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PubMed1999

Optical recording of cortical activity after in vitro perfusion of cerebral arteries with a voltage-sensitive dye.

Cortical neuronal architecture and connectivity can be analyzed with high-resolution optical imaging after staining the in vitro isolated guinea pig brain preparation by circulating the voltage-sensitive dye RH795 via the arterial system. To establish this new technique, electrical field potentials evoked in the piriform and entorhinal cortices by lateral olfactory tract stimulation were correlated to the optical signal. The depth analysis of the optical response was performed by evaluating the contribution of the mono- and poly-synaptic components of the signal generated in different layers after applying a pair-pulse stimulation protocol. The tangential propagation of neuronal activity in olfactory cortices was evaluated by gathering several 4.2 x 4.2 mm images recorded from adjacent cortical areas. The real-time optical imaging technique applied to the isolated guinea pig brain can be successfully utilized to study the integrative properties of cortical neurons ensembles.

Animals↗
PubMed2002

Detection of late epilepsy by the texture analysis of MR brain images in the lithium-pilocarpine rat model.

The aim of the study was to detect by texture analysis non easily visible anomalies of magnetic resonance (MR) images of piriform and entorhinal cortices relevant to the lithium-pilocarpine (Li-Pilo) model of temporal lobe epilepsy in rats. Status epilepticus was induced by Li-Pilo in twenty male rats 21 day-old. T(2)-weighted MR images of their brain, were obtained before injection of Li-Pilo and one day after status epilepticus. An hyperintense signal was found in the piriform and entorhinal cortices of six rats, which developed chronic epilepsy after a latent period of one to three months. Among the 14 other rats which displayed images similar to those obtained before injection, four remained healthy but 10 rats developed late epileptic symptoms, raising the problem of hidden cortical damage which may be too subtle to be detected by classic MRI examination. A numeric treatment of digital images was then undertaken by texture analysis, to derive image information from a purely computational point of view. The combined texture and discriminant analyses based on pixels pattern anomalies, selected 3 texture parameters derived from co-occurrence matrix which characterized structural abnormalities relevant to the hyperintense signal, not only in the modified images of 6 rats but also in images of 10 rats with apparently non modified images. These three texture's parameters allowed to classify the twenty rats of our experiment as follows: sixteen epileptic rats were effectively classified with cortical lesions, two non epileptic were correctly classified with healthy cortex, but two healthy rats were not correctly classified. This misclassification is discussed on the basis of the time dependence of the onset of seizure in the Li-Pilo model. These promising results suggest to apply this method to MRI examinations for an improvement of the early diagnostic of human epilepsy.

Animals↗
PubMed1998

Local cerebral glucose utilization in adult and immature GAERS.

In the present study, we compared the basal local cerebral metabolic rates for glucose (LCMRglcs) both in Wistar rats with genetic absence epilepsy (GAERS: genetic absence epilepsy rats from Strasbourg) and in control non epileptic (NE) rats selected in our breeding colony. LCMRglc was measured both in immature rats at postnatal day 21 (P21) at which age no spontaneous spike-and-wave discharges can be recorded in GAERS and at the adult age (6 months) when GAERS fully express thalamo-cortical spike-and-wave discharges recorded on the EEG. LCMRglcs were measured in 24 structures by the quantitative [14C]2-deoxyglucose autoradiographic technique. In adults GAERS, LCMRglc underwent a widespread increase recorded in all brain structures except in mediodorsal and ventromedian thalamus, and in the nucleus accumbens. These metabolic increases ranged from 17 to 50% over control levels in adult NE rats. In P21 GAERS, LCMRglc was similar to that of P21 NE rats in 16 areas. It increased over control levels of NE rats in two groups of structures. Metabolic increases were recorded in four limbic structures (entorhinal and piriform cortices, hippocampus and basolateral amygdala) where no spike-and-wave discharges were recorded in adult GAERS. Increases in LCMRglcs were also located in the substantia nigra pars reticulata, superior colliculus and globus pallidus which are structures involved in the control of seizure activity. In conclusion, our data suggest that the consequences of the genetic mutation(s) underlying the cellular and molecular events responsible for the expression of spike-and-wave discharges in adult GAERS is (are) able to increase metabolic activity in both limbic structures and the nigral inhibitory system before the occurrence of spike-and-wave discharges.

