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G Sperk

Publications and source records attributed to G Sperk.

At least 55 records · Page 3Linked to original sources
PubMed1995

Neurochemical characterization of preprotachykinin B(50-79) immunoreactivity in the rat.

Preprotachykinin B (PPT-B) contains two peptide sequences which are flanked by pairs of dibasic amino acids: the decapeptide neurokinin B and a 30 amino acid non-tachykinin peptide consisting of the amino acids 50-79 of PPT-B. Whereas the existence of neurokinin B is well established in brain and peripheral tissues, native PPT-B(50-79) has not been identified so far. We have previously studied the distribution of PPT-B(50-79)-immunoreactivity in the rat brain using antibodies directed against synthetic PPT-B(50-79). Now we adapted a radioimmunoassay for characterizing neurochemically PPT-B(50-79)-immunoreactivity in the rat. In the brain concentrations ranging from 2 to 180 fmol/mg wet tissue weight were measured using synthetic PPT-B(50-79) as standard. The highest concentrations were observed in the interpeduncular nucleus and in the hypothalamus (180 and 90 fmol/mg tissue, respectively). Intermediate concentrations (15 to 60 fmol/mg tissue) were present in cortical areas, in the hippocampus, the spinal cord and in the olfactory bulb. Modest levels were detected in the cerebellum. Considerably lower concentrations of PPT-B(50-79)-immunoreactivity were observed in peripheral tissues. They were highest in the adrenal medulla and in the urinary bladder (3.0 and 1.2 fmol/mg tissue, respectively). This distribution, as observed by radioimmunoassay, correlated to that previously revealed by immunocytochemistry. Tissue concentrations of total PPT-B(50-79) immunoreactivity, however, were slightly higher than those of neurokinin B. Gel filtration chromatography on Sephadex G50 and reversed phase HPLC revealed at least three PPT-B(50-79) immunoreactive peaks. About 90% of the PPT-B(50-79)-immunoreactivity was contained within 2 peaks of apparently higher molecular weight than PPT-B(50-79). A minor portion of PPT-B(50-79)-immunoreactivity comigrated with the synthetic peptide, suggesting that only minor amounts of PPT-B(50-79) are formed in vivo. The processing enzyme(s) cleaving protachykinin B at the pair of basic amino acids (Lys80-Arg81) located between PPT-B(50-79) and neurokinin B may not be acting at the Arg48-Arg49 site (followed by -Leu50) at the amino terminal end of PPT-B(50-79).

Amino Acid Sequence↗
PubMed1995

Somatostatin, neuropeptide Y, neurokinin B and cholecystokinin immunoreactivity in two chronic models of temporal lobe epilepsy.

Somatostatin-, neuropeptide Y-, neurokinin B- and cholecystokinin-containing neurons were investigated in the rat hippocampus in two chronic models of temporal lobe epilepsy, i.e. 30 days after rapid kindling or electrically induced status epilepticus (post-status epilepticus). After rapid kindling, somatostatin immunoreactivity was strongly increased in interneurons and in the outer and middle molecular layer of the dentate gyrus. In four of six post-status epilepticus rats (status epilepticus I rats), somatostatin immunoreactivity was slightly increased in the dorsal but decreased in the ventral dentate gyrus and molecular layer. Somatostatin immunoreactivity decreased in neurons of the dorsal hilus in the two other post-status epilepticus rats investigated, while a complete loss was found in the respective ventral extension (status epilepticus-II rats). These changes were associated with a different extent of neurodegeneration as assessed by Nissl staining. Similarly, neuropeptide Y immunoreactivity was enhanced in neurons of the hilus and in the middle and outer molecular layer of the dentate gyrus in the dorsal hippocampus of rapidly kindled and status epilepticus-I rats. Neuropeptide Y and neurokinin B immunoreactivity was enhanced in the mossy fibers of all post-status epilepticus rats, but not in the rapidly kindled rats. In status epilepticus-II rats, neuropeptide Y-and neurokinin B-positive fibers were also detected in the infrapyramidal region of the stratum oriens of CA3 and in the inner molecular layer of the dentate gyrus in the dorsal and ventral hippocampus respectively, labeling presumably sprouted mossy fibers. Increased staining of neuropeptide Y and neurokinin B was found in the alveus after rapid kindling. Cholecystokinin immunoreactivity was markedly increased in the cerebral cortex, Ammon's horn and the molecular layer of the dentate gyrus in the ventral hippocampus of rapidly kindled and post-status epilepticus rats. The lasting changes in the immunoreactive pattern of various peptides in the hippocampus may reflect functional modifications in the corresponding peptide-containing neurons. These changes may be involved in chronic epileptogenesis, which evolves in response to limbic seizures.

