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Biomedical subjects

H Prast

Publications and source records attributed to H Prast.

At least 19 recordsLinked to original sources
PubMed2004

7-nitroindazole, nNOS inhibitor, attenuates amphetamine-induced amino acid release and nitric oxide generation but not lipid peroxidation in the rat brain.

The aim of the present study was to elucidate whether amphetamine modulates the output of the neurotransmitters glutamate, aspartate, GABA and acetylcholine (ACh) in nucleus accumbens (NAc) as well as the formation of lipid peroxidation (LPO) and nitric oxide (NO). D,L-amphetamine (AMPH, 5 mg/kg, i.p., 4 times every 2 h) was injected into anaesthetized rats and the release of neurotransmitters in the NAc, tissue content of NO and LPO products were determined. While AMPH increased the release of aspartate, GABA and ACh in the NAc, the glutamate release was not affected. Levels of NO and LPO products were elevated in striatum and cortex. Pretreatment with the neuronal NO synthase inhibitor 7-nitroindazole (50 mg/kg, i.p.) was highly effective in abating the rise of the neurotransmitter release and NO generation but failed to influence the intensity of LPO elicited by the AMPH administration. These findings suggest that activation of NO synthesis is a potent factor in the AMPH-induced neurotransmitter release and that activation of NO synthesis and LPO by AMPH are not parallel processes.

Amino Acids↗
PubMed2004

Comparative effects of NO-synthase inhibitor and NMDA antagonist on generation of nitric oxide and release of amino acids and acetylcholine in the rat brain elicited by amphetamine neurotoxicity.

The aim of this study was to clarify the role of nitric oxide (NO) and lipid peroxidation (LPO) processes as well as the contribution of various neurotransmitters in pathophysiological mechanisms of neurotoxicity induced by amphetamine (AMPH). NO level was determined directly in brain tissues using electron paramagnetic resonance spectroscopy technique. The content of the products of lipid peroxidation (LPO) was measured spectrophotometrically as thiobarbituric acid reactive species (TBARS). The output of neurotransmitter amino acids (glutamate, aspartate, and GABA) and acetylcholine (ACH) was monitored in nucleus accumbens (NAc) by push-pull technique with HPLC detection. Repeated, systemic application of AMPH elevated striatal and cortical NO generation and LPO production. Moreover, administration of AMPH led to a marked and long-lasting increase of ACH release. Surprisingly, while glutamate output was not affected, aspartate release was enhanced 30 to 50 min after each AMPH injection. The release rate of GABA was also elevated. The selective NO-synthase inhibitor 7-nitroindazole (7-NI) was highly effective in abating the rise in the neurotransmitter release induced by the AMPH. The NOS inhibitor also abolished the increase of NO generation produced by AMPH, but did not influence the intensity of LPO elicited by the AMPH administration. Pretreatment with the noncompetitive NMDA receptor antagonist dizocilpine (MK-801) completely prevented increase of NO generation and TBARS formation induced by multiple doses of AMPH. Dizocilpine also abolished the effect of the psychostimulant drug on the release of neurotransmitters ACH, glutamate, aspartate, and GABA in the NAc. Our findings suggest a key role of NO in AMPH-induced transmitter release, but not in the formation of LPO products. It appears that AMPH enhances release of ACH and neurotransmitter amino acids through increased NO synthesis and induces neurotoxicity via NO and also by NO-independent LPO.

Acetylcholine↗
PubMed2002

Involvement of nitric oxide, cyclic GMP and phosphodiesterase 5 in excitatory amino acid and GABA release in the nucleus accumbens evoked by activation of the hippocampal fimbria.

