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PubMed1998

Postnatal expression of glucose-6-phosphate dehydrogenase in different brain areas.

The activity of glucose-6-phosphate dehydrogenase (G6PD) was studied in five brain areas of rats aged 5 to 90 days. The areas studied were: the olfactory bulb (OB), cortex, hippocampus, striatum and septum. The G6PD activity increased more than 2-fold from 5 to 90 days in the OB, while it was almost constant in the other areas. At every stage of development, the G6PD activity was significantly higher in the OB than in the other areas. The G6PD pattern was compared with 6-phosphogluconate dehydrogenase (6PGD), glutathione reductase (GR); glutathione peroxidase (GPX), catalase (CAT) and superoxide dismutase (SOD) in order to find synergistic interactions among activities of these enzymes during development. Over the considered period, the activity of 6PGD increased significantly in the OB, while no significant difference in activity was detected in the other areas. GR increased significantly and progressively at each developmental stage in all areas. GPX showed a progressive increase in the OB, while in other areas a significant increase was detected at 90 days only. CAT and SOD showed a different and independent pattern which differed from the G6PD pattern. CAT showed the highest level of activity at 5 days then progressively decreased or was constant until 90 days; SOD had the highest value at 5 days, than it decreased at 10 days and increased from 10 to 90 days. In all areas, G6PD activity showed three electrophoretic bands, whose relative activity changed with development. At histochemical level, we found a marked G6PD activity in the periglomerular zone of the OB, which increased with age, while other areas showed a homogeneous staining. The present results demonstrate that G6PD activity increases in the OB during the developmental stages and there is a coordinated simultaneous activation of 6PGD, GPX and GR. It is likely that this enzyme induction increases the antioxidant defense of periglomerular cells that are subject to a rapid renewal and thus much more exposed to oxidant stress.

Aging↗
PubMed1980

Efferent neurons of the rat olfactory bulb. (An experimental study using horseradish peroxidase).

1) Two efferent neurone populations - mitral and tufted cells - are present in the main structure of the rat olfactory bulb. 2) The tufted cells, whose axons leave the olfactory bulb, are scattered throughout the whole of the outer plexiform layer and some of them lie in the periglomelural layer. 3) The axons of some of the tufted cells lead to the rostral part of the prepyriform cortex (the anterior olfactory nucleus). 4) Our findings do not indicate that the tufted cells ensure monosynapltic interbulbar connection.

Animals↗
PubMed1997

Distribution of alpha 1a-, alpha 1b- and alpha 1d-adrenergic receptor mRNA in the rat brain and spinal cord.

The technique of in situ hybridization with specific ribonucleotide probes was used to determine the distribution patterns of mRNA encoding the alpha 1a-, alpha 1b- and alpha 1d-adrenoceptor (AR) subtypes in rat brain and spinal cord. The expression pattern of alpha 1a-AR mRNA has not been reported previously, and was found to be widespread throughout the rat central nervous system. High levels were found in regions of the olfactory system, several hypothalamic nuclei, and regions of the brainstem and spinal cord, particularly in areas related to motor function. Regions expressing moderate levels of mRNA for this receptor were the septum, bed nucleus of the stria terminalis, cerebral cortex, amygdala, cerebellum and pineal gland. Low expression levels were detected in the hippocampal formation. Most nuclei in the basal ganglia and thalamus expressed extremely low or undetectable levels of alpha 1a-AR mRNA. The expression patterns of the alpha 1b- and alpha 1d-AR mRNAs were similar to those described using oligonucleotide probes in earlier studies. High expression of alpha 1b-AR mRNA was noted in the pineal gland, most thalamic nuclei, lateral nucleus of the amygdala and dorsal and median raphe nuclei. Moderate expression levels were noted throughout the cerebral cortex, and in some olfactory, septal, and brainstem regions. The distribution of alpha 1d-AR mRNA was the most discrete of the three receptors examined. Expression was strong in the olfactory bulb, cerebral cortex, hippocampus, reticular thalamic nucleus, regions of the amygdala, motor nuclei of the brainstem, inferior olivary complex and spinal cord. Comparison of the distributions of the alpha 1a-, alpha 1b- and alpha 1d-AR mRNA suggests unique functional roles for each of these receptors.