Aging↗
PubMed2000

Involvement of cerebral cortical structures in the classical conditioning of eyelid responses in rabbits.

The classical conditioning of the eyelid motor system in alert behaving rabbits has been used to study the expression of Fos in the hippocampus, and in the occipital, parietal, piriform and temporal cortices. Animals were classically conditioned with both delay and trace conditioning paradigms. As conditioned stimulus, both short and long (20 and 100 ms) tones (600 Hz, 90 dB) or short, weak (20 ms, 1kg/cm(2)) air puffs were used. The unconditioned stimulus was always a long, strong (100 ms, 3 kg/cm(2)) air puff that started 250-270 ms after the onset of the conditioned stimulus. The expression of Fos was significantly increased after both delayed and trace conditioning in the hippocampus, and in the parietal and piriform cortices contralateral to the unconditioned stimulus presentation side, compared with equivalent ipsilateral structures in conditioned animals, or with Fos production in the same contralateral structures in pseudo-conditioned and control animals. Fos expression in some cortical sites was specific to tone versus air puff stimuli when used as conditioned stimulus. Thus, Fos expression was significantly increased in the contralateral temporal lobe when tones were used as conditioned stimulus, for both delayed and trace conditioning paradigms, but not when animals were conditioned to short, weak air puffs. The present results indicate a specific Fos activation in several cerebral cortical structures during associative eyelid conditioning.

Animals↗
PubMed1996

Kindling induces neuropsin mRNA in the mouse brain.

Neuropsin mRNA expression was analyzed and mapped in the mouse brains after kindling epileptogenesis by using in situ hybridization histochemistry. Dynamic increases of the neuropsin mRNA were observed in the layer II of prelimbic, somatosensory, auditory, perirhinal, entorhinal, and piriform cortices in an activity-dependent manner, though no neuropsin gene was expressed in these areas in control mice. In addition to the confirmation of our previous studies showing increases of mRNA in the hippocampus and amygdaloid complex, there were also remarkable increases of the neuropsin mRNA in the limbic areas, such as the accessory olfactory nucleus, the medial and lateral septal nucleus, the nucleus of diagonal band, the substantia innominata and the zona incerta. The dynamic activity-dependent changes of the gene expression and the site-specificity of neuropsin localization are suggesting that this molecule is implicated in cortical- and limbic-specific neuronal reorganization.

Animals↗
PubMed2000

Interruption of supramammillohippocampal afferents prevents the genesis and spread of limbic seizures in the hippocampus via a disinhibition mechanism.

In this study we describe the preventive effect of interruption of the supramammillohippocampal afferents on the Fos expression in the forebrain and epileptic discharges in the hippocampal electroencephalogram in rat model of kainic acid-induced limbic seizure. Little was known about the contribution of different degrees of neural activity of hippocampal principal cells to the genesis and spread of limbic seizures in the forebrain structures. Following kainic acid injection to the amygdala with or without concurrent injection of muscimol to the supramammillary nucleus, behavioral changes and electroencephalograms were observed in freely moving rats. The animals were processed for Fos immunocytochemical analysis at several time points. The latest expression of Fos at 2h was seen in hippocampal CA1-CA3, ventrolateral thalamic nuclei and mediodorsal caudate putamen, while the early Fos expression at 0.5h was seen in the piriform, entorhinal and other cortices, the thalamic midline nuclei and hypothalamic nuclei. Muscimol injection to the supramammillary nucleus prevented Fos expression in the CA1-CA3 region and reduced that in the forebrain regions with the latest Fos expression, but did not affect Fos expression in other forebrain regions with early Fos expression. This treatment also eliminated epileptic discharges and attenuated all waves in hippocampus. These findings indicate that an acute interruption of the facilitatory hypothalamic afferents by intrasupramammillary injection of muscimol may cause the inactivation of the disinhibition mechanism for hippocampal throughput at the dentate gyrus, resulting in the blockade of the genesis and spread of limbic seizures in the hippocampus.

Afferent Pathways↗
PubMed2000

The calcar femorale in cemented stem fixation in total hip arthroplasty.

