Neuropeptide Y-like Immunoreactivity Levels Research Articles

Cerebrospinal Fluid Neuropeptide Y-Like Immunoreactive Levels in Dementia of Alzheimer Type and Dementia with Frontotemporal Degeneration of Non-Alzheimer Type

Several neurochemical abnormalities are known in dementia of Alzheimer type (DAT). Little is known about the neurochemical changes in dementia with frontotemporal cortical degeneration of non-Alzheimer type (FTD), including Pick's disease. The present study evaluates the cerebrospinal fluid (CSF) levels of neuropeptide Y-like immunoreactivity (NPY-LI) correlated with duration of the disease. There was a significant difference between NPY-LI in DAT and FTD. NPY-LI is reduced in DAT but not in FTD. In FTD the CSF levels of NPY-LI tended to increase with the duration of the disease while in DAT the NPY-LI levels tended to decrease. This points towards a different involvement of NPY neurons in these two types of primary degenerative dementias.

Plasma neuropeptide Y and atrial natriuretic peptide concentrations in man.

1. In order to examine the concentration of neuropeptide Y-like immunoreactivity (NPY-LI) and atrial natriuretic peptide (ANP) in the circulation in man, blood was sampled from the iliac vein, the inferior vena cava, the superior vena cava, the pulmonary artery and the femoral artery in 13 patients undergoing cardiac catheterization. 2. Plasma NPY-LI levels were similar at all points sampled and no arteriovenous differences were found. Plasma ANP concentration in the pulmonary artery was greater than in peripheral venous blood but there was a strong correlation between the two. 3. The concentration of NPY-LI and ANP in peripheral venous blood reflects central venous and arterial concentrations.

α-Adrenoceptor Influence on Plasma Levels of Neuropeptide Y-Like Immunoreactivity and Catecholamines During Rest and Sympathoadrenal Activation in Humans

Antecubital venous plasma neuropeptide Y-like immunoreactivity (NPY-LI) and catecholamines were analyzed in six healthy volunteers performing a graded bicycle exercise without medication and after acute administration of clonidine, phentolamine, and nifedipine. During the control exercise, plasma noradrenaline (NA), adrenaline (A), and NPY-LI increased to 17-, 7-, and 3-fold the resting values, respectively, at a maximal workload. Clonidine (300 micrograms p.o.) reduced resting and exercising heart rate (HR) and systolic blood pressure (SBP). Plasma NA at rest decreased and NA, A, and NPY-LI were 40-60% lower during the exercise after clonidine compared to the control. Phentolamine (0.07 mg X kg-1 every 10 min i.v.) and nifedipine (20 mg p.o.) increased HR and reduced SBP during the exercise. Plasma NA at rest was elevated threefold and the exercise-induced increases in NA and A were also enhanced after phentolamine. Plasma NPY-LI at rest was unchanged by phentolamine, while it was increased five-fold, as compared to the control, at the highest workload. Nifedipine slightly enhanced plasma NA and NPY-LI but not A during exercise. It is suggested that NPY is released mainly at high levels of sympathetic activity and that blood-pressure-lowering drugs acting on alpha adrenoceptors acutely influence the release of both NA and NPY-LI from sympathetic nerves in humans.

Antidepressant drugs increase the concentration of neuropeptide Y (NPY)-like immunoreactivity in the rat brain

Rats were given imipramine or zimeldine orally for three weeks and the brain levels of neuropeptide Y-like immunoreactivity (NPY-LI) were measured. The concentration of NPY-LI in frontal cortical tissue was elevated by 40 and 60%, respectively. Imipramine increased the concentration of NPY-LI in the hypothalamus by 65% while zimeldine was without effect. The concentration of NPY-LI in the parietal cortex was unaffected by either of the drugs. These observations support the hypothesis that NPY might be involved in the pathophysiology of depressive illness.

Release of neuropeptide Y upon haemorrhagic hypovolaemia in relation to vasoconstrictor effects in the pig.

