Biomedical subjects

A A Mathé

Publications and source records attributed to A A Mathé.

At least 37 records · Page 2Linked to original sources

PubMed2000

Effects of acute and chronic electroconvulsive stimuli on cAMP and cGMP efflux in the rat striatum and hippocampus.

The effects of acute and chronic electroconvulsive stimuli (ECS) on extracellular concentrations of the cyclic nucleotides, cAMP and cGMP, from the striatum and hippocampus of awake rats were studied with in vivo microdialysis in conjunction with radioimmunoassay. Acute ECS, but not acute sham-ECS, significantly increased cAMP and cGMP efflux from the striatum by about 75 and 50%, respectively. Chronic ECS did not influence significantly basal efflux of cAMP or cGMP from the striatum or the hippocampus in comparison to control animals receiving chronically sham-ECS. Administration of a challenge ECS in animals treated chronically with sham-ECS resulted in an increase in cAMP and cGMP concentrations in the striatum by 20%, but it failed to affect significantly efflux of these nucleotides in animals treated chronically with ECS. Similarly, in the hippocampus, administration of a challenge ECS in animals treated chronically with sham-ECS resulted in an increase in cAMP and cGMP concentrations by about 40 and 65%, respectively, whereas it failed to affect significantly efflux of these nucleotides in animals treated chronically with ECS. Thus, acutely administered ECS increases cAMP and cGMP efflux in the striatum and hippocampus of rats, an effect that is greatly diminished in animals chronically receiving ECS. These findings suggest changes in the cAMP and cGMP signal transduction mechanisms in response to acute and chronic ECS that may be related to the therapeutic effects of this antidepressant and antipsychotic treatment.

Animals↗

PubMed1999

Alterations in neuropeptide Y levels and Y1 binding sites in the Flinders Sensitive Line rats, a genetic animal model of depression.

Previously, we observed specific alterations of neuropeptide Y (NPY) and Y1 receptor mRNA expression in discrete regions of the Flinders Sensitive Line rats (FSL), an animal model of depression. In order to clarify the correlation between mRNA expression and protein content, radioimmunoassay and receptor autoradiography were currently performed. In the FSL rats, NPY-like immunoreactivity (NPY-LI) was decreased in the hippocampal CA region, while Y1 binding sites were increased; NPY-LI was increased in the arcuate nucleus. Fluoxetine treatment elevated NPY-LI in the arcuate and anterior cingulate cortex and increased Y1 binding sites in the medial amygdala and occipital cortex in both strains. No differences were found regarding the Y2 binding sites. The results demonstrate a good correlation between NPY peptide and mRNA expression, and sustain the possible involvement of NPY and Y1 receptors in depression.

Amygdala↗

PubMed1999

Venlafaxine but not bupropion decreases cerebrospinal fluid 5-hydroxyindoleacetic acid in unipolar depression.

BACKGROUND: While the antidepressants venlafaxine and bupropion are known to have different neurochemical profiles in vitro, their effects on human cerebral metabolism in vivo have not been directly compared. METHODS: Cerebrospinal fluid (CSF) levels of 5-hydroxyindoleacetic acid (5-HIAA), serotonin, 3-methoxy-4-hydroxyphenylglycol (MHPG), homovanillic acid (HVA), and 3,4-dihydroxyphenylacetic acid (DOPAC) were examined in 14 never-hospitalized outpatients with unipolar depression and 10 age-similar healthy controls. Patients received a baseline lumbar puncture (LP), which was repeated after at least 6 weeks of randomized monotherapy with either venlafaxine or bupropion, while controls received only a baseline LP. RESULTS: Patients (n = 9) receiving venlafaxine showed a significant decrease (42%) in their CSF 5-HIAA concentrations after treatment, but no change in other CSF measures. In contrast, patients receiving bupropion (n = 8) showed no change in CSF measures compared to pretreatment values. CONCLUSIONS: While the mechanism for this differential effect of venlafaxine remains to be determined, the current study provides confirmation of the different aminergic effects of venlafaxine and bupropion.

Adult↗

PubMed1999

Neuropeptides and electroconvulsive treatment.