The calcar femorale is a vertical plate of bone lying deep to the lesser trochanter and is formed as a result of traction of the iliopsoas which separates the femoral cortex into two distinct layers, the calcar femorale and the medial femoral cortex. They fuse together proximally to form the medial femoral neck. A stem placed centrally will abut against the calcar femorale with little or no space for cement. Clearing of the calcar will offer space for a cement layer, which will support the stem proximally on the posterior aspect. We compared two consecutive groups of Charnley low-friction arthroplasties, with and without clearing of the calcar. In 330 patients who had an arthroplasty without clearing the calcar, there were ten revisions for aseptic loosening of the stem and six other stems were considered 'definitely loose', giving a rate of failure of 4.8%. In 111 patients in whom the calcar was cleared there was only one revision for aseptic loosening and no stems were classed as 'definitely loose', giving a rate of failure of 0.9%. Survivorship analysis has again shown the need for long-term follow-up; the differences became clear after ten years but because of the relatively small numbers, statistical analysis is not yet applicable. We now clear the calcar femorale routinely and advocate optimal access to the medullary canal and insertion of the stem in the area of the piriform fossa.

Adolescent↗
PubMed1995

Conditioned fear-induced changes in behavior and in the expression of the immediate early gene c-fos: with and without diazepam pretreatment.

The synthesis of Fos, the protein product of the immediate early gene c-fos, was used to map metabolically some of the neural substrates of conditioned fear in the rat. Analysis of the behaviors emitted by the rats during the test session provided strong evidence that the conditioning procedure was effective. Exposure to the environment in which they had previously received footshock significantly increased the number of Fos-like immunoreactive neurons in nearly 50 brain regions, both cortical and subcortical. Among the structures showing the most dramatic increases in fear-induced c-fos expression were the cingulate, piriform, infralimbic, and retrosplenial cortices, the anterior olfactory nucleus, claustrum, endopiriform nucleus, nucleus accumbens shell, lateral septal nucleus, various amygdalar nuclei, paraventricular thalamic nucleus, ventral lateral geniculate nucleus, the ventromedial, lateral, and dorsal hypothalamic nuclei, the ventral tegmental area, and the supramammillary area. These data demonstrate that a relatively simple classical conditioning procedure activates a large number of widely dispersed cortical and subcortical structures. Some of the structures showing increased c-fos expression have important autonomic functions and may therefore have reflected centrally mediated changes in blood pressure and respiration produced by the anxiogenic stimuli. In a second experiment, the effects of pretreatment with the anxiolytic drug diazepam (2.5, 5.0, or 10 mg/kg) were evaluated. The benzodiazepine produced dose-related decreases in the frequency of crouching (freezing) elicited by the aversively conditioned contextual cues. Diazepam also produced dose-related decreases in conditioned stress-induced c-fos expression in all but one structure, the effects being statistically significant in 38 of 60 sampled structures. Diazepam dose dependently increased fear-induced c-fos expression in the central nucleus of the amygdala. There was considerable regional variability with respect to sensitivity to diazepam, the retrosplenial cortex and the supramammillary area being the only two structures to show decreases after the lowest dose of diazepam. In contrast, the entorhinal cortex, nucleus accumbens core, ventromedial and posterior hypothalamic nuclei, median raphe, and locus coeruleus were particularly resistant to diazepam, all failing to show statistically significant decreases in conditioned fear-induced c-fos expression even at the highest dose. The extent to which diazepam decreased conditioned stress-induced c-fos expression was unrelated to previous estimates of benzodiazepine receptor density in the sampled structures.

Animals↗
PubMed2002

Functional magnetic resonance neuroimaging of drug dependence: naloxone-precipitated morphine withdrawal.