Animals↗
PubMed2003

Postnatal expression of Cdkl2 in mouse brain revealed by LacZ inserted into the Cdkl2 locus.

Transcripts of Cdkl2 encoding cycline-dependent kinase-like 2 increase in the deep cerebellar nuclei (DCN) of rabbits subjected to eyeblink conditioning. To examine the pattern of Cdkl2 expression and its activity dependence in mice, we prepared Cdkl2 mutant mice in which amino terminal coding exons were replaced by the LacZ using gene targeting. LacZ activity was first detected in the cerebral cortex from postnatal days 3 to 7 (P3-P7), and then gradually increased with age to reach nearly the maximal level by P28. In the adult brain, LacZ activity was detected in neurons in various brain regions including the olfactory bulb, cerebral cortex, hippocampus, thalamic nuclei, amygdaloid nuclei, geniculate nuclei, red nuclei, deep cerebellar nuclei, cranial nerve nuclei, and spinal cord. Loss of Purkinje cells in lurcher mice did not affect the pattern and level of LacZ activity in the DCN. Stimulation of primary neurons with glutamate, KCl, phorbol 12-myristate 13-acetate, and leukemia inhibitory factor appreciably increased the level of c-Fos but not of Cdkl2 transcripts. These results suggest that cdkl2 functions mainly in mature neurons and that mechanisms governing regulation of this gene expression in mice are distinct from those of immediate-early genes.

Animals↗
PubMed2002

Adenovirus-mediated WGA gene delivery for transsynaptic labeling of mouse olfactory pathways.

Detailed knowledge of neuronal connectivity patterns is indispensable for studies of various aspects of brain functions. We previously established a genetic strategy for visualization of multisynaptic neural pathways by expressing wheat germ agglutinin (WGA) transgene under the control of neuron type-specific promoter elements in transgenic mice and Drosophila. In this paper, we have developed a WGA-expressing recombinant adenoviral vector system and applied it for analysis of the olfactory system. When the WGA-expressing adenovirus was infused into a mouse nostril, various types of cells throughout the olfactory epithelium were infected and expressed WGA protein robustly. WGA transgene products in the olfactory sensory neurons were anterogradely transported along their axons to the olfactory bulb and transsynaptically transferred in glomeruli to dendrites of the second-order neurons, mitral and tufted cells. WGA protein was further conveyed via the lateral olfactory tract to the olfactory cortical areas including the anterior olfactory nucleus, olfactory tubercle, piriform cortex and lateral entorhinal cortex. In addition, transsynaptic retrograde labeling was observed in cholinergic neurons in the horizontal limb of diagonal band, serotonergic neurons in the median raphe nucleus, and noradrenergic neurons in the locus coeruleus, all of which project centrifugal fibers to the olfactory bulb. Thus, the WGA-expressing adenovirus is a useful and powerful tool for tracing neural pathways and could be used in animals that are not amenable to the transgenic technology.

Adenoviridae↗
PubMed1997

Developmental expression of platelet-derived growth factor alpha-receptor in neurons and glial cells of the mouse CNS.