Neuropeptides: corticotropin releasing factor (CRF), neuropeptide Y (NPY) and somatostatin (STS) have been associated with depression and anxiety, while neurotensin (NT), calcitonin gene-related peptide (CGRP) and tachykinins [neurokinin A (NKA) and substance P (SP)] are presumed to also play a role in the function of the dopaminergic system. Moreover, investigations in the past decade have shown that psychotomimetics and antipsychotic drugs as well as lithium affect brain synthesis, tissue concentrations, and release of some neuropeptides. In view of the above, experiments were carried out to explore whether changes in neuropeptides constitute one of the mechanisms of action of electroconvulsive treatment (ECT). Human cerebrospinal fluid (CSF) was studied before and after ECT, and brains from healthy and models of depression rats were investigated in electroconvulsive stimuli (ECS)-treated and sham-treated animals. The major findings were that a series of ECTs, in parallel to clinical recovery, increased CSF concentrations of NPY-like immunoreactivity (-LI), STS-LI, and CRF-LI, and in one study endothelin-LI. A series of ECS, but not a single treatment, reproducibly elevated concentrations of NPY-LI, NKA-LI, and STS-LI--but not NT-LI, SP-LI, galanin-LI, or CGRP-LI--in hippocampus, frontal cortex, and occipital cortex. No changes were measured in other regions, e.g., striatum. NPY and STS mRNAs were also increased indicating that ECS affects peptide synthesis. Generalized seizures induced by, e.g., kainic acid or pentylenetetrazole, had similar effects on neuropeptides. The changes persisted for at least 1 week after the last treatment. Pretreatment with compounds reducing seizures, such as benzodiazepines and MK-801; had no effect on magnitude of neuropeptide changes although the seizure duration was decreased by > 50%. On the basis of these findings, it is suggested that neuropeptides are involved in ECT's mechanisms of action. Since ECT is therapeutically efficient in both schizophrenia and depression and, taking into account that antipsychotic drugs and psychotomimetics as well as lithium selectively affect some neuropeptides, it is hypothesized that distinct combinations of neuropeptide and monoamine changes in selected neuronal populations constitute the underpinnings of ECT's effects on specific disease symptoms, conceivably independent of diagnosis.

Animals↗

PubMed1998

Neuropeptide Y, neurokinin A and neurotensin in brain regions of Fawn Hooded "depressed", Wistar, and Sprague Dawley rats. Effects of electroconvulsive stimuli.

1. Concentrations of neuropeptide Y (NPY)-, neurokinin A (NKA)- and neurotensin (NT)-like immunoreactivity (-LI) were measured in brain tissues of Fawn Hooded (FH) (a model of depression), Wistar (W) (control for depression) and Sprague Dawley (SD) rats (control for strain) with the aim to explore possible associations between neuropeptides and models of depression. 2. In addition, peptides were determined after six electroconvulsive stimuli (ECS) or six sham ECS ("baseline") in order to investigate ECS mechanisms of action. 3. Baseline NPY-LI concentrations were markedly lower in the hippocampus of the "depressed" FH compared to the W and SD animals. 4. Baseline NKA-LI concentrations were higher in the occipital cortex and NT-LI concentrations in the occipital cortex, frontal cortex, and hypothalamus of the FH and W compared to the SD rats. 5. ECS increased NPY-LI in the hippocampus, frontal cortex and occipital cortex of all three strains. In the hippocampus, the increase was significantly larger in the FH compared to the W and SD rats. ECS also increased NKA-LI in the hippocampus. 6. In contrast, ECS decreased NT-LI in the occipital cortex of the FH and W animals. 7. The results indicate that NPY may play a role in depression and that changes in NPY and NKA probably constitute one of the mechanisms of ECT action. More speculatively, NT may also be involved in depression.

Animals↗

PubMed1998

Changes in dietary fatty acids alter phospholipid fatty acid composition in selected regions of rat brain.

1. Eighty rats were randomized into four groups receiving one of the following diets: rat chow containing (1) 6% soybean oil, (2) 6% primrose oil, (3) 6% fish oil, (4) a combination of 4.5% primrose and 1.5% fish oil. 2. Following two months of each regimen, the rats were sacrificed by microwave irradiation and the brain's fatty acid composition was analysed with gas chromatography for each of the following regions: frontal cortex, striatum, occipital cortex, hippocampus, hypothalamus, cerebellum and pituitary. 3. Linoleic acid was decreased by both primrose and fish oil supplementations. The fish oil substitution resulted in a significant elevation of 20:3n-6, a decrease of 22:4n-6 and a non-significant decrease of 20:4n-6, probably reflecting inhibition of delta-5-desaturation. At the same time the fish oil diet significantly elevated 22:5n-3 while 22:5n-6 was decreased. 4. The primrose oil diet lowered the n-3/n-6 ratio in all regions except in the cerebellum. In contrast, the fish oil diet elevated the n-3/n-6 ratio in all regions. 5. The results demonstrate that changes in dietary fat composition can alter the fatty acid composition of the adult rat brain and that these effects are region specific. 6. This is of interest since metabolites of essential fatty acids may be involved in physiological and pathological processes in the brain and it has been hypothesized that dietary intake of fats may influence the outcome of psychiatric disorders such as schizophrenia.