This study investigated the potential utility of fMRI as a neuroimaging technique to examine drug dependence using a robust animal model of drug withdrawal. Two groups of rats chronically pretreated with incremental doses of morphine sulfate (2, 7, 15, 30, 40, 50, 50, and 50 mg/kg--subcutaneous injection) were subjected to opioid precipitated withdrawal (using the opioid antagonist, naloxone) and subsequently behaviorally assessed or gradient-echo imaged under urethane anesthesia. Whole brain, group statistical parametric maps revealed statistically significant changes in signal intensity following administration of 1 mg/kg naloxone (corrected for multiple comparisons: P < 0.05, T > 5.03). Control groups within the fully crossed designs did not exhibit any statistically significant changes in behavior or signal intensity changes. Regional patterns of modulated activity include the retrosplenial, piriform, insular, entorhinal, cingulate, visual and auditory cortices, posterior fields of the hippocampus, and in particular the dentate gyrus. Such areas are consistent with biochemical correlates of morphine withdrawal and time profiles derived from our behavioral observations (P < 0.02). A notable lack of signal intensity changes in a number of subcortical areas suggests a possible confound associated with fMRI under anesthesia. This paper reports the first whole brain fMRI examination of an animal model of drug withdrawal, we believe there is considerable scope for extrapolation of our methods to a multitude of pharmacological applications-most notably in conjunction with other techniques in the development of potential therapeutic agents for drug dependence.

Animals↗
PubMed1989

Endogenous homovanillic acid levels differ between rat and rabbit caudate, hippocampus, and cortical regions.

Endogenous dopamine (DA) levels and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC), 3-methoxytyramine (3MT) and homovanillic acid (HVA) were measured by high-performance liquid chromatography in the entorhinal-piriform (EnPi), cingulate (CIN), sensorimotor (SSM) and visual (VIS) cortices as well as is the caudate (CAU) and hippocampus (HIP) of Sprague-Dawley (SD) rats and New Zealand (NZ) rabbits. The DA, DOPAC and 3MT contents were similar in both species. The HVA levels however, although they followed DA distribution, were several-fold higher in NZ rabbits than in SD rats for all cortices, HIP and CAU. In addition, total metabolite contents and DA turnover (estimated from 'DA metabolite/DA' ratios) were significantly higher in NZ rabbits than in SD rats, suggesting an increased release and/or metabolism in the former species. The HVA/DA ratios were much higher for NZ rabbit regions than for SD rats, indicating an increased DA release in the former species since the DOPAC/DA ratios (index of intraneuronal degradation) were similar.

Animals↗
PubMed1996

Fos induction in subtypes of cerebrocortical neurons following single picrotoxin-induced seizures.

In adult rats single seizures of varying behavioural severities were caused by slow, systemic infusion of picrotoxin, an antagonist of the C1- channel at the GABAA receptor. We used a double labelling immunohistochemical method to define the subclasses of neurons that contained Fos protein following seizures. In four cortical regions (piriform, entorhinal, motor and sensory) neuronal subclasses were defined with antibodies against the calcium-binding proteins D-28K, parvalbumin and calretinin (aspiny neurons), and neurofilament protein (spiny neurons). The remaining spiny neuron population was estimated by subtraction of defined subclasses from total neuronal numbers determined from Nissl stain. After seizures, most of the calbindin D-28K immunoreactive interneurons (> 80%) and many of the unlabelled spiny neurons (60-80%) were FOs positive. Co-localisation of Fos was found in about 30% of parvalbumin, calretinin and neurofilament protein immunoreactive neurons. Paradoxically, mild seizures were associated with induction of Fos in up to 80% of cortical cells and more severe seizures with 60%, the difference being due to different levels of Fos induction in spiny neurons. These results also demonstrate that seizures induce Fos predominantly in excitatory cortical neurons.

Animals↗
PubMed2005

Learning-induced modulation of oscillatory activities in the mammalian olfactory system: the role of the centrifugal fibres.

In the mammalian olfactory system, oscillations related to odour representation have been described in field potential activities. Previous results showed that in olfactory bulb (OB) of awake rats engaged in an olfactory learning, odour presentation produced a decrease of oscillations in gamma frequency range (60-90 Hz) associated with a power increase in beta frequency range (15-40 Hz). This response pattern was strongly amplified in trained animals. The aim of this work was twofold: whether learning also induces similar changes in OB target structures and whether such OB response depends on its centrifugal inputs. Local field potentials (LFPs) were recorded through chronically implanted electrodes in the OB, piriform and enthorhinal cortices of freely moving rats performing an olfactory discrimination. Oscillatory activities characteristics (amplitude, frequency and time-course) were extracted in beta and gamma range by a wavelet analysis. First, we found that odour induced beta oscillatory activity was present not only in the OB, but also in the other olfactory structures. In each recording site, characteristics of the beta oscillatory responses were dependent of odour, structure and learning level. Unilateral section of the olfactory peduncle was made before training, and LFPs were symmetrically recorded in the two bulbs all along the acquisition of the learning task. Data showed that deprivation of centrifugal feedback led to an increase of spontaneous gamma activity. Moreover, under this condition olfactory learning was no longer associated with the typical large beta band. As a whole, learning modulation of the beta oscillatory response in olfactory structures may reflect activity of a distributed functional network involved in odour representation.

