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PubMed1992

Cholinergic suppression specific to intrinsic not afferent fiber synapses in rat piriform (olfactory) cortex.

1. Differences in the cholinergic suppression of afferent and intrinsic fiber synaptic transmission were studied in the rat piriform cortex. Extracellular and intracellular recording techniques were applied in an in vitro transverse slice preparation. Afferent and intrinsic fiber systems were differentially stimulated with electrodes placed in layer Ia or layer Ib, respectively. Synaptic responses were monitored in the presence of cholinergic agonists and antagonists. 2. Afferent and intrinsic fiber synaptic potentials measured extracellularly showed large differences in sensitivity to micromolar concentrations of the cholinergic agonists carbachol or (+/-)-muscarine, or to acetylcholine combined with neostigmine. Intrinsic fiber synaptic responses in layer Ib were strongly reduced in the presence of cholinergic agonists, whereas afferent fiber synaptic responses in layer Ia were largely unaffected. At a concentration of 100 microM, all three agonists caused a greater than 60% decrease in the height of the intrinsic fiber synaptic potential but less than 15% reduction in the afferent fiber synaptic potential. 3. Intracellular recordings confirmed that the cholinergic agonist carbachol selectively suppresses intrinsic fiber synaptic potentials but not afferent fiber synaptic potentials recorded from the same pyramidal cell. 4. Dose-response curves to carbachol were obtained for both fiber systems using extracellular recording of evoked field potentials. Carbachol suppressed intrinsic fiber synaptic potentials with a coefficient of dissociation (KD) estimated at 2.9 microM and an inhibitory concentration for 50% response estimated at 6.6 microM. 5. Carbachol produced a proportionately greater suppression of the first pulse than the second pulse of a pulse pair. This increase in the level of facilitation accompanying suppression suggests a presynaptic mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1991

Experimental superficial siderosis of the central nervous system. I. Morphological observations.

Autologous washed red blood cells were injected weekly over a period of three to six months into the cisterna magna of adult New Zealand white rabbits. After three months, the surface of the brain stem, cerebellum, and piriform cortex showed a distinct brown color, and staining of the gross specimens for iron produced an intense blue color which extended for a distance of 1-2 mm into the brain parenchyma. Enhanced iron stains of vibratome sections revealed the accumulation of reaction product in microglia and Bergmann glia of the cerebellar cortex, and in microglia and astrocytes of the piriform cortex. Ferritin immunocytochemistry revealed reaction product in cerebellar microglia and Bergmann glia which strongly resembled that obtained by the enhanced iron stain. In the piriform cortex, only microglia were reactive with anti-ferritin. Electron microscopy confirmed the accumulation of electron-dense ferritin granules only in the cytoplasm of microglia. Bergmann glia in the cerebellum and astrocytic processes in the piriform cortex were replete with intermediate filaments and contained an excess of glycogen. After six months, small granules of hemosiderin began to appear in cerebellar and piriform cortices. The observations support that the sequence of conversion of hemoglobin to ferritin and hemosiderin occurs in brain as in other organs.

Animals↗
PubMed2001

Olfactory learning modifies predisposition for long-term potentiation and long-term depression induction in the rat piriform (olfactory) cortex.

Learning-related modifications in predisposition for long-term potentiation (LTP) and long-term depression (LTD) were studied in brain slices of the rat piriform cortex following olfactory learning. Rats were trained to discriminate between pairs of odors until they demonstrated rule learning. We have previously shown that such training is accompanied by enhanced neuronal excitability and increased synaptic transmission in the intrinsic synaptic pathway. Here we show that the susceptibility for further enhancing synaptic connectivity by inducing LTP in slices from trained rats is markedly reduced after training, compared with slices from pseudo-trained and naive rats. Accordingly, while 900 stimuli at 1 Hz did not induce LTD in slices from control rats, it induced significant LTD in slices from trained rats. Post-tetanic potentiation (PTP) was also reduced after training, indicating that synaptic release is enhanced after odor learning, as previously suggested. We suggest that learning-related cellular modifications and activity-dependent synaptic plasticity share a common mechanism in the primary olfactory cortex. Our data also support the prediction generated according to the sliding modification threshold theory that learning should be accompanied by reduced capability of inducing LTP and increased susceptibility for LTD induction.