Animals↗

PubMed1998

Serotonergic 'vulnerability' in affective disorder: a study of the tryptophan depletion test and relationships between peripheral and central serotonin indexes in citalopram-responders.

A double-blind study of the tryptophan depletion (TD) challenge was performed on a sample consisting of 20 patients with a major depressive disorder in clinical remission after citalopram treatment. TD was induced by the intake of 43 g of an amino acid mixture containing the five large neutral amino acids. The control group received the same mixture, to which 2.3 g tryptophan had been added. Five of the 12 challenged patients showed a worsening of depressive symptoms during the day of the test. In contrast, there was no mood alteration in the eight control patients. Baseline cortisol levels were significantly higher in responders to TD compared to those in non-responders and controls. Platelet serotonin-receptor function and plasma prolactin levels were correlated. There was a significant positive correlation in the baseline data between rated mood state and plasma cortisol and a significant inverse correlation between related mood state and plasma tryptophan concentration. Thus low mood appeared to be associated with low serotonin precursor availability as well as with high cortisol levels.

Adult↗

PubMed1998

Neuropeptide Y levels in ethanol-naive alcohol-preferring and nonpreferring rats and in Wistar rats after ethanol exposure.

Neuropeptide Y (NPY) is a hexatriacontapeptide amide that is now well characterized as a neuromodulator in the central nervous system (CNS). When infused into the CNS, NPY produces both anxiolytic and orexigenic effects. NPY's anxiolytic effects appear to be mediated through receptors in the central amygdala, whereas its orexigenic effects are localized in discrete hypothalamic nuclei. Both food restriction and food deprivation produce increased levels of the peptide in the hypothalamus that are ameliorated by refeeding. However, the effects of alcohol consumption/deprivation on NPY levels remain unknown. The present study sought to determine if brain NPY levels were affected by either alcohol exposure and/or correlated with genetic differences in preference for drinking alcohol. In the first experiment, NPY-like immunoreactivity (NPY-LI) was compared in alcohol-naive, alcohol-preferring (P), and nonpreferring (NP) rats. After tissue extraction, NPY-LI was measured by radioimmunoassay: amygdala, hippocampus, frontal cortex, hypothalamus, and caudate. P rats were found to have significantly lower NPY-LI in amygdala (F = 4.69, p < 0.04), hippocampus (F = 7.03, p < 0.01), and frontal cortex (F = 4.7, p < 0.04), compared with NP rats. In the second experiment, heterozygous Wistar rats were exposed to alcohol for 14 hr/day for 7 weeks in alcohol vapor chambers (mean blood alcohol concentrations = 180 mg%) or control chambers. At 7 weeks of alcohol exposure, no significant changes in NPY-LI in were found. At 1 month after ethanol withdrawal, however, the ethanol-exposed animals had significantly higher NPY-LI in the hypothalamus (F = 4.78, p < 0.04) when compared with the nonexposed controls. Taken together, these studies suggest that exposure to chronic ethanol may affect NPY-LI at the level of the hypothalamus in a fashion similar to food restriction, because 4 weeks after alcohol withdrawal, significantly higher NPY levels are found. In addition, differences in NPY-LI in limbic areas and frontal cortex between alcohol-naive P and NP rats suggest that NPY may also play a role in risk for the development of alcohol preference either by modulating the "tension-reduction" properties of alcohol or by influencing consummatory behaviors.

Administration, Inhalation↗

PubMed1997

Decreased levels of preprotachykinin-A and tachykinin NK1 receptor mRNA in specific region of the rat striatum after electroconvulsive stimuli.

The effects of electroconvulsive stimuli on the expression of mRNAs coding for preprotachykinin-A and the substance P-sensitive tachykinin NK1 receptor were examined in subregions of the rat striatum. In the electroconvulsive stimuli-treated animals, a 43% decrease in preprotachykinin-A mRNA was detected in the dorso-lateral caudate-putamen as compared to sham electroconvulsive stimuli treated animals. A 75% decrease in numerical density of tachykinin NK1 receptor mRNA positive neurons was found in the caudal part of the nucleus accumbens core. These findings provide new evidence for selective effects of electroconvulsive stimuli on specific populations of neurons in the rat striatum.