The synthesis of platelet-derived growth factor-alpha receptor (PDGF-alphaR) is commonly attributed to oligodendrocyte progenitors during late embryonic and postnatal development. However, we recently demonstrated that mature neurons could also synthesize PDGF-alphaR, emphasizing a larger role for this receptor than previously described. In the present study, to analyze the pattern of PDGF-alphaR expression during postnatal development of the mouse CNS, we used in situ hybridization and immunohistochemistry on brain and spinal cord tissue sections. We found that, in addition to immature cells of the oligodendrocyte lineage, neurons of various CNS regions express PDGF-alphaR transcripts and protein as early as postnatal day 1 (P1). Whereas neuronal expression was maintained at all ages, the oligodendroglial expression strongly decreased after P21. In the adult, PDGF-alphaR was detected in very few oligodendrocyte progenitors scattered in the cerebral cortex or in white matter tracts, thus suggesting the presence of PDGF-alphaR on O-2Aadult progenitors. In the mature CNS, PDGF-alphaR transcripts and protein were mainly localized in neurons of numerous structures, such as the olfactory bulb, cerebral cortex, hippocampus, and brainstem nuclei and in motor neurons of the ventral horn of the spinal cord. The differential expression of PDGF-alphaR in oligodendroglia and neurons argues in favor of several roles of PDGF during development.

Aging↗
PubMed1997

Vesicular acetylcholine transporter (VAChT) protein: a novel and unique marker for cholinergic neurons in the central and peripheral nervous systems.

Acetylcholine (ACh) is synthesized in nerve terminals from choline and acetyl coenzyme A by the cytoplasmic enzyme choline acetyltransferase (ChAT). The neurotransmitter is thereafter transported into synaptic vesicles, where it is stored until release. cDNA clones encoding a vesicular ACh transporter (VAChT) were recently isolated. In this paper, we report on the generation of highly specific goat polyclonal antisera to the rat VAChT protein by using a synthetic carboxy-terminal 20-amino-acid peptide sequence as an immunogen. Characterization of the antisera revealed recognition of VAChT, but not vesicular monoamine transporter (VMAT) protein, in transfected CV-1 cells. VAChT immunoreactivity was also detected in cells that endogenously express the protein, such as in PC12 cells and in primary cultures of spinal motoneurons. Absorption controls showed that the VAChT antisera could be completely blocked at the 10(-5) M concentration by cognate peptide used for immunization. The antisera cross-reacted with the VAChT protein in rat and mouse but not in guinea pig, rabbit, or cat. Immunohistochemistry and confocal laser microscopy, using the goat VAChT antisera, showed strong immunoreactivity in discrete fibers and neuronal cell bodies of the central and peripheral nervous systems. Within cell bodies and axonal nerve terminals, as well as in dendrites, the staining appeared granular, presumably representing labeling of synaptic vesicles containing ACh. In the rat central nervous system, VAChT-positive cell bodies were demonstrated in the cerebral cortex, striatum, septum, nucleus basalis, medial habenula, mesopontine complex, cranial, and autonomic and spinal motor nuclei and in the intermediomedial region near the central canal. High densities of VAChT-immunoreactive axonal fibers were encountered in areas such as the olfactory bulb, cerebral cortex, striatum, basal forebrain, amygdala, thalamus, hypothalamus including median eminence, hippocampal formation, superior colliculus, interpeduncular nucleus, and pedunculopontine and laterodorsal tegmental nuclei. In cranial and spinal motor nuclei, particularly large varicosities were seen in close proximity to the motoneuron cell somata and their proximal dendrites. In the peripheral nervous system, VAChT immunoreactivity was also detected in motor endplates of skeletal muscle as well as in fibers of sympathetic and parasympathetic abdominal ganglia, heart atrium, respiratory tract, gastrointestinal tract, pancreas, adrenal medulla, male genitourinary tract, and salivary and lacrimal glands. Direct double labeling revealed colocalization of VAChT and ChAT immunoreactivity in neurons. The results show that VAChT antisera represent novel and unique tools for the study of cholinergic neurons in the central and peripheral nervous systems.

Animals↗
PubMed1999

Immunohistochemical localization of a novel acidic calmodulin-binding protein, NAP-22, in the rat brain.

