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Tomas Hokfelt - One of the best experts on this subject based on the ideXlab platform.

  • subtYpes Y1 and Y2 of the Neuropeptide Y receptor are respectivelY expressed in pro opiomelanocortin and Neuropeptide Y containing neurons of the rat hYpothalamic arcuate nucleus
    Neuroendocrinology, 1997
    Co-Authors: Christian Broberger, Marc Landry, H Wong, John N Walsh, Tomas Hokfelt
    Abstract:

    The arcuate nucleus of the hYpothalamus houses a number of neurochemicallY different cell populations. Among these, a dense cluster of small Neuropeptide-Y (NPY)-expressing neurons is located in its ventromedial subdivision and a pro-opiomelanocortin (POMC)-expressing neuron population in its ventrolateral part. Furthermore, both Neuropeptide Y Y1 and Y2 receptors (Y1-Rs and Y2-Rs) are expressed in the arcuate nucleus. Here we analYse the co-expression of NPY and POMC/adrenocorticotropic hormone with the Y1-R and Y2-R in arcuate neurons using immunohistochemistrY and in situ hYbridization. ManY, but not all, POMC neurons expressed Y1-R mRNA and protein. ConverselY, several Y1-R-positive, POMC-negative neurons were found. NPY-positive nerve terminals were found in close apposition to Y1-R-like immunoreactivitY localized close to the dendritic and somatic cell membranes. Y2-R mRNA was found in almost all NPY mRNA-expressing neurons, but also in a group of NPY mRNA-negative cells. These results show that the POMC neurons are targets for NPY, which is presumablY present in, and released from, fibres originating in the ventromedial arcuate nucleus and which maY plaY a role in NPY-induced feeding. Release of NPY, and possible coexisting messengers, maY be controlled bY presYnaptic Y2-R expressed in NPY neurons. Taken together, the findings support the division of Y1-Rs and Y2-Rs into post- and presYnaptic receptors, respectivelY.

  • subtYpes Y1 and Y2 of the Neuropeptide Y receptor are respectivelY expressed in pro opiomelanocortin and Neuropeptide Y containing neurons of the rat hYpothalamic arcuate nucleus
    Neuroendocrinology, 1997
    Co-Authors: Christian Broberger, Marc Landry, H Wong, John N Walsh, Tomas Hokfelt
    Abstract:

    The arcuate nucleus of the hYpothalamus houses a number of neurochemicallY different cell populations. Among these, a dense cluster of small Neuropeptide-Y (NPY)-expressing neurons is located in its v

  • the effects of intrathecal Neuropeptide Y on the spinal nociceptive flexor reflex in rats with intact sciatic nerves and after peripheral axotomY
    Neuroscience, 1994
    Co-Authors: Tomas Hokfelt, Z Wiesenfeldhallin
    Abstract:

    Abstract We examined the effects of intrathecallY administered Neuropeptide Y on the spinal nociceptive flexor reflex in decerebrate, spinalized, unanesthetized rats with intact sciatic nerves, or 11–39 daYs after unilateral transection of the sciatic nerve. In rats with intact sciatic nerve, intrathecal Neuropeptide Y at low doses (10 and 100ng) caused a brief facilitation of the flexor reflex. At a dose of 300 ng, the effect of Neuropeptide Y on the flexor reflex was biphasic i.e. a brief facilitation followed bY slight depression. At higher doses (1 and 10 μg), the effect of Neuropeptide Y was mainlY inhibitorY, causing substantial and usuallY prolonged depression of the flexor reflex magnitude. The reflex depression caused bY intrathecal Neuropeptide Y was not reversed bY the opioid antagonist naloxone or theα 2 adrenoceptor antagonist atipamezole. Intrathecal Neuropeptide Y at doses up to 1 and 10μg had no effect on reflex facilitation caused bY conditioning stimulation of C-fibers, intrathecal substance P or neurokinin A. Topical application of Neuropeptide Y (1 μg/μl) failed to influence the monosYnaptic reflex in normal rats. Eleven to 16 daYs after peripheral axotomY, the initial excitation of the flexor reflex to intrathecal Neuropeptide Y was significantlY enhanced in axotomized compared with normal rats. However, the depressive effect of Neuropeptide Y on the flexor reflex was unchanged. Neuropeptide Y did not influence the monosYnaptic reflex in axotomized rats at this period. In experiments performed on rats in which the sciatic nerve had been transected 31–39 daYs previouslY, the facilitatorY effect of Neuropeptide Y on the flexor reflex remained enhanced compared with normal rats. Furthermore, the inhibitorY effect of Neuropeptide Y also increased as 100 ng intrathecal Neuropeptide Y was able to produce reflex depression in a similar fashion as 300 ng Neuropeptide Y normallY and the reflex depression caused bY 1 μg Neuropeptide Y was stronger and longer lasting than in normal rats. Intrathecal Neuropeptide Y (100 ng-10 μg) in rats with intact sciatic nerves caused a moderate decrease in spinal cord dorsal surface blood flow as measured with a laser Doppler flowmeter. This effect of Neuropeptide Y was unchanged in axotomized rats. The present results support previous observations that spinal application of Neuropeptide Y in normal rats caused antinociception. As the depressive effect of Neuropeptide Y is independent of spinal opioid andα 2 -adrenergic sYstems, it maY be mediated bY its own receptors. The biphasic effect of Neuropeptide Y maY reflect its action on different subtYpes of Neuropeptide Y receptors. Experiments with Neuropeptide Y receptor antagonists are required to further define the role of endogenous Neuropeptide Y in nociception normallY and after peripheral axotomY.

Christian Broberger - One of the best experts on this subject based on the ideXlab platform.

G M Lees - One of the best experts on this subject based on the ideXlab platform.

  • reappraisal of the innervation of rat intestine bY vasoactive intestinal polYpeptide and Neuropeptide Y immunoreactive neurons
    Neuroscience, 1994
    Co-Authors: Kirsteen N Browning, G M Lees
    Abstract:

    Abstract The occurrence and distribution of neurons and nerve fibres showing vasoactive intestinal polYpeptide-like and Neuropeptide Y-like immunoreactivitY were re-examined in the enteric nervous sYstem of the small and large intestine of the adult rat using dual-labelling indirect immunofluorescence histochemistrY to detect the co-existence of these Neuropeptides. In the mYenteric plexus of both small and large intestine, a population of Neuropeptide Y-immunoreactive neurons that did not contain vasoactive intestinal polYpeptide was noted; it accounted for 29–53% of Neuropeptide Y neurons. Such neurons were also found in the submucosa but there theY constituted at most 2% of Neuropeptide Y-immunoreactive neurons. In both mYenteric and submucous plexuses, regional variations were observed in the number of immunoreactive neurons and in the proportion of dual-labelled neurons. In the mYenteric plexus, for example, the densitY of neurons with immunoreactivitY to these two Neuropeptides was constant throughout the small intestine, whereas it progressivelY increased distallY within the colon. In addition, a distinct but small subset of immunoreactive mYenteric neurons was found to have a novel soma morphologY, unclassifiable according to the criteria used for porcine or guinea-pig enteric neurons. Such neurons had one or more conspicuous processes, which were much longer than the short, lamellar somal processes of tYpical Dogiel TYpe I neurons; moreover, these protruded from an essentiallY smooth soma and terminated at distances of up to two cell diameters from their point of origin. Thus, our results suggest that the organization of the enteric nervous sYstem of the rat differs from that of other species and indicate that investigations of the co-localizations of Neuropeptides and biologicallY active mediators in the intestinal tract would be incomplete without reference to regional differences in the incidence and distribution of such neurochemicals.

Claude Burlet - One of the best experts on this subject based on the ideXlab platform.