Animals↗
PubMed1994

Central olfactory connections in the macaque monkey.

The connections between the olfactory bulb, primary olfactory cortex, and olfactory related areas of the orbital cortex were defined in macaque monkeys with a combination of anterograde and retrograde axonal tracers and electrophysiological recording. Anterograde tracers placed into the olfactory bulb labeled axons in eight primary olfactory cortical areas: the anterior olfactory nucleus, piriform cortex, ventral tenia tecta, olfactory tubercle, anterior cortical nucleus of the amygdala, periamygdaloid cortex, and olfactory division of the entorhinal cortex. The bulbar axons terminate in the outer part of layer I throughout these areas and are most dense in areas that are close to the lateral olfactory tract. Labeled axons also were found in the superficial part of nucleus of the horizontal diagonal band. Retrograde tracers injected into the olfactory bulb labeled cells in the nucleus of the diagonal band and in all of the primary olfactory cortical areas except the olfactory tubercle. Electrical stimulation of the olfactory bulb evoked short-latency unit responses and a characteristic field wave in the primary olfactory cortex. Multiunit activity in layer II tended to be of shorter latency than that in layer III and the endopiriform nucleus. Associational connections within the primary olfactory cortex were demonstrated with anterograde tracer injections into the piriform cortex and the entorhinal cortex. Injections into the piriform cortex near the lateral olfactory tract labeled axons in the deep part of layer I of many primary olfactory areas, but especially in areas near the tract. An injection into the rostral entorhinal cortex, distant to the lateral olfactory tract, labeled a complementary distribution of axons in deep layer I of olfactory areas medial and caudoventral to the tract. This organization resembles that reported in the primary olfactory cortex of the rat [Luskin and Price (1983) J. Comp. Neurol. 216:264-291]. The anterograde tracer injections into the piriform cortex and retrograde tracer injections into the orbital and medial prefrontal cortex and rostral insula label connections from the primary olfactory cortex to nine areas in the caudal orbital cortex, including the agranular insula areas Iam, Iai, Ial, Iapm, and Iapl and areas 14c, 25, 13a, and 13m. The piriform cortex projects most heavily to layer I of these areas. Only Iam, Iapm, and 13a receive a substantial projection to the deeper layers. Areas Iam, Iapm, and 13a were also the only areas that responded with multiunit action potentials to olfactory bulb stimulation in anesthetized animals.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMedDate not supplied

Amygdala adenosine A1 receptors have no anticonvulsant effect on piriform cortex-kindled seizures in rat.

Adenosine is an endogenous anticonvulsant that exerts its effects through A1 receptors. As the piriform/amygdala is a critical circuit for limbic seizure propagation, in this study, the role of basolateral amygdala A1 receptors on piriform cortex (PC)-kindled seizures was investigated. Rats were kindled by daily electrical stimulation of PC. In fully kindled animals, bilateral intra-amygdala N6-cyclohexyladenosine (CHA; 10-500 micromol/L, a selective A1 receptor agonist) had no effect on kindled-seizure parameters. However, bilateral intra-amygdala 2% lidocaine (reversal neuronal inhibitor) reduced the kindled seizure severity. There was significant increase in stage 4 latency and decrease in stage 5 duration. Bilateral lesion of basolateral amygdala of kindled animals (by electrical DC current) reduced the kindled seizure severity more dramatically. Our results showed afterdischarge duration, stage 5 duration, and seizure duration were decreased and stage 4 latency increased significantly. In addition, daily intra-amygdala CHA had no significant effect on PC kindling acquisition. Therefore, it may be concluded that although the basolateral amygdala neuronal activity has a critical role in the propagation of epileptic seizures from PC, the amygdala A1 receptors have no role in this regard. On the other hand, amygdala A1 receptors have no anticonvulsant or antiepileptogenic effect on PC-kindled seizures.

Adenosine↗
PubMed2005

Amygdala kindling differentially regulates the expression of the elements involved in TRH transmission.