It is known that the nucleus accumbens contains all elements of the nitric oxide (NO)-cyclic GMP (cGMP) system but the role of NO in this nucleus is not well understood. We investigated the contribution of the NO-cGMP system in the neurotransmission elicited by hippocampal nerve signals which are propagated to the nucleus accumbens via the fornix/fimbria. This glutamatergic hippocampus-accumbens projection was electrically stimulated for short periods in the urethane-anaesthetized rat. The nucleus accumbens was simultaneously superfused by the push-pull technique with compounds that influence the NO system and the released glutamate, aspartate and GABA were determined in the superfusate. Superfusion of the nucleus accumbens with the NO donor, PAPA/NO, enhanced basal release of the investigated amino acids with a complex concentration dependency. The release of glutamate and aspartate was also increased by the inhibitor of phosphodiesterase 5, UK-114,542. The PAPA/NO-elicited release of glutamate and aspartate was diminished by superfusion with the inhibitor of guanylyl cyclase, NS 2028. Basal release of amino acid transmitters was not influenced by NS 2028 and the NO synthase inhibitor, 7-NINA.Electrical stimulation of the fornix/fimbria increased the outflow of aspartate, glutamate and GABA in the nucleus accumbens. The stimulation-evoked release was abolished by superfusion of the nucleus with tetrodotoxin and strongly diminished by NS 2028, 7-NINA and N(G)-nitro-L-arginine methyl ester (L-name), while PAPA/NO facilitated stimulation-evoked release of these neurotransmitters. UK-114,542 also enhanced the evoked release of glutamate and aspartate while evoked GABA release was not influenced by the phosphodiesterase inhibitor. These findings indicate that NO plays the role of an excitatory transmitter in the nucleus accumbens and that nerve signals from the hippocampus propagated via fornix/fimbria induce NO synthesis in the nucleus accumbens. NO does not exert a tonic influence on basal release but facilitates release of aspartate, glutamate and GABA through increased cGMP synthesis. Phosphodiesterase 5 seems to be involved in the termination of the NO effect in glutamatergic but not in GABAergic neurons.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed2001

Importance of histamine in modulatory processes, locomotion and memory.

Acetylcholine modulates histaminergic transmission via M(1) receptors. On the other hand, cholinergic transmission is modulated by neighbouring histaminergic neurons via H(1), H(2) and H(3) receptors. Dopaminergic and GABAergic neurons are also involved in these modulatory mechanisms. Furthermore, the release of histamine is modulated by glutamatergic neurons and nitric oxide of neuronal origin. The release of histamine in the brain oscillates according to circadian, slow ultradian and fast ultradian rhythms. Ultradian fluctuations have also been observed in the theta- and delta-frequency bands of the EEG spectral power. Simultaneous recordings of histamine outflow and EEG in the hypothalamus revealed that the ultradian histamine release rhythm coincides temporally with ultradian fluctuations in the EEG spectral power. Histamine receptor ligands used in pharmacotherapy, like H(1) and H(2) antagonists, modify the frequency of the EEG fluctuations. Brain histamine seems to be involved in memory processes, since inhibition of histamine synthesis deteriorates, while H(3) antagonists, histamine and histidine improve short-term memory. The latter finding may open new horizons in pharmacological treatment of memory disorders.

Activity Cycles↗
PubMed2001

Endocrine-disrupting nonylphenols--ultra-trace analysis and time-dependent trend in mussels from the German bight.

A very sensitive and efficient analytical procedure is presented for the determination of 4-nonylphenols (NP) in blue mussels by use of off-line coupling of high-performance liquid chromatography (HPLC) and gas chromatography with mass spectrometric detection (GC-MS). Combined steam distillation and solvent extraction were used to extract the analytes from the mussel samples. Before quantification by GC-MS the raw extracts were purified by normal-phase HPLC. 4-n-Nonylphenol was used as internal standard. The detection limit was 15 ng NP absolute, calculated from the blank value. The method was applied to the determination of NP in blue mussel samples from the German North Sea sampled over a period of 10 years. Collection, homogenization, and storage of the mussels were performed according to the Standard Operating Procedures of the German Environmental Specimen Bank since 1985. The total NP concentrations in the mussels decreased significantly from 1985 (4 microgram kg (-1)) to 1995 (1.1 microgram kg (-1)).

Animals↗
PubMed2001

Nitric oxide as modulator of neuronal function.

The gas NO is a messenger that modulates neuronal function. The use of NO donors and NO synthase inhibitors as pharmacological tools revealed that this free radical is probably implicated in the regulation of excitability and firing, in long-term potentiation and long-term depression, as well as in memory processes. Moreover, NO modulates neurotransmitter release. In vivo and in vitro studies have shown that, in all brain structures investigated, endogenous NO modulates the release of several neurotransmitters, such as acetylcholine, catecholamines, excitatory and inhibitory amino acids, serotonin, histamine, and adenosine. In most cases, enhanced NO level in the tissue increases the release of neurotransmitters, although decreasing effects have also been observed. Cyclic 3'-5' guanosine monophosphate and glutamate mediate the modulation of transmitter release by NO. Recent observations suggest that the release of some transmitters is dually influenced by NO. Thus, besides modulation by presynaptically located auto- and heteroreceptors, NO released from nitrergic neurons seems to play a universal role in modulating the release of transmitters in the brain.