NAP-22 is a neuronal tissue-enriched acidic calmodulin-binding protein with a molecular mass of 22,000 and is recovered in the membrane fraction during biochemical fractionation. We observed the distribution pattern of this protein in the rat brain using an immunohistochemical method by light and electron microscopy. NAP-22 immunoreactivity was detected through the whole brain, and the most dense staining was observed in the forebrain including cerebral cortex, hippocampal formation, olfactory bulb, basal ganglia and thalamus. Immunoreactivity was distributed densely at the neuropil, whereas nerve cells and nerve fibres had little or no reaction. In the brain stem, immunonegative large nerve cell bodies were surrounded by immunopositive varicosities. In the cerebellar cortex, mossy fibre terminals and parallel fibres showed immunoreactivity, whereas Purkinje cells did not. Intracellular distribution was observed in the cerebral and cerebellar cortices. NAP-22 immunoreactivity was noted in the axon terminals, dendritic spines and thin nerve fibres. In these structures, reaction products were associated mainly with synaptic vesicles, pre- and postsynaptic membranes and microtubules. This study demonstrates that the immunoreactivity of NAP-22 is distributed widely in the brain, especially in the synapse, and suggests that this protein is involved in synaptic transmission both in the pre- and postsynaptic region.

Animals↗
PubMed2000

Neural correlates of olfactory recognition memory in the rat orbitofrontal cortex.

The orbitofrontal cortex (OF) is strongly and reciprocally connected with the perirhinal (PR) and entorhinal areas of the medial temporal lobe and plays an important role in odor recognition memory. This study characterized firing patterns of single neurons in the OF of rats performing a continuous odor-guided delayed nonmatch to sample (DNMS) task. Most OF neurons fired in association with one or more task events, including the initiation of trials, the sampling of odor stimuli, and the consumption of rewards. OF neurons also exhibited sustained odor-selective activity during the memory delay, and a large proportion of OF cells had odor-specific enhanced or suppressed responses on stimulus repetition. Most OF neurons were activated during several task events, or associated with complex behavioral states. The incidence of cells that fired in association with the critical match/non-match judgement was increased as the DNMS rule was learned, and was higher in OF than in perirhinal and entorhinal cortex. Furthermore, the classification of match and nonmatch trials was correlated with accuracy in performance of that judgement. These findings are consistent with the view that OF is a high order association cortex that plays a role both in the memory representations for specific stimuli and in the acquisition and application of task rules.

Action Potentials↗
PubMed1992

Opioid receptors and inhibition of dopamine-sensitive adenylate cyclase in slices of rat brain regions receiving a dense dopaminergic input.

In slices of rat nucleus accumbens, olfactory tubercle, frontal cortex and mediobasal hypothalamus exposed to dopamine (DA), the activation of DA D1 receptors stimulated cyclic AMP (cAMP) formation whereas, in nucleus accumbens slices only, activation of D2 receptors appeared to inhibit D1 receptor-stimulated adenylate cyclase at the same time. Activation of mu-opioid receptors by [D-Ala2,MePhe4,Gly-ol5]enkephalin (DAMGO; 1 microM), but not of delta-opioid receptors by 1 microM [D-Pen2,D-Pen5]enkephalin (DPDPE), inhibited (by 35-40%) DA-stimulated cAMP production in slices of nucleus accumbens and olfactory tubercle. When adenylate cyclase was stimulated by selective D1 receptor activation, i.e. by DA in the presence of (-)-sulpiride, DPDPE reduced cAMP formation (by about 45%) in nucleus accumbens slices but not in slices of the other brain regions. The kappa-agonist, U 50,488, did not affect DA- or D1 receptor-stimulated adenylate cyclase activity in any of the brain regions. Preincubation of nucleus accumbens slices with the irreversible delta-ligand, fentanyl isothiocyanate (FIT; 1 microM), not only antagonized the inhibitory effect of DPDPE but also prevented the antagonism by naloxone of the inhibitory effect of DAMGO. Therefore, in nucleus accumbens opioids may inhibit DA-sensitive adenylate cyclase through activation of a mu/delta-opioid receptor complex, whereas in olfactory tubercle mu-receptors appear to mediate the inhibition of adenylate cyclase activity. Opioids do not seem to affect DA-stimulated cAMP formation in frontal cortex and mediobasal hypothalamus.