Subthreshold electrical stimulation of the amygdala (kindling) activates neuronal pathways increasing the expression of several neuropeptides including thyrotropin releasing-hormone (TRH). Partial kindling enhances TRH expression and the activity or its inactivating ectoenzyme; once kindling is established (stage V), TRH and its mRNA levels are further increased but TRH-binding and pyroglutamyl aminopeptidase II (PPII) activity decreased in epileptogenic areas. To determine whether variations in TRH receptor binding or PPII activity are due to regulation of their synthesis, mRNA levels of TRH receptors (R1, R2) and PPII were semi-quantified by RT-PCR in amygdala, frontal cortex and hippocampus of kindled rats sacrificed at stage II or V. Increased mRNA levels of PPII were found at stage II in amygdala and frontal cortex, and of pro-TRH and TRH-R2, in amygdala and hippocampus. At stage V, pro-TRH mRNA levels increased and those of PPII, decreased in the three regions; TRH-R2 mRNA levels diminished in amygdala and frontal cortex and of TRH-R1 only in amygdala. In situ hybridization analyses revealed, at stage II, enhanced TRH-R1 mRNA levels in dentate gyrus and amygdala while decreased in piriform cortex; those of TRH-R2 increased in amygdala, CA2, dentate gyrus, piriform cortex, thalamus and subiculum and of PPII, in CAs and piriform cortex. In contrast, at stage V decreased expression of TRH-R1 occurred in amygdala, CA2/3, dentate gyrus and piriform cortex; of TRH-R2 in CA2, thalamus and piriform cortex, and of PPII in CA2, and amygdala. The magnitude of changes differed between ipsi and contralateral side. These results support a trans-synaptic modulation of all elements involved in TRH transmission in conditions that stimulate the activity of TRHergic neurons. They show that reported changes in PPII activity or TRH-binding caused by kindling relate to regulation of the expression of TRH receptors and degrading enzyme.

Amygdala↗
PubMed1985

Ontogeny of dopamine, serotonin and spirodecanone receptors in rat forebrain--an autoradiographic study.

Sections from freshly frozen neonatal rat brain, ages 0-21 days, were incubated with [3H]spiperone (SP). Initial studies characterized the binding sites for SP in terms of association and dissociation rates, saturability and pharmacology. The binding sites were found to be predominantly dopamine D2 receptors in sections centered in the striatum and these receptors were similar to receptors in adult brain. Autoradiographic studies using in vitro techniques examined the anatomic distribution of [3H]SP binding sites. Using domperidone, ketanserin and (+)butaclamol it was possible to differentiate dopamine D2, serotonin S2 and spirodecanone receptors. Dopamine receptors were found at birth in striatum and nucleus accumbens and increased in density with age. In the first two weeks postnatally there was an apparent dorsolateral to ventromedial gradient in the striatum. Serotonin S2 receptors were found in the cortex, lateral olfactory tubercles and nucleus accumbens and claustrum. These receptors increased in density with age but to a much lesser extent than dopamine receptors. Spirodecanone receptors were first apparent in the piriform cortex by day 5. They became very dense with age in particular regions, i.e., layer II of cortex, piriform cortex, medial olfactory tubercles, lateral septum and in patches in the nucleus accumbens. These studies delineate with a high resolution at an anatomical level the major receptor sites for neuroleptic drugs in the developing rat forebrain. They describe the developmental pattern of these receptors and provide a basis for further studies on their control and function during development.

Animals↗
PubMed2003

Trans-neuronal regulation of cortical apoptosis in the adult rat olfactory system.