Action Potentials↗
PubMed1993

Nervous system distribution of the serotonin 5-HT3 receptor mRNA.

The serotonin 5-HT3 receptor subtype has been implicated in many brain functions. Antagonists of this receptor have anxiolytic and antiemetic effects in humans and in animal models. To determine with cellular resolution the distribution of 5-HT3 receptor mRNA, in situ hybridization was performed in sections of mouse brain and dorsal root ganglia. Scattered labeled cells were observed throughout cortical regions, with highest densities in the piriform, cingulate, and entorhinal areas. Strong hybridization signals were seen in the hippocampal formation, where expression appeared primarily in interneurons. Labeled cells were most abundant in the posteroventral hippocampal region, particularly in the lacunosum moleculare layer of CA1. This distribution suggests that 5-HT3 receptors may mediate the known serotonergic inhibition of pyramidal cell populations via excitation of inhibitory interneurons. Labeled cells were also observed in the major subdivisions of the amygdaloid complex, the olfactory bulb, the trochlear nerve nucleus, the dorsal tegmental region, the facial nerve nucleus, the nucleus of the spinal tract of the trigeminal nerve, and the spinal cord dorsal horn. In the periphery, intense hybridization signals were seen in a subpopulation of cells in dorsal root ganglia. The data correlate generally with physiological, behavioral, and receptor autoradiographic studies, provide cellular resolution, and reveal regions of receptor expression not previously observed. The distribution of 5-HT3 receptor mRNA is consistent with roles for the receptor in cognition and affect and in the modulation of sensory input.

Amygdala↗
PubMed1993

The patterns of afferent innervation of the core and shell in the "accumbens" part of the rat ventral striatum: immunohistochemical detection of retrogradely transported fluoro-gold.

Recent data have emphasized the neurochemically distinct nature of subterritories in the accumbens part of the rat ventral striatum termed the core, shell, and rostral pole. In order to gain a more comprehensive understanding of how afferents are distributed relative to these subterritories, immunohistochemical detection of retrogradely transported Fluoro-Gold was carried out following iontophoretic injections intended to involve selectively one of the subterritories. The data revealed that a number of cortical afferents of the medial shell and core originate in separate areas, i.e., the dorsal peduncular, infralimbic, and posterior piriform cortices (to medial shell) and the dorsal prelimbic, anterior agranular insular, anterior cingulate, and perirhinal cortices (to core). The lateral shell and rostral pole are innervated by cortical structures that also project either to the medial shell or core. The orbital, posterior agranular insular, and entorhinal cortices, hippocampus, and basal amygdala were observed to innervate the accumbens in a topographic manner. Following core injections, strong bilateral cortical labeling was observed. Few labeled cortical cells were observed contralaterally following injections in the medial shell. Intermediate numbers of labeled neurons were observed in contralateral cortices following lateral shell injections. Robust subcortical labeling in a variety of structures in the ventral forebrain, lateral hypothalamus, deep temporal lobe, and brainstem was observed after shell injections, particularly those that involved the caudal dorsomedial extremity of the shell, i.e., its "septal pole." Selective ipsilateral labeling of subcortical structures in the basal ganglia circuitry was observed following injections in the core and, to a lesser extent, lateral shell. It was concluded that a number of afferent systems exhibit varying degrees of segregation with respect to the accumbal subterritories.

Afferent Pathways↗
PubMed1992

Subcortical structures and pathways involved in convulsive seizure generation.