Adenylyl Cyclase Inhibitors↗
PubMed1997

Comparative distribution of myristoylated alanine-rich C kinase substrate (MARCKS) and F1/GAP-43 gene expression in the adult rat brain.

Myristoylated alanine-rich C-kinase substrate (MARCKS) and F1/GAP-43 (B-50/neuromodulin) are both major specific substrates for protein kinase C (PKC) and appear to play an important role in the regulation of neuroplastic events during development and in the adult brain. Since PKC isozymes are differentially expressed in brain and the expression of F1/GAP-43 and MARCKS are differentially regulated by PKC through posttranslational mechanisms, the present study examined the relative distribution of both mRNAs in the adult brain by using in situ hybridization histochemistry. MARCKS hybridization was most pronounced in the olfactory bulb, piriform cortex (layer II), medial habenular nucleus, subregions of the amygdala, specific hypothalamic nuclei, hippocampal granule cells, neocortex, and cerebellar cortex, intermediate in the superior colliculus, hippocampal CA1, and certain brainstem nuclei including the locus coeruleus, and low-absent in regions of the caudate-putamen, geniculate, thalamic nuclei, lateral habenular nucleus, and hippocampal CA3 pyramidal and hilar neurons. Consistent with previous reports, prominent F1/GAP-43 hybridization was observed in neocortex, medial geniculate, piriform cortex (layer II), substantia nigra pars compacta, hippocampal CA3 pyramidal cells, thalamic and hypothalamic nuclei, lateral habenular nucleus, locus coeruleus, raphe nuclei, and cerebellar granule cells, intermediate in regions of the thalamus, hypothalamus, and amygdala, and low-absent in regions of the olfactory bulb, caudate-putamen, medial habenular nucleus, hippocampal granule cells, and superior colliculus. Overall, F1/GAP-43 was highly expressed in a greater number of regions compared to MARCKS and, in a number of regions, including the hippocampus, habenular complex, ventral tegmentum, geniculate, and certain brain stem nuclei, a striking inverse pattern of expression was observed. These results indicate that MARCKS gene expression, like that of F1/GAP-43, remains elevated in select regions of the adult rat brain which are associated with a high degree of retained plasticity. The potential role of PKC in the regulation of MARCKS and F1/GAP-43 gene expression in brain is assessed.

Animals↗
PubMed1993

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) effects on enkephalinergic neurons in various regions of mouse brain.

In order to elucidate the effects of MPTP on enkephalinergic neurons, dopamine (DA), norepinephrine (NE), proenkephalin (PE) mRNA and met-enkephalin (ME) were measured in striatum, olfactory tubercle, and prefrontal cortex of C57/B16 mice 1 day-2 weeks following treatment with 96 mg/kg MPTP HCl (24 mg/kg i.p., twice/day for 2 days). DA and its metabolites were depleted 70% in striatum and 40% in olfactory tubercle within 1 day. In cortex, DA was unchanged, whereas homovanillic acid and NE were depleted 50 and 40% respectively by 3 days. ME increased in all three brain regions at different times whereas PE mRNA showed a different pattern in each region, with an increase in olfactory tubercle, a decrease in cortex, and in striatum, a decrease at 1 day followed by an increase at 3 days. Thus enkephalinergic neurons in each region respond differently to MPTP treatment. In striatum and olfactory tubercle. DA is depleted sufficiently to release its tonic inhibition on the enkephalinergic neurons, thereby leading to increased enkephalin synthesis. In cortex, the change in NE metabolism appears to cause a decrease of ME release and thereby a depression of PE synthesis. The possible relationship between these results and the changes observed in Parkinson's disease are discussed.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2002

Effect of quercetin on plasma extravasation in rat CNS and dura mater by ACE and NEP inhibition.