Animals↗
PubMed1995

Hippocampal granule cells express glutamic acid decarboxylase-67 after limbic seizures in the rat.

Temporal lobe epilepsy is the most common form of epilepsy. Decreased GABA-ergic inhibition has been suggested as one cause of hyperexcitability. On the other hand, increased expression of glutamic acid decarboxylase, the rate-limiting enzyme of GABA synthesis, has been found in interneurons of the hippocampus in patients with temporal lobe epilepsy and in rats after kainic acid-induced limbic seizures, indicating increased GABA-ergic transmission. Here we report differential expression of two genes encoding different molecular forms of glutamic acid decarboxylase (GAD), GAD65 and GAD67, after kainic acid-induced seizures in the rat. There is a rapid but transient elevation of GAD67 mRNA levels in granule cells 6-24 h after kainic acid injection, followed by enhanced GAD immunoreactivity in the terminal field of mossy fibers. In interneurons in the hilus of the dentate gyrus, a sustained and progressing increase in the expression of both GAD65 and GAD67 messenger RNA occurs. These observations indicate that consitutively glutamatergic mossy fibers may be capable of synthetizing and utilizing the inhibitory transmitter GABA in sustained limbic seizures. Enhanced expression of glutamic acid decarboxylases within interneurons and in granule cells/mossy fibers suggest augmented GABA-ergic neurotransmission supporting selfprotective, anticonvulsive mechanisms in limbic epilepsy.

Animals↗
PubMed1994

Kainic acid induced seizures cause a marked increase in the expression of neurokinin-3 receptor mRNA in the rat cerebellum.

Marked changes in the expression of the tachykinin peptide neurokinin B (NKB) have been recently observed in animal models of epilepsy. In this study we investigated mRNA levels encoding the receptor for NKB, the neurokinin-3 receptor (NK-3R), after limbic seizures induced by kainic acid (KA) in the rat. NK-3R mRNA levels were determined by nuclease protection assay at various time intervals after i.p. injection of KA in the rat. Increases of more than 200% were observed in NK-3R mRNA in the cerebellum after 7 and 30 days. In the hippocampus a moderate, reversible increase (of 70%, 1 day after KA) was seen. In the frontal cortex a reduction of NK-3R mRNA (2 days after KA) was found. In the amygdala, levels of the transcript were decreased (by 50% and more) at all intervals investigated. The decreases in mRNA levels in the amygdala are consistent with the severe damage observed in this brain area. The increases in NK-3R mRNA in the cerebellum point to the development of receptor supersensitivity and suggest a functional role of NKB in this animal model of epilepsy.

Animals↗
PubMed1994

Differential NPY mRNA expression in granule cells and interneurons of the rat dentate gyrus after kainic acid injection.