Convulsive seizures in animal models usually involve one or more of the following components: (1) limbic motor seizures, (2) explosive running-bouncing clonic seizures, and (3) tonic extensor seizures. Each of these components depends on specific and experimentally separable anatomic substrates. Limbic motor seizures depend on forebrain structures for their initiation and propagation, with the prepiriform, piriform, and entorhinal cortices playing a prominent role in conjunction with hippocampus, amygdala, substantia innominata, and mediodorsal thalamus. In contrast, seizures involving running-bouncing clonus or tonic extension depend on neural substrates in the brainstem and do not appear to require the integrity of the forebrain for their development or expression. The inferior colliculus is a region from which running-bouncing seizures can be elicited by chemical or electrical stimulation. Tonic extensor seizures depend on the integrity of the nucleus reticularis pontis oralis, but a specific locus responsible for triggering these seizures has yet to be identified. Under conditions of chronic or repeated seizure activity over prolonged time periods, seizures evoked from the hindbrain can recruit forebrain circuits; conversely, repeated stimulation of forebrain limbic circuits (e.g., kindling) can modify susceptibility to brainstem convulsions. These long-term alterations may result from changes in the activity of seizure "gating" pathways, which are circuits that influence seizure susceptibility by modulating the threshold for the initiation and/or propagation of the seizures. In general, these pathways are not part of any core seizure propagation pathway per se. In many cases, the gating substrates are relatively nonselective as to the type of seizure they can influence. In this category, the substantia nigra and its related circuits within the basal ganglia serve a prominent role. In addition, ascending noradrenergic projections have been implicated in the regulation of seizure threshold. Other gating mechanisms involve thalamic circuitry and pathways originating in cerebellum.

Animals↗
PubMed1980

Mesolimbicocortical dopamine terminal fields are necessary for normal locomotor and investigatory exploration in rats.

Rats explore a novel open field or novel object less after denervation of mesolimbicocortical dopaminergic terminal fields produced by bilateral 6-hydroxydopamine (6-OHDA) microinjections into the anterolateral hypothalamus after pretreatment with desmethylimipramine (DMI). These behavioral deficits were correlated with complete or nearly complete loss of fluorescent dopaminergic (DA) terminals in the nucleus accumbens, olfactory tubercle, dorsal bed nucleus of the stria terminalis, lateral septal nucleus and the deep layers of the frontal and piriform cortices. There were also fewer A10, medial A9, and A8 DA fluorescent cells after the 6-OHDA-DMI injections; this suggests retrograde degeneration of the cells of origin of the mesolimbicocortical DA system. When the DMI pretreatment was omitted, identical bilateral 6-OHDA microinjections also produced severe loss of norepinephrine (NE) fibers in the neocortex, hippocampus, lateral hypothalamus and ventral bed nucleus of the stria terminalis. The addition of this noradrenergic damage did not change the exploratory deficits observed after mesolimbicocortical DA denervation alone. Systemic administration of the DA agonist apomorphine, but not the adrenergic agonist clonidine, to the 6-OHDA-DMI rats repaired the deficits in exploration of a novel open field or novel object. The increased locomotion in a novel open field and investigation of a novel object produced by apomorphine in 6-OHDA-DMI rats were blocked by the DA antagonist, pimozide. This is evidence that apomorphine restored exploratory responses by stimulating dopaminergic receptors. The exploratory responses produced by apomorphine were also blocked by testing rats in a familiar open field or with a familiar novel object. This is evidence that apomorphine facilitates exploratory responding to novel stimuli by 6-OHDA-DMI rats, but that the same dose of apomorphine does not increase activity when 6-OHDA-DMI rats are confronted by familiar stimuli. We conclude: (1) that mesolimbicocortical dopaminergic terminals are necessary for normal exploratory behavior in rats; and (2) that DA released by these terminals may facilitate optimal sensorimotor integration in these terminal fields during spontaneous exploratory behavior.

Animals↗
PubMed1997

Cortical input to the basal forebrain.