Previous work has identified a population of neurons within the anterior piriform cortex that undergo rapid apoptosis following de-afferentation by olfactory bulbectomy in adult rats. The specific initiation signal for apoptosis in this paradigm is unknown, but may include an activity-dependent trans-neuronal cascade. The present report examined the effect of adult-onset unilateral naris occlusion, which reduces olfactory bulb afferent excitation of piriform cortex, on apoptosis (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling [TUNEL]) in the rat anterior piriform cortex. Adult Long-Evans hooded rats received unilateral naris occlusion or a control manipulation and were sacrificed after 1, 5, 7, 10 or 20 days later. For comparison, a second group of rats received a unilateral bulbectomy and were sacrificed 24 h later. Counts of TUNEL-stained cell profiles were performed for layers I/II and layer III of the anterior piriform cortex ipsilateral and contralateral to the manipulation. The results confirmed that unilateral bulbectomy produced a dramatic increase in TUNEL labeling in layers I/II of the ipsilateral piriform cortex 24 h after bulbectomy. Unilateral naris closure also produced enhanced TUNEL labeling, although the magnitude of the effect was less than that produced by bulbectomy, and enhanced TUNEL labeling was apparent both ipsilateral and contralateral to the sealed naris compared to controls. Deprivation-induced TUNEL labeling was detectable by 24 h post-closure, peaked at 5 days and was no different from controls by 20 days post-closure. Neither bulbectomy nor naris closure affected TUNEL labeling in layer III. Together, these results suggest that there is a population of superficial cells in piriform cortex whose survival is tightly regulated by sensory input.

Animals↗
PubMed1995

Comparative localization of serotonin1A, 1C, and 2 receptor subtype mRNAs in rat brain.

Serotonin (5-HT) mediates its effects on neurons in the central nervous system through a number of different receptor types. To gain better insight as to the localization of 5-HT responsive cells, the distribution of cells expressing mRNAs encoding the three 5-HT receptor subtypes 1A, 1C, and 2 was examined in rat brain with in situ hybridization using cRNA probes. 5-HT1A receptor mRNA labeling was most pronounced in the olfactory bulb, anterior hippocampal rudiment, septum, hippocampus (dentate gyrus and layers CA1-3), entorhinal cortex, interpeduncular nucleus, and medullary raphe nuclei. 5-HT1C receptor mRNA labeling was the most abundant and widespread of the three 5-HT receptor subtypes examined. Hybridization signal was densest in the choroid plexus, anterior olfactory nucleus, olfactory tubercle, piriform cortex, septum, subiculum, entorhinal cortex, claustrum, accumbens nucleus, striatum, lateral amygdala, paratenial and paracentral thalamic nuclei, subthalamic nucleus, substantia nigra, and reticular cell groups. 5-HT2 receptor mRNA was localized to the olfactory bulb, anterior hippocampal rudiment, frontal cortex, piriform cortex, entorhinal cortex, claustrum, pontine nuclei, and cranial nerve motor nuclei including the oculomotor, trigeminal motor, facial, dorsal motor nucleus of the vagus, and hypoglossal nuclei. The distributions of mRNAs for the three different 5-HT receptor subtypes overlap with regions that bind various 5-HT receptor-selective ligands and are present in nearly all areas known to receive serotonergic innervation. The results of this study demonstrate that neurons which express these 5-HT receptor subtypes are very widespread in the central nervous system, yet possess unique distributions within the rat brain. Moreover, previously unreported regions of 5-HT receptor subtype expression were observed, particularly with the 5-HT2 receptor riboprobe in the brainstem. Finally, several brain areas contain multiple 5-HT receptor subtype mRNAs, which leads to the possibility that individual cells may express more than one 5-HT receptor subtype.

Animals↗
PubMed1996

Reciprocal and topographic connections between the piriform and prefrontal cortices in the rat: a tracing study using the B subunit of the cholera toxin.

In the present study, the reciprocal connections between the piriform cortex and the prefrontal areas are described on the basis of experiments using the anterograde and the retrograde transport of the cholera toxin B subunit (CTb). Following CTb injections placed in the anterior part of the piriform cortex, retrogradely labeled cells and anterogradely labeled fibers were mainly found in the ventrolateral and lateral orbital areas as well as in the anterior part of the agranular insular cortex. Following injections placed in the posterior part of the piriform cortex, the CTb labeling was primarily observed in the infralimbic area and the posterior part of the agranular insular cortex. Thus, we described a topographical organization of the direct reciprocal connections between the anterior and the posterior parts of the piriform cortex parts and some prefrontal areas. This could support a differential modulation of the olfactory processing along the rostrocaudal dimension of the piriform cortex.

Animals↗
PubMed1997

Soman-induced seizures rapidly activate astrocytes and microglia in discrete brain regions.