Neuropeptide Y is co-stored with noradrenaline in peripheral sympathetic nerves, but is not present in the adrenal chromaffin cells in the pig. Plasma levels of neuropeptide Y-like immunoreactivity and catecholamines were studied upon haemorrhagic shock in the anaesthetized pig. The animals were bled in two successive steps (30 and 10 ml kg-1), resulting in a reduction of the mean arterial blood pressure by 44% and 53%, respectively. Plasma levels of noradrenaline increased abruptly after the first bleeding from 1.21 +/- 0.27 to 26.5 +/- 6.3 nmol l-1. Plasma neuropeptide Y showed a progressive increase from 62 +/- 8 pmol l-1 in the basal state to 365 +/- 98 pmol l-1 at 60 min after the first bleeding. After the second bleeding plasma neuropeptide Y and noradrenaline showed a largely parallel increase and finally reached levels of 2524 +/- 580 pmol l-1 and 316 +/- 117 nmol l-1, respectively. A veno-arterial gradient of neuropeptide Y and noradrenaline indicating local release was present over the spleen after both bleeding steps. The overflow of neuropeptide Y was delayed about 15 min compared to noradrenaline after the initial bleeding. Depletion of the neuropeptide Y content after shock in the heart and skeletal muscle supported local release also from these organs. Infusions of neuropeptide Y to obtain similar plasma concentrations as during shock (nM range) caused reduction in blood flow as determined by the radionuclide-labelled microsphere technique in several organs including spleen and skeletal muscle (threshold response at 319 +/- 22 pmol l-1) but not in heart and brain. In conclusion, both neuropeptide Y and noradrenaline were markedly elevated in plasma upon haemorrhagic shock, suggesting release from sympathetic nerve terminals. Neuropeptide Y could therefore have a role as a sympathetic neurotransmitter, and during severe stress, circulating plasma levels are in the range where vasoconstriction is evoked by exogenous NPY.

Stress-induced changes of circulating neuropeptide Y in the rat: comparison with catecholamines

Circulating concentrations of neuropeptide Y-like immunoreactivity (NPY), noradrenaline (NA) and adrenaline (AD) were measured in conscious, chronically catheterized rats submitted to various stress protocols. Basal plasma levels of NPY, NA and AD (194 ± 52 fmol/ml, 0.90 ± 0.11 pmol/ml and 0.52 ± 0.07 pmol/ml) were increased by handling (+132%, +76% and +629%, respectively) and rose further during electric shock treatment. Adrenalectomy resulted in the complete disappearance of circulating adrenaline but did not alter either control or stress values of noradrenaline. In comparison circulating levels of NPY were reduced, but not significantly in adrenalectomized animals. Insulin stress induced a large increase in plasma AD levels and cold stress induced an increase in plasma NA levels, without any parallel change in NPY concentrations. These results demonstrate that NPY, which is colocalized with catecholamines in the peripheral nervous system, is also released during stress responses and that its release parallels more closely changes in circulating NA than AD. Furthermore, stress-induced changes in circulating NPY-like immunoreactivity do not originate from the adrenal gland but mainly from the peripheral nervous system, and the release of NPY is dependent upon the nature of the stimulus.

A comparison of somatostatin and neuropeptide Y distribution in monkey brain

The concentrations of both somatostatin-like immunoreactivity (SLI) and neuropeptide Y-like immunoreactivity (NPYLI) were measured in all major cortical and subcortical regions of monkey brain. High concentrations of both SLI and NPYLI were found in cerebral cortex where they were significantly correlated, supporting a colonization of the two peptides in cortical neurons. There were no significant differences between the right and left hemispheres. Subdissections of the basal ganglia showed that concentrations of both SLI and NPYLI were 3-fold higher in the nucleus accumbens than in the remainder of the striatum, where concentrations of the peptides were evenly distributed. SLI and NPYLI levels were significantly correlated in the striatum, supporting a colocalization of the two neuropeptides in striatal neurons. Concentrations were low in the globus pallidus. Limbic system nuclei including the amygdala, bed nucleus of the stria terminalis and substantia innominata had relatively high concentrations of both SLI and NPYLI. In several subcortical regions concentrations of the neuropeptides were dissociated, suggesting separate neuronal populations. The distribution of both neuropeptides in monkey brain closely resembles that in human brain. The high levels in cerebral cortex and basal ganglia suggest that somatostatin and neuropeptide Y may play a role both in cognition and in normal motor function.