Animals↗
PubMed2001

The nitric oxide system modulates the in vivo release of acetylcholine in the nucleus accumbens induced by stimulation of the hippocampal fornix/fimbria-projection.

Nerve signals from the hippocampus to the nucleus accumbens (NAc) are transmitted through a glutamatergic pathway via the fornix/fimbria fibres. The aim of the present study was to investigate whether cholinergic neurons are activated by this projection and whether the nitric oxide (NO) system is also involved in the signal transduction within this nucleus. For this purpose, the NAc of urethane-anaesthetized rats was superfused, by the push-pull technique, with compounds that influence the NO system while the fornix/fimbria was electrically stimulated for short periods. The amount of acetylcholine (ACh) released in the superfusate was then determined. Electrical stimulation of the fornix/fimbria increased the ACh output in the NAc. This effect was abolished by superfusion with tetrodotoxin and decreased by superfusion with the glutamate receptor antagonists AP-5 and DNQX indicating the involvement of action potentials and glutamate. Superfusion with the inhibitor of neuronal NO synthase, NS 2028 also diminished stimulation-evoked ACh release. The NO donor PAPA/NO increased basal release. Simultaneous application of PAPA/NO and electrical stimulation led to an over-additive increase of ACh release. The effect of PAPA/NO on stimulation-evoked release was also abolished by NS 2028. The selective inhibitor of phosphodiesterase type 5 (PDE 5), 5-[2-ethoxy-5-(morpholinylacetyl)phenyl]-1,6-dihydro-1-methyl-3-propyl-7H-pyrazolo[4,3-d]pyrimidin-7-one methanesulphanate monohydrate also enhanced stimulation-induced release of ACh. Our findings indicate, that action potentials propagated by the fornix/fimbria to the NAc release glutamate which increases ACh release predominantly via NMDA receptors. In addition, nitrergic neurons are activated to enhance NO synthesis. The released NO seems to exert, via cGMP, a potent facilitatory role in the transduction and processing of signals from the hippocampus within the NAc, while the PDE 5 decreases the effects of NO.

Acetylcholine↗
PubMed2001

Role of histaminergic and cholinergic transmission in cognitive processes.

Mutual modulatory and functional interactions exist between the histaminergic and cholinergic systems in the brain. The activity of histaminergic neurons is permanently modulated by neighboring cholinergic neurons via muscarinic M(1) receptors, cholinergic transmission by histaminergic neurons through H(1), H(2), H(3A) and H(3B) receptors. In the nucleus accumbens, glutamatergic neurons originating from the hippocampus modulate cholinergic transmission in a direct way via stimulation of NMDA receptors located on cholinergic neurons. Additionally, glutamatergic neurons of the hippocampus modulate the activity of cholinergic neurons in an indirect way by stimulating histaminergic neurons within the nucleus accumbens. Reciprocal regulatory influences and neurotransmission are subjected to the global modulatory influence of nitric oxide. Both histaminergic and cholinergic systems in the nucleus accumbens are implicated in the response to aversive stimuli. Memory acquisition is associated with activation of cholinergic transmission in the nucleus accumbens, while stimulation of histaminergic neurons facilitates memory in a way that is independent of the cholinergic system. Hence, both histaminergic and cholinergic transmission within the nucleus accumbens and interactions between the two systems seem to play a predominant role in cognition.

Journal Article↗
PubMed1999

Influence of NOS inhibitors on changes in ACH release and NO level in the brain elicited by amphetamine neurotoxicity.

We studied the possible role of neurotoxicity in the d,l-amphetamine (AMPH)-induced release of acetylcholine (ACH) in the nucleus accumbens (Nac) and the involvement of endogenous NO in this process. For determination of ACH release the Nac was superfused using the push-pull-technique. NO was directly measured using the electron paramagnetic resonance technique. Repeated administration of AMPH increased ACH release by about 400%. N-nitro-L-arginine (L-NNA) and 7-nitroindazole (7-NI) nearly abolished the AMPH-induced increase in ACH release. AMPH increased NO as well as lipid peroxidation (LPO) products in the cortex. L-NNA and 7-NI substantially diminished NO increase. AMPH-evoked LPO was only slightly reduced by these compounds. It is concluded that AMPH enhances ACH release through increased NO synthesis and induces neurotoxicity via NO and by LPO independent NO generation.

Acetylcholine↗
PubMed1999

Serotonin (5-HT) in brains of adult patients with Down syndrome.