Using in situ hybridization histochemistry neuropeptide Y (NPY) mRNA expression was investigated after intraperitoneal injection of kainic acid (KA) and after local application of KA or quinolinic acid into the dentate gyrus of the rat. Enhanced concentrations of NPY mRNA were observed in interneurons of the hilus, including presumptive fusiform neurons and pyramidal-shaped basket cells already 4 hours after initiation of limbic seizures by KA (10 mg/kg, i.p.). Increased NPY expression persisted in neurons resistant to seizure-induced cell death (6-48 h after i.p. KA). Exceptionally high hybridization signals were found in interneurons of the hilus and the CA1 and CA3 sectors 8 months after KA-induced limbic seizures. In the granule cell layer only a transient but pronounced increase in NPY mRNA was observed 12-24 h after injection. Only moderate changes were observed in this cell layer at later intervals. Anticonvulsant treatment with thiopental, after a brief period of generalized seizures, prevented the increase in NPY mRNA in granule cells but not in interneurons. No change in NPY message was found also in granule cells of rats which responded with mild "wet dog shake" behavior but not with motor seizures to KA injection. Local injections of low doses of KA (0.05-0.2 nmol) or quinolinic acid (6.5-100 nmol) into the dentate gyrus of the hippocampus under deep thiopental anesthesia, after 24 h, resulted in increased concentrations of NPY message in interneurons of the ipsilateral, but not of the contralateral hilus and not in granule cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Neuropeptide Y inhibits potassium-stimulated glutamate release through Y2 receptors in rat hippocampal slices in vitro.

1. We investigated the effects of neuropeptide Y (NPY), peptide YY (PYY), NPY13-36, NPY18-36, [Leu31][Pro34]NPY and of pancreatic polypeptide Y (PPY) on calcium-dependent, potassium-stimulated glutamate release in superfused rat hippocampal slices. 2. NPY, PYY and the Y2 receptor agonist NPY13-36 equipotently inhibited the release of glutamate. The half-maximal response was observed at about 10 nM in a dose-dependent manner (3 to 100 nM). Maximal inhibition of 50 to 60% was obtained at 100 nM. At higher concentrations of the peptides (300 nM and 1 microM) this inhibition was partially or entirely reversed. Porcine NPY13-36 and NPY18-36 inhibited glutamate release by about 44% at 100 nM. 3. The specific Y1 receptor agonist, [Leu31][Pro34]NPY, caused an insignificant increase in glutamate release at 100 to 300 nM concentrations. PPY had no effect on potassium-evoked glutamate release in hippocampal slices at concentrations of 30 nM to 1 microM. 4. The experiments support previous electrophysiological data. They suggest a potent inhibitory action of NPY through NPY-Y2 receptors on the release of the excitatory amino acid glutamate in rat hippocampus. Especially under conditions of increased NPY synthesis, such as in epilepsy, this mechanism may be of pathophysiological relevance.

Animals↗
PubMed1993

Electrical kindling of the hippocampus is associated with functional activation of neuropeptide Y-containing neurons.

The release of neuropeptide Y (NPY) was measured from hippocampal slices of rats at stage 2 (preconvulsive stage) and stage 5 (full seizure expression) of electrical kindling of the dorsal hippocampus (upper blade of the dentate gyrus). Spontaneous release in naive rats (9.0 +/- 0.8 fmol/ml every 10 min) was independent of external Ca2+ but was reduced by 38 +/- 3.6% (P < 0.05) during 20 min incubation with 5 microM tetrodotoxin. Spontaneous efflux in naive rats did not differ from that in shams (implanted with electrodes but not stimulated) or in rats kindled to stage 2 and stage 5. Twenty-five, 50 and 100 mM KCl induced a concentration-dependent release of NPY (P < 0.05 and P < 0.01 at 25 and 50-100 mM respectively) from slices of shams. The effect of 100 mM KCl was reduced by 94 +/- 1% (P < 0.01) in the absence of Ca2+. Two days after the last stage 2 stimulation and 1 week after the last stage 5 seizure, NPY release was significantly larger than in shams at all KCl concentrations in the stimulated and contralateral hippocampus (P < 0.05 and P < 0.01). Forty-eight hours after one single after-discharge and 1 month after the last stage 5 seizure, 50 mM KCl induced a significantly larger release of NPY in the stimulated and contralateral hippocampus (P < 0.01 and P < 0.05), although the effect was less than during kindling.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1993

Kainic acid seizures cause enhanced expression of cholecystokinin-octapeptide in the cortex and hippocampus of the rat.