The effects of quercetin on substance P-induced plasma protein extravasation (PE) in the rat dura mater, cerebellum, olfactory bulb and cortex and also its modulation by endopeptidases, angiotensin-converting enzyme (ACE) and neutral endopeptidase (NEP) were studied. PE was assessed by photometric measurement of extravasated Evans blue. Substance P (SP) and NEP or ACE inhibitors increased the PE in dura mater. Pretreatment with captopril or phosphoramidon potentiated PE induced by SP in the dura mater and cerebellum, respectively. Quercetin increased the PE in the dura mater, cerebellum and cortex. Further results suggested that the PE induced by SP in the dura mater was enhanced by pretreatment with quercetin, similar to that observed with selective peptidase inhibitors. Quercetin-stimulated extravasation in all tissues was abolished by NK-1 receptor blockade. These results suggest that quercetin increases PE in the dura mater and CNS tissues by inhibiting NEP and/or ACE, showing that the effect induced in the dura mater, cerebellum and cortex occurs through endogenous SP accumulation.

Animals↗
PubMed1994

An in situ hybridization study on interleukin-1 beta mRNA induced by transient forebrain ischemia in the rat brain.

Expression of interleukin-1 beta (IL-1 beta) mRNA in the rat brain after transient forebrain ischemia was investigated by in situ hybridization histochemistry. Thirty min after the start of recirculation, IL-1 beta mRNA was induced in the several brain regions, including the olfactory bulb, cerebral cortex, hippocampus, striatum and thalamus where neuronal degeneration was reported to be observed after transient forebrain ischemia. The hybridization signals were observed both on the glial cells and around the vascular walls.

Animals↗
PubMed2005

An extrahippocampal projection from the dentate gyrus to the olfactory tubercle.

BACKGROUND: The dentate gyrus is well known for its mossy fiber projection to the hippocampal field 3 (CA3) and its extensive associational and commissural connections. The dentate gyrus, on the other hand, has only few projections to the CA1 and the subiculum, and none have clearly been shown to extrahippocampal target regions. RESULTS: Using anterograde and retrograde tracer techniques in the Madagascan lesser hedgehog tenrec (Afrosoricidae, Afrotheria) it was shown in this study that the dentate hilar region gave rise to a faint, but distinct, bilateral projection to the most rostromedial portion of the olfactory tubercle, particularly its molecular layer. Unlike the CA1 and the subiculum the dentate gyrus did not project to the accumbens nucleus. A control injection into the medial septum-diagonal band complex also retrogradely labeled cells in the dentate hilus, but these neurons were found immediately adjacent to the heavily labeled CA3, while the tracer injections into the rostromedial tubercle did not reveal any labeling in CA3. CONCLUSION: The dentate hilar neurons projecting to the olfactory tubercle cannot be considered displaced cells of CA3 but represent true dentato-tubercular projection neurons. This projection supplements the subiculo-tubercular projection. Both terminal fields overlap among one another as well as with the fiber terminations arising in the anteromedial frontal cortex. The rostromedial olfactory tubercle might represent a distinct ventral striatal target area worth investigating in studies of the parallel processing of cortico-limbic information in tenrec as well as in cat and monkey.

Animals↗
PubMed1996

Localization of natriuretic peptide-activated guanylate cyclase mRNAs in the rat brain.

