neonatal rat did not alter the sex differences in Bnip3 mRNA levels. The transient increase in Bnip3 mRNA expression correlates with naturally occurring cell death in the neonatal rat cortex and hippocampus. Thus, Bnip3 may be a mediator of developmental apoptosis in the postnatal rat brain.

Animals↗

PubMed2007

Changes in estrogen receptor-alpha mRNA in the mouse cortex during development.

Estrogen plays a critical role in brain development and is responsible for generating sex differences in cognition and emotion. Studies in rodent models have shown high levels of estrogen binding in non-reproductive areas of the brain during development, including the cortex and hippocampus, yet binding is diminished in the same areas of the adult brain. These binding studies demonstrated that estrogen receptors decline in the cortex during development but did not identify which of the two estrogen receptors was present. In the current study, we examined the expression of estrogen receptor alpha (ERalpha) and estrogen receptor beta (ERbeta) in the mouse cortex during the first month of life. Messenger RNA was isolated from cortical tissue taken from C57BL/6 mice on postnatal day (PND) 1, 4, 10, 18 and 25 and expression levels were determined by real-time PCR. ERalpha mRNA expression in the mouse cortex at PND 25 was significantly reduced as compared to PND 1 (p<0.01). ERbeta mRNA expression at PND 25 was significantly increased as compared to PND 1 (p<0.05). Although the increase in ERbeta mRNA was statistically significant, the ERbeta levels were extremely low in the isocortex compared to ERalpha mRNA levels, suggesting that ERalpha may play a more critical role in the developmental decrease of estradiol binding than ERbeta. Additionally, we measured ERalpha mRNA expression in organotypic explant cultures of cortex taken from PND 3 mice. Explants were maintained in vitro for 3 weeks. mRNA was isolated at several time points and ERalpha and ERbeta mRNA was measured by real-time RT-PCR. ERalpha and ERbeta mRNA levels reflected a similar pattern in vitro and in vivo, suggesting that signals outside the cortex are not needed for this developmental change. This study lays the groundwork for an understanding of the mechanisms of the developmental regulation of ERalpha mRNA.

Aging↗

PubMed2005

Effects of the metabotropic glutamate receptor agonist, ACPD, on the extracellular concentrations of GABA and acetylcholine in the prefrontal cortex of the rat during the normal process of aging.

The aim of the present study was to investigate the effects of activation of metabotropic glutamate receptors (mGluR) on the extracellular concentrations of GABA and acetylcholine in the prefrontal cortex of freely moving rats of different groups of age. Perfusion, through the microdialysis probe, of the agonist of mGluR, (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD; 100, 500 and 1000 microM), in the prefrontal cortex of young rats produced a dose-related increase of the dialysate concentrations of GABA. The effects of perfusion of ACPD on the concentrations of GABA were attenuated in middle-aged rats. In the prefrontal cortex of aged rats, perfusion of ACPD produced no changes in dialysate concentrations of GABA at any of the doses used. Conversely, perfusion of ACPD (100, 500 and 1000 microM) in the prefrontal cortex of young, middle-aged and aged rats did not modify the dialysate concentrations of acetylcholine. Basal concentrations of acetylcholine in the prefrontal cortex of middle-aged and aged rats were significantly lower than those in young rats. In contrast, basal dialysate concentrations of GABA were not significantly different in young, middle-aged and aged rats. These results suggest that the interaction GABA-glutamate in the prefrontal cortex, mediated by mGluRs, changes with age.

Acetylcholine↗