Down syndrome (DS) is a genetic disease with developmental brain abnormalities resulting in early mental retardation and precocious, age dependent Alzheimer-type neurodegeneration. Furthermore, non-cognitive symptoms may be a cardinal feature of functional decline in adults with DS. As the serotonergic system plays a well known role in integrating emotion, cognition and motor function, serotonin (5-HT) and its main metabolite, 5-hydroxyindol-3-acetic acid (5-HIAA) were investigated in post-mortem tissue samples from temporal cortex, thalamus, caudate nucleus, occipital cortex and cerebellum of adult patients with DS, Alzheimer's disease (AD) and controls by use of high performance liquid chromatography (HPLC). In DS, 5-HT was found to be age-dependent significantly decreased in caudate nucleus by 60% (DS: mean +/- SD 58.6 +/- 28.2 vs. Co: 151.7 +/- 58.4 pmol/g wet tissue weight) and in temporal cortex by about 40% (196.8 +/- 108.5 vs. 352.5 +/- 183.0 pmol/g), insignificantly reduced in the thalamus, comparable to controls in cerebellum, whereas occipital cortex showed increased levels (204.5 +/- 138.0 vs. 82.1 +/- 39.1 pmol/g). In all regions of DS samples, alterations of 5-HT were paralleled by levels of 5-HIAA, reaching significance compared to controls in thalamus and caudate nucleus. In AD, 5-HT was insignificantly reduced in temporal cortex and thalamus, unchanged in cerebellum, but significantly elevated in caudate nucleus (414.3 +/- 273.7 vs. 151.7 +/- 58.4 pmol/g) and occipital cortex (146.5 +/- 76.1 vs. 82.1 +/- 39.1 pmol/g). The results of this study confirm and extend putatively specific 5-HT dysfunction in basal ganglia (caudate nucleus) of adult DS, which is not present in AD. These findings may be relevant to the pathogenesis and treatment of cognitive and non-cognitive (behavioral) features in DS.

Adult↗
PubMed1999

Histaminergic neurons modulate acetylcholine release in the ventral striatum: role of H3 histamine receptors.

To investigate whether histaminergic neurons influence the activity of cholinergic neurons, the ventral striatum was superfused through a push-pull cannula and the release of endogenous acetylcholine was determined in the superfusate. Local inhibition of histamine synthesis by superfusion with alpha-fluoromethylhistidine (FMH) gradually decreased the release rate of acetylcholine. Superfusion with histamine increased the release of acetylcholine. The releasing effect of histamine was greatly inhibited when the striatum was simultaneously superfused with the D2/D3 agonist quinpirole and the D1 antagonist (+/-)-7-bromo-1-(fluoresceinylthioureido)phenyl-8-hydroxy-3-methyl -2,3,4,5-tetrahydro-1H-3-benzapine (SKF 83566). The effect of histamine on acetylcholine release was abolished by the GABA(A) receptor antagonist bicuculline. Superfusion with the H3 receptor agonists imetit or immepip increased acetylcholine release rate in the striatum. The releasing effects of the two H3 agonists were FMH resistant, while superfusion with quinpirole and SKF 83566 abolished the H3 receptor agonist-induced acetylcholine release. Superfusion with the H3 receptor antagonist thioperamide enhanced acetylcholine release rate. The releasing effect of thioperamide was abolished after inhibition of histamine synthesis by FMH. The release of acetylcholine by thioperamide was also abolished on simultaneous superfusion with quinpirole and SKF 83566. The findings show that, in the striatum, the activity of cholinergic neurons is permanently modulated by neighbouring histaminergic nerve terminals and axons. The release of acetylcholine is also permanently inhibited by neighbouring GABAergic neurons. The enhanced release of acetylcholine by the H3 receptor agonists imetit and immepip is due to stimulation of H3 heteroreceptors, while the increase of acetylcholine release by the H3 receptor antagonist thioperamide is elicited via blockade of H3 autoreceptors. Histamine released from histaminergic nerve terminals increases the release of acetylcholine in part by inhibition of dopamine release which, in turn, decreases GABAergic transmission. A dopamine-independent way seems also to be involved in the histamine-evoked acetylcholine release.

Acetylcholine↗
PubMed1999

Histaminergic neurons modulate acetylcholine release in the ventral striatum: role of H1 and H2 histamine receptors.