Immunocytochemistry and in situ hybridization techniques were used for investigating changes in cholecystokinin immunoreactivity and mRNA in the cerebral cortex and hippocampus after kainic acid-induced limbic seizures in the rat. Marked increases in cholecystokinin mRNA concentrations were observed in layers II/III and V/VI of the cerebral cortex, in CA1 pyramidal neurons of the hippocampus, and in presumptive basket cells of the dentate gyrus 1 and 2 days after the acute seizures. Whereas cholecystokinin mRNA contents returned to normal in the cerebral cortex and the CA1 sector at later intervals, high concentrations were observed in basket cells even 2 months after the initial seizures. Accordingly, cholecystokinin-like immunoreactivity was intensified in the cerebral cortex, CA1 sector and in presumed basket cells of the hippocampus 30 days after kainic acid. Besides its high content in basket cells, cholecystokinin-like immunoreactivity was primarily present in neuronal fibers or diffusely distributed in the respective brain area. In the hippocampus, strongly enhanced staining for cholecystokinin was also observed in the alveus, the stratum lacunosum moleculare, and in the inner molecular layer, suggesting increased concentrations of the peptide in afferent and efferent fibers of the hippocampus. The present experiments suggest a strong activation of cholecystokinin systems in the brain after kainic acid-induced limbic seizures in the rat. This is indicated by pronounced increases in cholecystokinin mRNA in the cortex and individual cell types of the hippocampus (basket cells, granule cells, and CA1 pyramidal neurons). The subsequent increases in cholecystokin immunoreactivity even surpass those in mRNA. The observed changes may be part of the self-defense mechanisms that protect the animals during subsequent epileptic episodes.

Amygdala↗
PubMed1993

Kainic acid seizures in the rat: differential expression of chromogranin A, carboxypeptidase H and peptidylglycine alpha-amidating monooxigenase in subfields of the hippocampal formation.

Using in situ hybridization histochemistry concentrations of mRNAs encoding chromogranin A (ChA), carboxypeptidase H (CPH) and peptidylglycine alpha-amidating monooxigenase (PAM) have been investigated in the hippocampus after kainic acid (KA)-induced limbic seizures in the rat. Increased concentrations (by 150%) of ChA and CPH mRNAs were found in the granule cell layer 24 h after KA injection. At the same time PAM mRNA levels were only slightly elevated (by 50%). Whereas the increases in CPH and PAM transcripts were only transient, ChA mRNA concentrations in the granule cell layer were elevated up to 2 months after the initial seizures. In contrast, in the pyramidal cell layers of all hippocampal subfields (CA1 to CA3) ChA mRNA concentrations were significantly reduced (by 40-70%) 1-60 days after KA. PAM and CPH messages were slightly reduced in the pyramidal cell layer of CA1 but not in CA2 and CA3. The experiments demonstrate that KA-induced limbic seizures cause sustained changes in the expression of ChA mRNA. At the same time the expression of two enzymes involved in post-translational processing of neuropeptides, PAM and CPH, becomes only transiently altered. Synthesis of ChA may be regulated differently in the strata granulosum and pyramidale during epileptic seizures.

Animals↗
PubMed1993

Effects of antidepressant drug treatment on levels of NPY or prepro-NPY-mRNA in the rat brain.