Neurons in the piriform cortex and the pontine nucleus locus coeruleus express elevated levels of the immediate early gene protein product, Fos, within 30-45 minutes of a seizurogenic dose of the anticholinesterase, soman (Zimmer et al., [1997] J. Comp. Neurol. 378:468-481). By 24 hours following soman injection, there is marked neuropathology in the piriform cortex. These findings suggest selective, regional vulnerability in response to the seizurogenic actions of soman. In the present study, we determined that soman-induced seizures also cause selective, rapid activation of astrocytes and microglia in the piriform cortex and other brain regions. Animals were killed at different intervals between 1 hour and 24 hours after a convulsive dose of soman. Brain sections were processed for immunocytochemical detection of astrocytes with antibodies against glial fibrillary acidic protein, and microglia and macrophages with antibodies against the complement receptor 3 protein, OX-42. The results demonstrate that following soman administration: (1) there is a rapid increase in glial fibrillary acidic protein staining in astrocytes of the piriform cortex (1 hour); (ii) reactive astrocytes are specifically restricted to layer II and the superficial boundaries of layer III of the piriform cortex. These are the same layers in which neurons express Fos within 30-45 minutes following soman administration; (3) between 1 and 4 hours, resting (ramified) microglia in the piriform cortex and the hippocampus alter their morphology to resemble active microglia. From 4-8 hours, active microglia undergo morphological changes characteristic of reactive microglia that resemble macrophages. Taken together, these observations indicate that astrocytes and microglia in brain regions susceptible to soman become rapidly "reactive" in response to seizures. The highly specific anatomical codistribution of reactive glia and Fos-expressing neurons suggests that intensely active neurons provide local signals that trigger reactive changes in neighboring glia.

Animals↗
PubMed1998

Spatiotemporal distribution of a late synchronized activity in olfactory pathways following stimulation of the olfactory bulb in rats.

The evoked potential recorded in the rat piriform cortex in response to electrical stimulation of the olfactory bulb is composed of an early component occasionally followed by a late component (60-70 ms). We previously showed that the late component occurrence was enhanced following an olfactory learning. In the present study carried out in naive rats, we investigated the precise conditions of induction of this late component, and its spatiotemporal distribution along the olfactory pathways. In the anaesthetized rat, a stimulating electrode was implanted in the olfactory bulb. Four recording electrodes were positioned, respectively, in the olfactory bulb, the anterior and posterior parts of the piriform cortex, and the entorhinal cortex. Simultaneous recording of signals evoked in the four sampled structures in response to stimulation of the olfactory bulb revealed that the late component was detected in anterior and posterior piriform cortex as well as in entorhinal cortex, but not in the olfactory bulb. The late component occurred reliably for a narrow range of low intensities of stimulation delivered at frequencies not exceeding 1 Hz. Comparison of late component amplitude and latency across the different recorded sites showed that this component appeared first and with the greatest amplitude in the posterior piriform cortex. In addition to showing a functional dissociation between anterior and posterior parts of the piriform cortex, these data suggest that the posterior piriform cortex could be the locus of generation of this late high amplitude synchronized activity, which would then propagate to the neighbouring regions.

Animals↗
PubMed2001

Spatiotemporal analysis of Fos expression associated with cocaine- and PTZ-induced seizures in prenatally cocaine-treated rats.

We previously reported that prenatal cocaine exposure (40 mg/kg s.c., E10-E20) increased susceptibility to convulsant-induced seizures later in life, with female rats becoming more sensitive to seizures induced by cocaine and pentylenetetrazol (PTZ), and males more sensitive to PTZ-induced seizures (Snyder-Keller and Keller, 1995, 2000). In order to determine the locus of enhanced seizure susceptibility in the brains of prenatally cocaine-treated rats, we examined the distribution and density of Fos-immunoreactive cells after cocaine- and PTZ-induced seizures in mature rats. Subconvulsive cocaine doses induced c-fos in cortical areas as well as densely dopamine-innervated regions such as striatum and nucleus accumbens. Following cocaine-induced seizures, intense c-fos induction was observed in piriform cortex, amygdala, and hippocampus. Quantification of the number of Fos-immunoreactive cells in the brains of prenatally cocaine-treated versus prenatally saline-treated rats revealed differences in piriform cortex and amygdala that were indicative of a lower threshold in prenatally cocaine-treated female rats. Following PTZ-induced seizures, the same pattern of limbic structures were recruited with increasing seizure severity. Only females exhibited changes in the number of Fos-immunoreactive cells as a result of prenatal cocaine treatment. Pretreatment with the noncompetitive NMDA antagonist MK-801 blocked both cocaine- and PTZ-induced seizures, and Fos expression in limbic areas was also blocked. The dopamine D1 antagonist SCH 23390 blocked cocaine-induced seizures and associated c-fos induction, but not PTZ-induced seizures or Fos. Examination of the pattern of Fos expression at 15-20 min postseizure revealed that the initial site of c-fos induction associated with PTZ-induced seizures appeared to be the piriform cortex, whereas cocaine-induced seizures induced early expression in both piriform cortex and lateral amygdala. These findings suggest that neural alterations residing in the piriform cortex and amygdala are likely to account for the increased seizure susceptibility of prenatally cocaine-treated rats.