Physiological actions of atrial natriuretic peptide (ANP) and C-type natriuretic peptide (CNP) are elaborated by membrane-bound natriuretic peptide receptors (NPRs). These receptors possess intracellular guanylate cyclase domains that mobilize cyclic guanosine monophosphate upon binding of peptide. Two distinct NPR subtypes have been described in brain: the NPR-A selectively binds ANP, whereas NPR-B exhibits high affinity for CNP. To define further the potential domains of ANP and CNP action in brain, the present study used in situ hybridization histochemistry to map NPR-A and NPR-B mRNA-expressing cell populations. Significant levels of neuronal NPR-A mRNA expression were observed only in the mitral cell layer of the olfactory bulb, medial habenula, subfornical organ, and area postrema. Expression of NPR-A mRNA was observed in forebrain white matter tracts, suggesting synthesis in glial cells. In contrast, NPR-B mRNA was widely expressed throughout the neuraxis. In the telencephalon, signal was abundant throughout limbic cortex and neocortex, olfactory bulb, hippocampus, and amygdala. Intense NPR-B mRNA hybridization was observed in preoptic-hypothalamic neuroendocrine circuits and in motor nuclei of cranial nerves. Intermediate expression of NPR-B mRNA was observed in brainstem nuclei controlling autonomic function. Labeling for NPR-B but not NPR-A mRNA was observed in pituicytes in the neural lobe of the pituitary and in scattered cells of the anterior pituitary. These results suggest that CNP is the primary biologically active natriuretic peptide in brain. In contrast with NPR-B, NPR-A appears to be expressed largely in restricted cell populations containing high levels of ANP and in circumventricular organs. These data implicate the NPR-A in autoregulation of ANP neurons and central registration of cardiac ANP release.

Animals↗
PubMed1985

Effects of lesions in the amygdala and periventricular hypothalamus on striatal somatostatin-like immunoreactivity.

Somatostatin has been found in substantial amounts in the basal ganglia by radioimmunoassay and has been demonstrated in both neurons and nerve terminals. Since the levels of somatostatin have been shown to vary in Huntington's and Alzheimer's disease it was of interest to see whether such changes could be produced experimentally. Lesions of the periventricular nucleus of the hypothalamus and knife cuts adjacent to this nucleus had no effect on striatal somatostatin-like immunoreactivity (SLI). Similarly lesions of medio-dorsal frontal cortex, and those isolating pyriform cortex or the olfactory bulb had no effect on striatal SLI. Removal of the amygdala resulted in significant increases in SLI in the ipsilateral striatum and nucleus accumbens, suggesting loss of an inhibitory interaction. Stria terminalis lesions failed to reproduce this effect suggesting that it is mediated via amygdalo-striatal projections traveling in the dorsal longitudinal bundle. Other findings support a somatostatin projection to the amygdala from the bed nucleus of the stria terminalis and one from the amygdala to the ventromedial hypothalamus.

Amygdala↗
PubMed1996

Alteration in protein phosphorylation associated with olfactory bulb kindling.

Kindling is a model of neuronal plasticity underlying both epilepsy and memory. One of the cellular mechanisms associated with the increased synaptic efficacy is the modification of the structural configuration of synaptic membrane proteins. The present study examined changes in protein phosphorylation associated with olfactory bulb kindling. The differences in the degree of protein phosphorylation in four brain regions, i.e., olfactory bulb, pyriform cortex, hippocampus and frontal cortex, were examined in kindled, non-kindled and implanted control rats. Two phosphoproteins (45k and 48k, named according to their mol. wt.) in frontal cortex were altered after kindling. There was a two-fold increase in phosphorylation of a 48k phosphoprotein in the frontal cortex of kindled rats compared to controls. This phosphorylation was stimulated by Ca2+/calmodulin, and depressed by ACTH1-24. The 45k phosphoprotein in frontal cortex of kindled rats was decreased to 52% of the controls. The changes in protein phosphorylation found in frontal cortex are consistent with the hypothesis that permanent information storage may reside in cortical areas, while hippocampus and pyriform cortex may be the major relaying centers. This phenomenon could theoretically model an information storage process occurring in the cortex following relay of experiential input from subcortical areas.

Animals↗