The effects of acute and chronic treatment with the tricyclic antidepressant drugs, imipramine, clomipramine and desipramine on levels of neuropeptide Y (NPY) and prepro-NPY-mRNA were studied in different areas of the rat brain. Chronic treatment with imipramine (6.3-25 mg/kg/day) for 10-30 days caused an approx. 15-25% reduction in NPY immunoreactivity in the frontal cortex, but only insignificant changes in striatum, hippocampus, amygdala and hypothalamus. Slight and insignificant changes in the concentrations of prepro-NPY-mRNA were also detected by Northern blot analysis in these brain areas. Only in the hypothalamus was a 20% increase in prepro-NPY-mRNA found. NPY or prepro-NPY-mRNA levels were not altered 3 or 24 h after a single injection of imipramine. The effects of clomipramine and desipramine, at doses of 25 mg/kg daily for 10 days, were investigated in the frontal cortex and in the hippocampus. Except for a slight decrease in prepro-NPY-mRNA in the frontal cortex after desipramine no significant changes in NPY tissue levels or prepro-NPY-mRNA concentrations were observed in the frontal cortex and the hippocampus. In summary, treatment with the three tricyclic antidepressant drugs had no consistent effects on the brain NPY system. These data do not support the previous suggestion that antidepressant drugs may exert their actions by increasing NPY levels in the brain.

Animals↗
PubMed1992

Distribution of neurons expressing neurokinin B in the rat brain: immunohistochemistry and in situ hybridization.

Neurokinin B (NKB) belongs to the family of neuropeptides named tachykinins. Members of this family such as substance P or neurokinin A have been proposed to function as neurotransmitters or neuromodulators. Searching for possible sites of action of NKB in the central nervous system, we have now investigated its distribution within the rat brain by immunohistochemical techniques and in situ hybridization. For immunohistology two different antisera directed against amino acid sequences within preprotachykinin B were used. One antiserum had been raised against a synthetic derivative of NKB; the other one was directed towards the amino acids 50-79 of preprotachykinin B, which are referred to as peptide 2. Essentially the same distribution of immunoreactive perikarya was obtained with both antisera and it closely corresponded to the cellular localization of preprotachykinin B mRNA. Neurons containing NKB immunoreactivity and mRNA were present in many areas including cerebral cortex, hippocampal formation, amygdaloid complex, bed nucleus of the stria terminalis, ventral pallidum, habenula, medial preoptic area, arcuate nucleus, and lateral mammillary bodies. Dense immunoreactive fibers were observed in various parts of the brain and were most prominent in the olfactory bulb and tubercle, the lateral olfactory tract, medial hypothalamus, around blood vessels of the median eminence and interpeduncular nucleus, amygdaloid nuclei, stria terminalis, subbrachial nucleus, and medial geniculate nucleus. Fibers of less intense staining were seen among other brain areas in the substantia nigra, the reticular formation, and the area of the nucleus of the solitary tract. Surgical lesion of the fasciculus retroflexus revealed that the dense fiber network observed in the interpeduncular nucleus originates from the ventral and dorsal parts of the medial habenula. Our data suggest a widespread and distinct distribution of neurons expressing NKB within the central nervous system, suggesting possible neuromodulatory roles of this neuropeptide for various brain functions.

Amino Acid Sequence↗
PubMed1992

Temporal lobe epilepsy of the rat: differential expression of mRNAs of chromogranin B, secretogranin II, synaptin/synaptophysin and p65 in subfield of the hippocampus.

We have investigated by in situ hybridization changes in the content of mRNAs encoding for chromogranin B, secretogranin II, synaptin/synaptophysin and p65 after kainic acid-induced seizures and pentylenetetrazol kindling. Kainic acid seizures resulted in marked but transient increases in secretogranin II mRNA concentrations in the granule cell layer and throughout the pyramidal cell layers of the hippocampus (by 100-500%) as well as in various areas of the cerebral cortex (by up to 900%) and the thalamus (up to 300%) 12 h after injection of the toxin. Chromogranin B mRNA concentrations were persistently increased in granule cells (but not in pyramidal cells) of the hippocampus (suprapyramidal blade, 450%) and in cortical areas (250%) at all time intervals after kainic acid injection (12 h to 60 days). Accordingly chromogranin B immunoreactivity was enhanced in the terminal field of mossy fibers and in the inner part of the molecular layer 30 days after kainic acid. Secretogranin II immunoreactivity was also markedly increased in CA1, the paraventricular thalamic nucleus and in the central amygdala. In rats kindled with pentylenetetrazol only chromogranin B (by 200%) but not secretogranin II mRNA was increased in dentate granule cells. In contrast to the mRNAs of these secretory proteins concentrations of mRNAs encoding synaptin/synaptophysin and p65, two membrane proteins of synaptic vesicles, were not altered in any of these brain structures. These data demonstrate that in brain the biosynthesis of chromogranin B and secretogranin II is regulated like that of neuropeptides which is consistent with a role of these secretory polypeptides as precursors of functional peptides. Activation of neurons induces an increased synthesis of neuropeptides but not a concomitant synthesis of membrane proteins of synaptic vesicle. This might lead to an increased quantal content available for transmission.