Animals↗
PubMed2003

Epileptiform ictal discharges are prevented by periodic interictal spiking in the olfactory cortex.

Interictal potentials are commonly observed between seizures in human epilepsies and in animal models of epilepsy. It is uncertain whether interictal spiking in partial epilepsies is causally related with the onset of an ictal discharge. To analyze the reciprocal correlation between interictal and ictal epileptiform events, we performed extracellular recordings in the limbic system of the in vitro isolated guinea pig brain preparation. Arterial perfusion of bicuculline (50 microM) in vitro consistently induced a focal ictal discharge in the hippocampal-entorhinal region that in one third of the experiments was associated with periodic interictal spikes in the piriform cortex. In the absence of active interictal spiking, the piriform cortex was secondarily invaded by the ictal discharge initiated in the hippocampal-entorhinal region, whereas no secondary ictal entrainment was observed in the presence of periodic piriform cortex spikes at circa 0.1 to 0.2 Hz. Similarly, ictal events never occurred when arterial perfusion of bicuculline was preceded by a local injection of the same drug in the piriform cortex, a procedure that induces a sustained interictal spiking. A reduced responsiveness to incoming paroxysmal discharges generated in the hippocampus was observed during the interval between two interictal spikes in the piriform cortex.

Action Potentials↗
PubMed1999

Identification of the mammalian homolog of the splicing regulator Suppressor-of-white-apricot as a thyroid hormone regulated gene.

Mammalian brain development is controlled by thyroid hormone through the regulation of target genes. In this study, we describe for the first time that a splicing regulator gene is under thyroid hormone control in the rat brain during the critical period of neuronal differentiation. By differential display, we have identified the mammalian homolog of the Drosophila splicing regulator Suppressor-of-white-apricot (SWAP) as a thyroid hormone-regulated gene in an immortal line of rat neuroblasts, E18 cells. Using Northern blotting and in situ hybridization, we found that expression of SWAP is under thyroid control in the developing rat brain. SWAP gene expression is highest during the first 10 days of life (P0-P10), preferentially in cerebral cortex, cerebellum, subventricular epithelium, piriform cortex, hippocampus, amygdala, and caudate putamen. At later stages (P15-P30) SWAP expression decreases, being detectable only in the cerebellum, hippocampus, and layers II/III of cerebral and piriform cortexes. We found that hypothyroidism causes an abnormal high level of SWAP RNA expression at P5-P15 throughout the brain except the cerebellum. Significantly, thyroid hormone treatment in vivo of hypothyroid animals led to a normalization of SWAP RNA expression. Furthermore, similar hormone treatment caused a decrease in SWAP expression in control rats. By modulating the expression of SWAP and perhaps other splicing regulators thyroid hormone may exert wide regulatory effects on multiple genes. The regulation of SWAP gene defines a novel mechanism of action of thyroid hormone which can be important for its effects in the developing brain.

Amino Acid Sequence↗
PubMed2006

Spontaneous oscillatory burst activity in the piriform-amygdala region and its relation to in vitro respiratory activity in newborn rats.