Animals↗

PubMed1997

A comparison between microwave irradiation and decapitation: basal levels of dynorphin and enkephalin and the effect of chronic morphine treatment on dynorphin peptides.

Opioid peptides were analysed in tissue extracts of various brain structures and the pituitary gland from rats sacrificed by microwave irradiation, and compared with peptide levels in tissue extracts from decapitated rats. Dynorphin A, dynorphin B and Leu-enkephalinArg6, derived from prodynorphin, and Met-enkephalinArg6Phe7 from proenkephalin, were measured. Basal immunoreactive levels of dynorphin A and B were consistently higher in extracts from microwave-irradiated rats, whereas in these extracts immunoreactive levels of Leu-enkephalinArg6, an endogenous metabolite of dynorphin peptides, were either lower than, the same as or higher than in decapitated rats. Immunoreactive levels of Met-enkephalinArg6Phe7 were higher in microwave-irradiated rats. Effects of morphine treatment on prodynorphin peptide levels were evaluated and compared with previous findings in decapitated rats. Dynorphin immunoreactive levels were higher in the nucleus accumbens and striatum of morphine-tolerant rats than in corresponding areas in saline-treated rats. These results indicate tissue-specific metabolism of prodynorphin peptides and show that metabolism of opioid peptides occurs during the dissection procedure after decapitation of the rat even though precautions are taken to minimize degradation.

Animals↗

PubMed1997

Basal and stimulated C-fos mRNA expression in the rat brain: effect of chronic dietary lithium.

The mechanisms underlying the therapeutic efficacy of lithium in affective disorders are poorly understood; however, previous studies have established an influence of lithium on receptor-coupled and postreceptor signal transduction mechanisms, including the transcription factor c-fos. We investigated the effect of chronic lithium on basal, stress-, muscarinic-, and haloperidol-induced c-fos mRNA expression in various rat brain regions. Chronic lithium produced significant reductions in basal c-fos expression in the frontal cortex and hippocampus, confirming our previous report. Stress-induced c-fos was significantly attenuated in the frontal cortex, hippocampus, and pituitary, was increased in the occipital cortex, and unchanged in the hypothalamus by chronic lithium. Pilocarpine-induced c-fos was significantly reduced in the frontal cortex and hippocampus by chronic lithium, but was enhanced in the occipital cortex and hypothalamus. Haloperidol-induced c-fos was augmented in the striatum and pituitary, but reduced in the frontal cortex by chronic lithium treatment. In regions in which haloperidol did not induce fos expression in control animals, fos levels after haloperidol were reduced after chronic lithium. One week after discontinuation of the lithium treatment, basal c-fos levels remained significantly lower in the frontal cortex and hippocampus, whereas the effects of stress, pilocarpine, or haloperidol on fos were normalized in most regions, except in the hippocampus, where the attenuated fos response to injection stress persisted. We suggest that repression of basal fos expression and inhibition and activation of inducible fos may be factors to be considered in the longer-term effects of lithium, leading to changes in expression of genes that regulate fos and are regulated by Fos, and ultimately to alterations in the functional activity of neural systems involved in the pathophysiology of affective disorder.

Amino Acid Isomerases↗

PubMed1997

Effects of electroconvulsive stimuli and MK-801 on neuropeptide Y, neurokinin A, and calcitonin gene-related peptide in rat brain.

Rats were pretreated with 0.9% NaCl, or 0.1 or 1.0 mg/kg MK-801, an anticonvulsant and a psychotomimetic drug, and 60 minutes later given ECS or sham ECS. After six sessions the animals were sacrificed and neuropeptide Y (NPY-), neurokinin A (NKA-), and calcitonin gene-related peptide (CGRP-) like immunoreactivity (-LI) measured with radioimmunoassays. ECS increased NPY-LI in frontal cortex, striatum, occipital cortex and hippocampus, and NKA-LI in occipital cortex and hippocampus. MK-801 increased CGRP in a dose-response manner in frontal cortex, and NKA-LI in occipital cortex. Although the higher MK-801 dose reduced seizure duration by 50%, the ECS induced NPY-LI increase in striatum, occipital cortex and hippocampus, and NKA-LI in occipital cortex was not diminished. In contrast, there was a parallel decrease in seizures and NPY-LI and NKA-LI changes in frontal cortex and hippocampus, respectively. Investigation of neuropeptides in brain may contribute to understanding of the mechanisms of action of antidepressive and antipsychotic treatments and of psychotomimetic drugs.