Animals↗
PubMed1992

Limbic seizures cause pronounced changes in the expression of neurokinin B in the hippocampus of the rat.

Immunohistological and in situ hybridization techniques were used to study the influence of kainic acid-induced seizures and of pentylenetetrazol kindling on neurokinin B immunoreactivity and neurokinin B mRNA in the rat hippocampus. Pronounced increases in neurokinin B immunoreactivity were observed in the terminal field of mossy fibres 10-60 days after intraperitoneal injection of kainic acid. These slow but persistent increases in immunoreactivity were accompanied by markedly enhanced expression of neurokinin B mRNA in the granule cells and in hilar interneurons adjacent to the granule cell layer. These changes were preceded by transient increases in neurokinin B mRNA and immunoreactivity in CA1 pyramidal cell layer two and 10 days after kainic acid, which, however, subsided later on. Pentylenetetrazol kindling caused similar increases in neurokinin B mRNA expression in granule cells and in CA1 pyramidal cells, but not in hilar interneurons. In CA1, increased neurokinin B message was present two days after termination of the kindling procedure but not after 10 days. Sixty days after kainic acid injection, neurokinin B immunoreactivity extended to the inner-third of the molecular layer of the dentate gyrus. After pentylenetetrazol kindling, a neurokinin B-immunoreactive band was observed in the infrapyramidal region of CA3. Lesions of the dentate granule cells by local injection of colchicine in kainic acid-treated rats abolished the supragranular neurokinin B-positive staining, whereas it was almost unchanged after transection of the ventral hippocampal commissure. These observations suggest that neurokinin B immunoreactivity may be located in ipsilateral mossy fibres undergoing collateral sprouting to the inner molecular layer or to the infrapyramidal region in CA3, respectively. Preprotachykinin A mRNA, which encodes for neurokinin A and substance P, and substance P immunoreactivity were not changed in the hippocampus of epileptic rats compared with untreated animals. The observed changes in neurokinin B immunoreactivity and mRNA indicate that specific functional and morphological changes may be induced in hippocampal neurons by recurrent limbic seizures.

Animals↗
PubMed1992

Functional changes in neuropeptide Y- and somatostatin-containing neurons induced by limbic seizures in the rat.

The influence of sustained epileptic seizures evoked by intraperitoneal injection of kainic acid on the gene expression of the neuropeptides somatostatin and neuropeptide Y and on the damage of neurons containing these peptides was studied in the rat brain. Injection of kainic acid induced an extensive loss of somatostatin and, though less pronounced, of neuropeptide Y neurons in the inner part of the hilus of the dentate gyrus. Neuropeptide Y-immunoreactive neurons located in the subgranular layer of the hilus, presumably pyramidal-shaped basket cells, were spared by the treatment. Although neuropeptide Y messenger RNA was not detected in granule cells of control rats, it was found there after kainic acid seizures at all time intervals investigated (12 h to 90 days after injection of kainic acid). High concentrations of neuropeptide Y messenger RNA were especially observed 24 h after injection of kainic acid. At this time neuropeptide Y messenger RNA was also transiently observed in CA1 pyramidal cells. Neuropeptide Y synthesis in granule cells in turn gave rise to an intense immunoreactivity of the peptide in the terminal field of mossy fibers which persisted for the entire time period (90 days) investigated. In addition, neuropeptide Y messenger RNA concentrations were also drastically elevated in presumptive basket cells located at the inner surface of the granule cell layer, especially at the "late" time intervals investigated (30-90 days after kainic acid). These data support the concept that extensive activation of granule cells by limbic seizures contributes to the observed neuronal cell death in CA3 pyramidal neurons and interneurons of the hilus. Consecutively, basket cells containing neuropeptide Y and presumably GABA might be activated and participate in recurrent inhibition of granule cells. Neuropeptide Y-immunoreactive fibers observed in the inner molecular layer at "late" time intervals after kainic acid may result either from collateral sprouting of mossy fibers or from basket cells extensively expressing the peptide. It is speculated that neuropeptide Y synthesized and released at a high rate from granule cells and basket cells may exert a protective action against seizures.