The amygdala is important for the formation of emotions that are affected by olfactory information. The piriform cortex is involved in information processing related to olfaction. To investigate functional interactions between the piriform cortex and amygdala and their relation to medullary respiratory activity, we developed a novel in vitro preparation including the limbic system, brainstem, and spinal cord of newborn rats. With the use of optical and electrophysiologic recordings, we analyzed spontaneous neuronal activity in the piriform-amygdala complex in limbic-brainstem-spinal cord preparations from 0- to 1-day-old rats. For optical recordings, the preparation was stained with a voltage-sensitive dye, and inspiratory activity was monitored from the fourth cervical (C4) ventral root. Spontaneous oscillatory burst activity (up to 10/min) was detected from the rostral cut surface of limbic and para-limbic regions including the piriform cortex and amygdala. The burst activity initially appeared in the piriform cortex and then propagated to the amygdala. We averaged the imaging data in the limbic area with the use of C4 inspiratory activity as a trigger signal. The results suggest functional coupling of the rhythmic burst activity in the piriform-amygdala complex to medullary inspiratory activity, which was confirmed electrophysiologically by cross-correlation analysis of these signals. This rhythmic burst activity may be involved in the development of neuronal circuits that process information related to olfaction, emotion, and respiration.

Amygdala↗
PubMed2005

Methylphenidate regulates c-fos and fosB expression in multiple regions of the immature rat brain.

Methylphenidate (Ritalin, MPH) is a common psychostimulant used to treat childhood attention-deficit hyperactivity disorder (ADHD). Little is known about the long-term developmental effects on gene expression and behavior, which may occur with extended MPH use. We reported previously that the striatum is a major target of MPH, consistent with human MRI studies. In the present study, we tested the hypothesis that MPH is likely to have widespread effects in extra-striatal regions of the brain. We used the expression of two immediate early genes, c-fos and fosB, as probes to map the response of the immature rat brain to single (1 day) versus repeated (14 days) MPH treatment (2 or 10 mg/kg; s.c.) from postnatal day 25 to 38. Consistent with previous reports, the striatum is a major target of acute MPH action, as indicated by elevated levels of cFOS-immunoreactivity (-ir). Increases in c-fos expression were also seen in the nucleus accumbens, cingulate/frontal cortex and piriform cortex, and Islands of Calleja. FosB expression was elevated only in the striatum following a single stimulation. Chronic MPH treatment (10 mg/kg/day for 14 days) resulted in an attenuation of c-fos expression in the striatum and Islands of Calleja. However, levels of cFOS-ir remained elevated in the nucleus accumbens and frontal cortex. In contrast to the inhibitory effect of repeated MPH exposure on c-fos expression, FOSB-ir was further elevated in the striatum, and an increase was observed in the cingulate/frontal and piriform cortices. Thus, chronic MPH differentially regulated expression of c-fos and fosB in several brain regions. Our data suggest that MPH may exert its stimulant effects at multiple sites in the immature brain, which has implications for long-term treatment in children.

Analysis of Variance↗
PubMed1998

Alterations in calmodulin mRNA expression and calmodulin content in rat brain after repeated, intermittent amphetamine.

To assess whether calmodulin (CaM) gene expression could have a role in behavioral sensitization induced by repeated, intermittent amphetamine, CaM protein and mRNA of the three separate CaM genes were measured in several different brain areas from rats repeatedly administered saline or amphetamine. Rats were injected twice weekly for five weeks, followed by one week of withdrawal. CaM protein and mRNA were measured in dorsal striatum, limbic forebrain, prefrontal cortex, ventral mesencephalon and piriform cortex. There were increases of CaM protein content and decreases of CaM I mRNA in the dorsal striatum and prefrontal cortex. CaM II mRNA was also decreased in the dorsal striatum. A decrease of CaM protein and an increase of CaM I mRNA were found in the ventral mesencephalon. There was no change of CaM protein in the limbic forebrain, although a decrease of CaM I mRNA was detected. CaM protein and mRNA were not altered in the piriform cortex. Our findings demonstrate that both CaM content and mRNA are altered after an amphetamine regimen leading to sensitization. The fact that the changes in CaM content and mRNA are in dopaminergic brain areas associated with sensitization suggests that CaM could contribute to neurochemical events underlying behavioral sensitization to amphetamine.

Alternative Splicing↗