To investigate whether H1 and H2 histamine receptors are implicated in the modulation of acetylcholine release by endogenous histamine, the ventral striatum of the conscious, freely moving rat was superfused by the push-pull superfusion technique with drugs and the release of acetylcholine was determined in the superfusate. Superfusion with the H1 receptor agonist 2-thiazolylethylamine (TEA, 50 micromol/l) enhanced the release of acetylcholine, while the H1 receptor antagonist triprolidine (50 micromol/l) reduced acetylcholine outflow and abolished the TEA-evoked release of the neurotransmitter. The inhibitory effect of triprolidine was not influenced either on simultaneous superfusion with 10 micromol/l (+/-)-7-bromo-1-(fluoresceinylthioureido)phenyl-8-hydroxy-3-methyl -2,3,4,5-tetrahydro-1H-benzazepine (SKF-83566, D1 dopamine receptor antagonist) and 50 micromol/l quinpirole (D2/D3 dopamine receptor agonist) or on superfusion with the GABAA receptor antagonist bicuculline (50 micromol/l). The H2 receptor antagonists ranitidine or famotidine (50 micromol/l each) greatly enhanced acetylcholine release rate in the ventral striatum. Presuperfusion with alpha-fluoromethylhistidine (FMH, 1 mmol/l), which inhibits neuronal synthesis of histamine, abolished the famotidine-induced release of acetylcholine. The releasing effect of famotidine was also abolished on simultaneous superfusion with 10 micromol/l SKF-83566 and 50 micromol/l quinpirole. The release of acetylcholine elicited by famotidine was reversed to a decreased acetylcholine outflow when the striatum was superfused with the GABA(A) receptor antagonist bicuculline (50 micromol/l) prior to famotidine. Superfusion with the H2 receptor agonist impromidine (1 micromol/l) decreased acetylcholine outflow, while the H2 agonist dimaprit (50 micromol/l) exerted the opposite effect. The releasing effect of dimaprit was not influenced by FMH (1 mmol/l), but it was abolished in the presence of SKF-83566 (10 micromol/l) and quinpirole (50 micromol/l). In the presence of bicuculline the release of acetylcholine by dimaprit was enhanced and prolonged. It seems possible that dimaprit and impromidine stimulate different subtypes of H2 receptors. The findings suggest that the release of acetylcholine in the striatum is modulated by neighbouring histaminergic neurons in a complex way. Stimulation of H1 histamine receptors, probably located on cholinergic neurons, enhances acetylcholine release. Stimulation by histamine of H2 receptors located on cholinergic or GABAergic neurons enhances the release of acetylcholine, while stimulation of H2 receptors located on dopaminergic neurons exerts the opposite effect.

Acetylcholine↗
PubMed1999

Histological changes and neurotransmitter levels three months following perinatal asphyxia in the rat.

The involvement of excitatory amino acids (EAA) in the pathogenesis of hypoxic-ischemic states is well-documented. Information on the role of overexcitation by EAA in perinatalasphyxia (PA), however, is limited and data from adult models cannot be directly extrapolated to immature systems. Moreover, most adult models of ischemia are representing stroke rather than PA. We decided to study long term effects in a non-invasive rat model of PA resembling the clinical situation three months following the asphyctic insult. Morphometry on Nissl - stained sections was used to determine neuronal death in frontal cortex, striatum, hippocampus CA1, hypothalamus and cerebellum L1, and the amino acids glutamate, glutamine, aspartate, GABA, taurine, arginine as well as histamine, serotonin and 5-hydroxy-indoleacetic acid were determined in several brain regions and areas. Morphometry revealed that neuronal loss was present in the hippocampal area CA1 in all groups with PA and that morphological alterations were significantly higher in the cerebellar granular layer. The prominent light microscopical finding in all areas of asphyctic rats studied was decreased Nissl-staining, suggesting decreased cellular RNA levels. Glutamate, aspartate and glutamine were significantly elevated in the hypothalamus of asphyctic rats probably indicating overstimulation by EAA. Excitotoxicity in this area would be compatible with findings of emotional / behavioral deficits observed in a parallel study in our model of PA. Our observations point to and may help to explain behavioral and emotional deficits in Man with a history of perinatal asphyxia.

Animals↗
PubMed1998

Melatonin facilitates short-term memory.

The olfactory social memory test, based on the recognition of a juvenile rat by a male adult rat, was used to investigate whether melatonin influences memory. Intracerebroventricular (i.c.v.) injection of 1.1 nmol melatonin shortened recognition time, while the melatonin ML1 receptor antagonist luzindole (1 nmol) exerted the opposite effect. The facilitating influence of melatonin was abolished in the presence of 0.5 nmol luzindole. The findings suggest that endogenous melatonin facilitates short-term memory.