Animals↗
PubMed1991

Effect of neuropeptide Y on jejunal water and ion transport in humans.

Neuropeptide Y is a neurotransmitter in enteric and postganglionic sympathetic neurons. In animal models of intestinal water and ion transport, neuropeptide Y decreases stimulated secretion but has no consistent effect on basal transport. In the present study, the effect of neuropeptide Y on jejunal water and electrolyte transport in healthy volunteers was investigated under basal conditions and during intestinal secretion induced by intraluminal administration of prostaglandin E2. The triple-lumen tube technique was used for perfusion of the small intestine with a plasmalike electrolyte solution containing polyethylene glycol as a nonabsorbable volume marker. After an initial control period (saline IV) neuropeptide Y was administered IV at a dose of 400 pmol.kg-1.h-1. Neuropeptide Y significantly increased net absorption of water, sodium, potassium, and chloride under basal conditions. The peptide significantly reduced the secretion of these electrolytes induced by an intraluminal prostaglandin E2 concentration of 5 mumol/L and reduced net water secretion by 36%. The results of the current study suggest that neuropeptide Y can change intestinal water and ion transport from secretion toward absorption.

Adult↗
PubMed1991

Regional heterogeneity in the distribution of neurotransmitter markers in the rat hippocampus.

A detailed neurochemical analysis of the distribution of markers for the most relevant neurotransmitter systems within the rat hippocampal formation has been performed. The hippocampi, obtained from unfrozen brains of male Sprague-Dawley rats were subdissected into tissue parts containing mainly CA1, CA3 or the dentate gyrus, respectively. Each part was further divided into ventral and dorsal halves. In these six hippocampal subregions the concentrations of noradrenaline, dopamine, serotonin, 3-methoxy-4-hydroxyphenylglycol, 5-hydroxyindoleacetic acid and the putative neurotransmitter amino acids glutamate, aspartate, GABA, glycine and taurine, and the levels of somatostatin and neuropeptide Y and the activities of choline acetyltransferase, acetylcholinesterase and glutamate decarboxylase were measured. A marked heterogeneity in the subregional distribution of markers for various neurotransmitter systems within the hippocampal formation was observed. Each neuronal marker was characterized by an individual pattern of distribution. Most of the markers showed a concentration-gradient, increasing from dorsal to ventral; only taurine was more abundant in the dorsal than in the ventral parts and no dorsoventral difference was seen for aspartate, glycine and neuropeptide Y. The highest molar ratios of total 3-methoxy-4-hydroxyphenylglycol to noradrenaline and 5-hydroxyindoleacetic acid to serotonin were found in the dorsal hippocampus. The levels of noradrenaline, GABA and glutamate decarboxylase activity were highest in the dentate gyrus and lowest in CA1. The concentrations of somatostatin were highest in CA1; those of serotonin were highest in CA3. Highest activities of choline acetyltransferase and acetylcholinesterase were found in the dentate gyrus; lowest activities were found in CA3. In CA3 the lowest values of glutamate, aspartate, taurine and somatostatin were also found. The heterogeneity in the distribution of individual neurochemical markers allows insights into possible functional differences of hippocampal subregions and provides a relevant basis for future neurochemical investigations in this brain area.

Animals↗