The arborization pattern and postsynaptic targets of corticofugal axons in basal forebrain areas have been studied by the combination of anatomical tract-tracing and pre- and postembedding immunocytochemistry. The anterograde neuronal tracer Phaseolus vulgaris leucoagglutinin was iontophoretically delivered into different neocortical (frontal, parietal, occipital), allocortical (piriform) and mesocortical (insular, prefrontal) areas in rats. To identify the transmitter phenotype in pre- or postsynaptic elements, the tracer staining was combined with immunolabeling for either glutamate or GABA, or with immunolabeling for choline acetyltransferase or parvalbumin. Tracer injections into medial and ventral prefrontal areas gave rise to dense terminal arborizations in extended basal forebrain areas, particularly in the horizontal limb of the diagonal band and the region ventral to it. Terminals were also found to a lesser extent in the ventral part of the substantia innominata and in ventral pallidal areas adjoining ventral striatal territories. Similarly, labeled fibers from the piriform and insular cortices were found to reach lateral and ventral parts of the substantia innominata, where terminal varicosities were evident. In contrast, descending fibers from neocortical areas were smooth, devoid of terminal varicosities, and restricted to the myelinated fascicles of the internal capsule en route to more caudal targets. Ultrastructural studies obtained indicated that corticofugal axon terminals in the basal forebrain areas form synaptic contact primarily with dendritic spines or small dendritic branches (89%); the remaining axon terminals established synapses with dendritic shafts. All tracer labeled axon terminals were immunonegative for GABA, and in the cases investigated, were found to contain glutamate immunoreactivity. In material stained for the anterograde tracer and choline acetyltransferase, a total of 63 Phaseolus vulgaris leucoagglutinin varicosities closely associated with cholinergic profiles were selected for electron microscopic analysis. From this material, 37 varicosities were identified as establishing asymmetric synaptic contacts with neurons that were immunonegative for choline acetyltransferase, including spines and small dendrites (87%) or dendritic shafts (13%). Unequivocal evidence for synaptic interactions between tracer labeled terminals and cholinergic profiles could not be obtained in the remaining cases. From material stained for the anterograde tracer and parvalbumin, 40% of the labeled terminals investigated were found to establish synapses with parvalbumin-positive elements; these contacts were on dendritic shafts and were of the asymmetrical type. The present data suggest that corticofugal axons innervate forebrain neurons that are primarily inhibitory and non-cholinergic; local forebrain axonal arborizations of these cells may represent a mechanism by which prefrontal cortical areas control basal forebrain cholinergic neurons outside the traditional boundaries of pallidal areas.

Animals↗
PubMed1993

Are differences in dorsal hippocampal kindling related to amygdala-piriform area excitability?

It has been suggested that several structures associated with the amygdala-piriform (A-P) area are important, if not critical, for convulsive generalization of limbic seizures. In experiment 1, when examining the development of convulsive seizures kindled from the dorsal hippocampus (cornus ammonis; DH), a broad range of kindling rates was observed. Independent of electrode location within the hippocampus, kindling rates were correlated positively with both local and, more dramatically, distant excitability (measured by the duration of the primary and secondary hippocampal afterdischarges, respectively) at all stages of epileptogenesis. Because kindling rates were bimodally distributed, we bisected the distribution into 'faster' and 'slower' kindling rats. Here we examined the magnitude of both electrophysiological and behavioral differences between 'faster' and 'slower' rats and their changes over time. The 'faster' rats had longer primary and secondary afterdischarge (AD) durations than 'slower' rats throughout all stages of kindling. With the appearance of generalized convulsions, the 'faster' rats showed longer latencies to clonus onset, with longer clonus and AD durations than 'slower' rats. Also, the generalized convulsions of 'faster' rats appeared during a much enlarged secondary AD period, while 'slower' rats convulsed during primary AD. In both groups, convulsions were invariably associated with increased discharge in A-P associated structures. We interpreted the differences between 'faster' and 'slower' DH rats to reflect genetic differences in excitability in both local and A-P associated structures. If the DH kindling profile of the 'faster' rats differed from 'slower' rats largely because of naturally greater excitability in A-P associated structures, then experimentally increased excitability in those structures (via amygdala kindling) in a random sample of rats should duplicate much of the 'faster' DH kindling profile. In experiment 2, this outcome was observed. In conclusion, we suggest that either natural or induced differences in the excitability of A-P associated structures affect both the genesis and the profile of convulsive generalization of limbic kindled seizures.

Amygdala↗