Animals↗
PubMed1998

Glial cells participate in histamine inactivation in vivo.

The ability of glial cells to take up histamine in vitro suggests that these cells may be involved in histamine inactivation. This prompted us to study the possible interactions between neuronal and glial processes which determine the histamine concentration in the synaptic cleft. In vitro experiments showed that the glial metabolic toxin, fluoroacetate (20 and 40 mmol/l) depressed histamine uptake into cultured astroglial cells and dissociated hypothalamic cells of rats. For in vivo experiments, the push-pull superfusion technique was used. In anaesthetized rat, the anterior hypothalamic area was superfused through the push-pull cannula with artificial cerebrospinal fluid (aCSF) or with aCSF which contained fluoroacetate and the release of endogenous histamine was determined in the superfusate. Hypothalamic superfusion with fluoroacetate (20 mmol/l) led to a pronounced increase in extracellular histamine. The effect of fluoroacetate was inhibited by 5 micromol/l tetrodotoxin. Superfusion with Ca++-free, Mg++-rich (12 mmol/l) aCSF inhibited the basal release rate of histamine. Under these conditions, 20 mmol/l fluoroacetate did not modify the level of the amine in the superfusate. These data demonstrate that depression of glial function enhances the concentration of histamine in the extracellular space by slowing down the uptake of the amine into the glial cells. Thus, under in vivo conditions, glial cells are directly involved in the continuous removal of neuronal histamine from the synaptic cleft.

Animals↗
PubMed1998

Influence of catecholamine receptor agonists and antagonists on the ultradian rhythm of the EEG in the posterior hypothalamus.

The power of delta and theta frequency bands of the EEG in the posterior hypothalamus of the rat fluctuates according to an ultradian rhythm. To investigate, whether catecholamine receptor ligands influence the ultradian EEG rhythm, drugs were applied intracerebroventricularly into the lateral ventricle of anaesthetized rats. Injection of the alpha1-adrenoceptor agonist (+/-)-methoxamine (150 nmol) abolished, while 25 nmol of the compound prolonged the cycle duration of the rhythmic changes in the delta and theta frequency bands. Injected into the lateral ventricle, the alpha2-adrenoceptor agonists 6-ethyl-5,6,7,8-tetrahydro-4H-oxazol[4,5-d] azepin-2-amine (B-HT 933) or clonidine (150 nmol each) prolonged the duration of the cycles of both frequency bands. The beta1/2-receptor agonists (+/-)-orciprenaline (300 nmol) and (R)-(-)-isoprenaline (150 nmol) slowed down the cycle durations of both frequency bands. The beta1-receptor agonist (+/-)-xamoterol (300 nmol) also prolonged the cycle durations of the delta and theta frequency bands. The beta1-receptor antagonist (S)-(-)-atenolol was ineffective (150 and 300 nmol). The beta2-receptor agonist (+/-)-salbutamol (300 nmol) shortened the duration of the ultradian rhythm in the two frequency bands, while the beta2-receptor antagonist (+/-)-1-[2,3-(dihydro-7-methyl-1 H-inden-4-yl) oxy]-3-[(1-methylethyl)amino]-2-butanol (ICI 118,551) (300 nmol) exerted the opposite effect. On the other hand, the D1 receptor agonist (+/-)-1-phenyl-2,3,4,5-tetrahydro-1H)-3-benzazepine-7,8-diol (SKF 38393) and the D2 agonist (4aR,8aR)-(-)-quinpirole (150 nmol each) slowed down the frequency of the ultradian rhythm. The powers of alpha and beta frequency bands were not significantly influenced by the catecholamine receptor ligands used in this study. The findings suggest that, in the posterior hypothalamus, the ultradian rhythm of the delta and theta frequency bands are prolonged when beta1-receptors are stimulated and shortened on stimulation of beta2-adrenoceptors. Endogenous catecholamines released from their neurons seem to shorten the duration of the rhythmic fluctuations by stimulating beta2-receptors and to slow down the frequency of the cyclic fluctuations by stimulating alpha2-adrenoceptors. The ultradian rhythm is also slowed down on stimulation of D1 and D2 receptors by endogenous dopamine. Together with previous observations, the results indicate that the ultradian EEG rhythm is susceptible to modulatory mechanisms mediated by catecholaminergic neurons.

Activity Cycles↗