  • k stimulated Neuropeptide Y release into the paraventricular nucleus and relation to feeding behavior in free moving rats
    Neuropeptides, 1993
    Co-Authors: A Strickerkrongrad, G Barbanel, Bernard Beck, Arlette Burlet, Jeanpierre Nicolas, Claude Burlet
    Abstract:

    Neuropeptide Y (NPY) stronglY stimulates food intake when it is injected in the central nervous sYstem and especiallY in the hYpothalamus. The major site of NPY sYnthesis in the hYpothalamus is the arcuate nucleus which projects to the paraventricular nucleus. These two nuclei form the arcuate-paraventricular axis, a local circuit in the control of food intake. It was demonstrated that Neuropeptide Y concentration in the paraventricular nucleus can be modified bY ingestive or metabolic factors. ActuallY, these modifications cannot be associated with the existence of a release of Neuropeptide Y in this nucleus. That is whY we used push-pull perfusion during the light phase in freelY-behaving rats with food and water available. Perfusates were collected with standard artificial cerebrospinal fluid (CSF) as medium and hYperosmotic CSF obtained bY addition of potassium chloride (55 mM). HYperosmotic perfusion was repeated a second time for some animals. Results clearlY demonstrated that Neuropeptide Y is released into the paraventricular nucleus during normal perfusion with a mean value of 35.5 ± 1.5 pg/tube. The potassium perfusion produced an increase in the release of Neuropeptide Y (peak at 71.4 ± 7.1 pg/tube; p < 0.01), and this phenomenon was reproduced with the second potassium stimulation (peak at 47.7 ± 2.3 vs pg/tube; p < 0.05). Neuropeptide Y release returned to normal values after or between stimulations. Behavioral analYsis showed that these stimulations were associated with an increase in food intake. Neuropeptide Y is therefore phYsiologicallY released into the paraventricular nucleus of the hYpothalamus. This release is associated with ingestive behavior and might be induced through voltage-dependent channels sensible to the high depolarisation associated with potassium excess in the extracellular fluid.

Annamaria Vezzani - One of the best experts on this subject based on the ideXlab platform.

  • seizure susceptibilitY and epileptogenesis are decreased in transgenic rats overexpressing Neuropeptide Y
    Neuroscience, 2002
    Co-Authors: Annamaria Vezzani, M Michalkiewicz, T Michalkiewicz, D Moneta, Teresa Ravizza, Cristina Richichi, Marisa Aliprandi, F Mule, L Pirona, Marco Gobbi
    Abstract:

    Functional studies in epileptic tissue indicate that Neuropeptide Y and some of its peptide analogs potentlY inhibit seizure activitY. We investigated seizure susceptibilitY in transgenic rats overexpressing the rat Neuropeptide Y gene under the control of its natural promoter. Seizures were induced in adult transgenic male rats and their wild-tYpe littermates bY i.c.v. injection of 0.3 microg kainic acid or bY electrical kindling of the dorsal hippocampus. Transgenic rats showed a significant reduction in the number and duration of electroencephalographic seizures induced bY kainate bY 30% and 55% respectivelY (P<0.05 and 0.01). Transgenic rats were also less susceptible to epileptogenesis than wild-tYpe littermates as demonstrated bY a 65% increase in the number of electrical stimuli required to induce stage 5 seizures (P<0.01). This phenotYpe was associated with a strong and specific expression of Neuropeptide Y mRNA in area CA1, a brain area involved in the seizure network. We conclude that endogenous Neuropeptide Y overexpression in the rat hippocampus is associated with inhibition of seizures and epileptogenesis suggesting that this sYstem maY be a valuable target for developing novel antiepileptic treatments.

  • somatostatin Neuropeptide Y neurokinin b and cholecYstokinin immunoreactivitY in two chronic models of temporal lobe epilepsY
    Neuroscience, 1995
    Co-Authors: Christoph Schwarzer, John Williamson, Eric W. Lothman, Annamaria Vezzani, G. Sperk
    Abstract:

    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.