Neuropeptide Y in the adrenal gland: Characterisation, distribution and drug effects

The occurrence of neuropeptide Y-like immunoreactivity in the adrenal gland was investigated by means of radioimmunoassay, chromatography and immunohistochemistry. The adrenal levels of neuropeptide Y-like immunoreactivity varied considerably between species with lowest amounts in the rat and highest in the cow where immunoreactivity was observed in chromaffin cells and nerve fibres in the capsule and cortex. The distribution of neuropeptide Y-like immunoreactivity in the cow medulla overlapped that of enkephalin-like immunoreactivity. Chromatographic characterisation of rat and cow adrenal extracts showed that the majority of the neuropeptide Y-like immunoreactivity was similar in molecular weight and solubility properties to porcine neuropeptide Y. Rat adrenal contained additional material some of which may represent oxidised neuropeptide Y. The administration of insulin and reserpine to rats in vivo showed that the turnover of adrenal neuropeptide Y-like immunoreactivity is regulated by the splanchnic nerve. Splanchnic activation following insulin-induced hypoglycaemia elicited a 60% depletion of neuropeptide Y-like immunoreactivity 2 h post insulin injection. A smaller (maximum 40%) depletion of neuropeptide Y-like immunoreactivity was measured 24 h after reserpine injections which may be explained by splanchnic activation. Five days after reserpine injections the levels of adrenal neuropeptide Y-like immunoreactivity were increased to 200% of control levels and remained slightly elevated at 25 days. Adrenal enkephalinlike immunoreactivity showed similar but not identical changes following reserpine. The reserpine-induced elevation in neuropeptide Y-like immunoreactivity at the 5-day time point was abolished in rats with a chronic bilateral splanchnectomy. This evidence indicates that neuropeptide Y may be considered as a new adrenal medullary hormone.

Reserpine-induced depletion of neuropeptide Y from cardiovascular nerves and adrenal gland due to enhanced release.

The mechanisms underlying reserpine-induced depletion of neuropeptide Y-like immunoreactivity (NPY-LI) in relation to tissue content of noradrenaline (NA) and cardiovascular impairment were studied in guinea-pigs. Reserpine pretreatment (5 mg/kg SC) caused a 5-fold increase in plasma levels of NPY-LI with a maximum after 4 h. This was associated with a progressive fall in systemic arterial blood pressure and heart rate (to about 50% of basal values). The contents of NPY-LI and NA in nerves of the heart and quadriceps muscle were then reduced by about 75% and 85%, respectively. The adrenal content of NPY-LI was reduced by 40% 8 h after reserpine, while the adrenaline content was uninfluenced. Pretreatment with guanethidine depleted NA in the heart but did not influence plasma levels or tissue content of NPY-LI per se. The reserpine-induced increase in plasma NPY-LI and the depletion of NPY-LI in the heart and skeletal muscle was to a large extent prevented by guanethidine. The reserpine-induced bradycardia and hypotension were reduced after guanethidine pretreatment. Chlorisondamine pretreatment depressed heart rate, blood pressure and plasma levels of NPY-LI. Furthermore, chlorisondamine inhibited the reserpine-induced increase in plasma NPY-LI and prevented the reduction in tissue content of NPY-LI in the heart, skeletal muscle and adrenal.(ABSTRACT TRUNCATED AT 250 WORDS)

Co-release of neuropeptide Y and catecholamines during physical exercise in man

Venous plasma levels of neuropeptide Y-like immunoreactivity (with chromatographic properties of synthetic neuropeptide Y) increased in parallel with catecholamines, heart rate and blood pressure during graded physical exercise in man. The plasma levels of neuropeptide Y correlated better with the levels of noradrenaline than adrenaline, suggesting release of a neural origin. Taken together with previous results, this suggests that neuropeptide Y is released together with noradrenaline upon sympathetic activation during physiological conditions in man. Determinations of plasma neuropeptide Y may therefore be valuable in the assessment of sympathetic nerve activity.