Analysis of Variance↗

PubMed1997

Impaired neuropsychological performance in euthymic patients with recurring mood disorders.

BACKGROUND: Both patients suffering from schizophrenia and patients suffering from recurring mood disorder show cognitive impairments as established by a variety of neuropsychological tests. The aim of the present study was to investigate the neuropsychological performance of euthymic patients who had recurring mood disorder and the possible relationship between episodes of hospitalization and cognitive impairments. METHOD: Twenty-six euthymic patients with a DSM-III-R recurring mood disorder diagnosis were investigated by using the Synonym Reasoning and Block-Test Battery and a part of the Halstead-Reitan Test Battery. RESULTS: An overall lowered performance in the test results was found. There was a significant positive relationship between four different tests and the number of hospitalization episodes; the patients with impaired cognitive functioning had significantly more hospitalization episodes than patients with normal cognitive functioning. CONCLUSION: The results suggest that a subgroup of patients with recurring mood disorder are defined by more relapses and episodes of hospitalization and show cognitive dysfunctions even when euthymic.

Adult↗

PubMed1996

Effects of chronic lithium and electroconvulsive stimuli on cholecystokinin mRNA expression in the rat brain.

This study compares the effect of lithium (Li+) and electroconvulsive stimuli (ECS), two treatments commonly used in the treatment of affective disorders, on CCK mRNA expression in the rat brain. Two groups of rats receiving either 4 week Li+ or vehicle food supplementation and two groups receiving 6 ECS or 6 sham ECS during 2 weeks were studied. A significant decrease in CCK mRNA levels was seen in the caudate putamen both after Li+ as compared to vehicle and ECS as compared to sham ECS, 27 and 25%, respectively. A small (10%), yet significant, decrease was also seen in the inner entorhinal cortex after Li+. The results indicate that both Li+ and ECS inhibit CCK synthesis in the caudate putamen and are consistent with other findings of presumed decreased dopaminergic action in this part of the brain following these treatments.

Animals↗

PubMed1996

The psychotomimetic drugs D-amphetamine and phencyclidine release calcitonin gene-related peptide in the limbic forebrain of the rat.

Calcitonin gene-related peptide (CGRP) is the major product of the calcitonin gene in brain and exerts a number of actions in the central nervous system (CNS). In particular the finding that CGRP affects dopamine (DA) release and metabolism has raised the possibility that it may play a role in several neuropsychiatric disorders. Consequently, we have here studied the effects of two psychotomimetic drugs, namely, d-amphetamine (AMPH) and phencyclidine (PCP), on CGRP concentrations in brain microdialysates from freely moving rats. The animals were stereotaxically implanted with vertical concentric probes in the medial prefrontal cortex (mPFC), the ventral striatum (vSTR), or the hippocampus; and the experiments were performed 48 hr after surgery. The dialysis probes were perfused with a modified Ringer's solution at the rate of 5 microliters/min. AMPH 1.5 mg/kg, PCP 2.5 mg/kg, or NaCl 0.9% were injected s.c.; and the perfusates were collected at 60 min intervals before and after the injections and used for CGRP-like immunoreactivity (-LI) determination by radioimmunoassay (RIA). In separate experiment, KCl (100 mM), veratridine (50 microM), or tetrodotoxin (2 microM), were added to the perfusate and infused in the vSTR. Baseline levels of CGRP-LI were detected in dialysates from all three regions. Both AMPH and PCP caused a significant and sustained increase (maximum about 300%) in CGRP-LI concentrations, in particular from the mPFC and vSTR, while saline had no effect. KCl and veratridine also increased CGRP-LI in dialysates during the first posttreatment period, while tetrodotoxin induced a significant but delayed decrease in CGRP-LI levels. Finally, cervical dislocation also elevated CGRP-LI in dialysates from the mPFC and the vSTR. Our findings demonstrate that 1) CGRP-LI can be measured in vivo in microdialysates from mPFC, vSTR, and hippocampus; 2) the release in vSTR is action potential-dependent; and 3) systemic administration of AMPH or PCP results in a long-lasting release of CGRP-LI in the mPFC and vSTR, thus demonstrating a novel action of these drugs in the brain. Since other studies have shown that major antipsychotic drugs appear to reduce CGRP release in brain, our study provides, in principle, support for a role of CGRP in psychotic disorders.

Analysis of Variance↗

PubMed1995

Effects of D-amphetamine and phencyclidine on behavior and extracellular concentrations of neurotensin and dopamine in the ventral striatum and the medial prefrontal cortex of the rat.

The effects of systemically administered phencyclidine (PCP; 2.5 mg/kg, s.c.) and D-amphetamine (1.5 mg/kg, s.c.) on the extracellular concentrations of neurotensin-like immunoreactivity (NT-LI) and dopamine (DA) in the ventral striatum (vSTR) and the medial prefrontal cortex (mPFC) were studied in freely moving rats using microdialysis. In separate animals, the effects of PCP and D-amphetamine on open field activity were also analyzed. PCP, but not D-amphetamine, caused a significant increase (156% over baseline) of NT-LI levels in the vSTR which was relatively short lasting, i.e., of less than 2 h duration. In contrast, both drugs significantly increased NT-LI concentrations in the mPFC by almost 100% during the same period. PCP and D-amphetamine also significantly increased extracellular levels of DA in the vSTR by 83 and 364%, respectively. However, the peak effect of PCP on DA appeared later than that of D-amphetamine, i.e., at 150 and 60 min, respectively, after drug administration. Also in the mPFC, both PCP and D-amphetamine significantly increased DA concentrations by 98 and 284%, respectively. Generally, effects on DA levels of both PCP and D-amphetamine were, in contrast to their effects on NT-LI levels, clearly more long-lasting, i.e., of 3-4 h duration. Behaviorally, D-amphetamine produced a more pronounced, general activation than PCP, with a faster onset of activation, i.e. within 30 vs 90 min after administration. However, both drugs produced long-lasting effects on the spatial organization of behavioral activity, which lasted for 3-4 h. In conclusion, the more pronounced behavioral stimulation by D-amphetamine (1.5 mg/kg, s.c.) vs PCP (2.5 mg/kg, s.c.) in the rat may largely be explained by its more potent DA-releasing effect in the brain. Initial behavioral suppression by PCP, e.g., of rearing, as well as its rather poor locomotor stimulant action in general, might relate to release of NT in the vSTR. The long-lasting, behavioral disorganization by both PCP and D-amphetamine may, however, be related to increased release of DA rather than NT in the mesolimbocortical areas.

Animals↗

PubMed1995

Concurrent analysis of neuropeptides and biogenic amines in brain tissue of rats treated with electroconvulsive stimuli.

We developed a method for measuring neuropeptides and monoamines in the same rat brain tissue and applied this method to study the effects of electroconvulsive stimuli (ECS) on these compounds. Rats were treated with repeated ECS or sham ECS. After sacrifice by focused microwave irradiation, brains were dissected and immediately frozen. The tissues were extracted in acetic acid. After lyophilization the samples were reconstituted in phosphate buffer and divided in three fractions: (1) was further purified on a cation-exchange column before catecholamines were measured on a high-performance liquid chromatography (HPLC) system, (2) for measuring serotonin on the HPLC system, (3) for measuring peptide concentrations by specific radioimmunoassays. Confirming our previous findings, ECS significantly increased neuropeptide Y-like immunoreactivity (-LI) in hippocampus and frontal cortex and neurokinin A-LI in the hippocampus, while no changes in substance P- and neurotensin-LI were detected. New findings were a decrease in noradrenaline concentrations in the frontal and occipital cortex and hippocampus, an increase in dopamine concentrations in the frontal and occipital cortex and no serotonin change. In summary, we have developed methods to measure both peptides and monoamines in the same brain tissue specimens, and have shown that ECS leads to changes in both neuropeptides and classical neurotransmitters in distinct brain regions.

Animals↗

PubMed1995

Region-specific effects of chronic lithium administration on neuropeptide Y and somatostatin mRNA expression in the rat brain.

The aim of this study was to examine the effects of 4-week lithium (Li+) food supplementation on neuropeptide mRNA expression in the rat brain. In situ hybridisation was used to determine the effects on the expression of neuropeptide Y (NPY) and somatostatin (SS) mRNA. Increases in NPY mRNA levels were seen in the hippocampus, layers II-III of the entorhinal cortex, nucleus accumbens shell and in the medial caudate-putamen. Increases in SS mRNA expression were seen in the layers IV-VI of the entorhinal cortex and in the lateral caudate putamen. Thus, Li+ appears to affect discrete populations of NPY and SS mRNA expressing neurons, with possible relevance to beneficial effects of Li+ in affective disorders.

Animals↗