NPY Induces Stress Resilience via Downregulation of in Principal Neurons of Rat Basolateral Amygdala.

Neuropeptide Y (NPY) expression is tightly linked with the development of stress resilience in rodents and humans. Local NPY injections targeting the basolateral amygdala (BLA) produce long-term behavioral stress resilience in male rats via an unknown mechanism. Previously, we showed that activation of NPY Y receptors hyperpolarizes BLA principal neurons (PNs) through inhibition of the hyperpolarization-activated, depolarizing H-current, The present studies tested whether NPY treatment induces stress resilience by modulating NPY (10 pmol) was delivered daily for 5 d bilaterally into the BLA to induce resilience; thereafter, the electrophysiological properties of PNs and the expression of in the BLA were characterized.

Neuropeptide Y input to the rat basolateral amygdala complex and modulation by conditioned fear.

Within the basolateral amygdaloid complex (BLA), neuropeptide Y (NPY) buffers against protracted anxiety and fear. Although the importance of NPY's actions in the BLA is well documented, little is known about the source(s) of NPY fibers to this region. The current studies identified sources of NPY projections to the BLA by using a combination of anatomical and neurochemical approaches.

EP24.15 as a Potential Regulator of Kisspeptin Within the Neuroendocrine Hypothalamus.

The neuropeptide kisspeptin (Kiss1) is integral to the advent of puberty and the generation of cyclical LH surges. Although many complex actions of Kiss1 are known, the mechanisms governing the processing/regulation of this peptide have not been unveiled. The metallo enzyme, endopeptidase 24.

Differential activation of neuronal cell types in the basolateral amygdala by corticotropin releasing factor.

Enhanced corticotropin releasing factor (CRF) release in the basolateral amygdala (BLA) is strongly associated with the generation of behavioral stress responses through activation of the CRF-R1 receptor subtype. Stress and anxiety-like behavior are modulated in part by the balance of peptide actions such as excitatory CRF and inhibitory neuropeptide Y (NPY) receptor activation in the BLA. While the actions of CRF are clear, little is known about the cell type influenced by CRF receptor stimulation.

Cell-specific expression of calcineurin immunoreactivity within the rat basolateral amygdala complex and colocalization with the neuropeptide Y Y1 receptor.

Neuropeptide Y (NPY) produces potent anxiolytic effects via activation of NPY Y1 receptors (Y1r) within the basolateral amygdaloid complex (BLA). The role of NPY in the BLA was recently expanded to include the ability to produce stress resilience and long-lasting reductions in anxiety-like behavior. These persistent behavioral effects are dependent upon activity of the protein phosphatase, calcineurin (CaN), which has long been associated with shaping long-term synaptic signaling.

Neuropeptide Y in the amygdala induces long-term resilience to stress-induced reductions in social responses but not hypothalamic-adrenal-pituitary axis activity or hyperthermia.

Resilience to mental and physical stress is a key determinant for the survival and functioning of mammals. Although the importance of stress resilience has been recognized, the underlying neural mediators have not yet been identified. Neuropeptide Y (NPY) is a peptide known for its anti-anxiety-like effects mediated via the amygdala.

Influence of dehydration on the expression of neuropeptide Y Y1 receptors in hypothalamic magnocellular neurons.

Regulation of vasopressin (VP) and oxytocin (OT) secretion involves integration of neural signals from hypothalamic osmoreceptors, ascending catecholaminergic and peptidergic cell groups in the brain stem, and local and autoregulatory afferents. Neuropeptide Y (NPY) is one factor that stimulates the release of VP and OT from the supraoptic (SON) and paraventricular nuclei of the hypothalamus via activation of Y1 receptors (Y1R). The current studies were designed to assess the regulation and distribution of NPY Y1R expression in the SON of male rats that were either given 2% NaCl drinking water (24-72 h) or water deprived (48 h).

Differential mechanisms of antianalgesia induced by endomorphin-1 and endomorphin-2 in the ventral periaqueductal gray of the rat.

The effects of pretreatment with endomorphin-1 (EM-1) and endomorphin-2 (EM-2) given into the ventral periaqueductal gray (vPAG) to induce antianalgesia against the tail-flick (TF) inhibition produced by morphine given into the vPAG were studied in rats. Pretreatment with EM-1 (3.5-28 nmol) given into vPAG for 45 min dose-dependently attenuated the TF inhibition produced by morphine (9 nmol) given into vPAG.

Increased release of immunoreactive dynorphin A1-17 from the spinal cord after intrathecal treatment with endomorphin-2 in anesthetized rats.

We previously demonstrated pretreatment with antiserum against dynorphin A1-17 attenuates endomorphin-2-induced analgesia and antianalgesia, suggesting that these endomorphin-2 effects are mediated by the release of dynorphin A1-17. Lumbar-cisternal spinal perfusion was used to measure the release of immunoreactive dynorphin A1-17 into spinal perfusates from urethane-anesthetized rats following endomorphin-2 or endomorphin-1 treatment within the perfusion solution. Treatment with endomorphin-2 (5-50 nmol) for 3 min caused a dose-dependent increase of immunoreactive dynorphin A1-17 in spinal perfusates, with a maximal increase detected between 24 and 48 min after endomorphin-2 treatment, while levels returned to baseline within 60 min.

Opposite conditioned place preference responses to endomorphin-1 and endomorphin-2 in the mouse.

An unbiased conditioned place preference paradigm was used to evaluate the reward effect of selective endogenous mu-opioid ligands, endomorphin-1 and endomorphin-2, in male CD-1 mice. Pre- and post-conditioning free-movement were measured on day 1 and day 5, respectively. Conditioning sessions were conducted twice daily from day 2 through day 4 consisting of the alternate injection of conditioning drug or vehicle.

Nonopioidergic mechanism mediating morphine-induced antianalgesia in the mouse spinal cord.

Intrathecal (i.t.) pretreatment with a low dose (0.

Differential conditioned place preference responses to endomorphin-1 and endomorphin-2 microinjected into the posterior nucleus accumbens shell and ventral tegmental area in the rat.

An unbiased conditioned place preference (CPP) paradigm was used to evaluate the reward effects of endogenous mu-opioid receptor ligands endomorphin-1 (EM-1) and endomorphin-2 (EM-2) from the mesolimbic posterior nucleus accumbens (Acb) shell and the ventral tegmental area (VTA) in CD rats. EM-1 (1.6-8.

Region-dependent G-protein activation by kappa-opioid receptor agonists in the mouse brain.

The G-protein activations induced by kappa-opioid receptor agonists, (-)U50,488H, U69,593 and TRK-820 in the mouse lower midbrain, striatum and limbic forebrain were determined by monitoring guanosine-5'-o-(3-[35S]thio)triphosphate ([35S]GTP gamma S) binding. All kappa-opioid receptor agonists produced approximately 40, 20 and 10% increases of [35S]GTP gamma S binding over baseline in the lower midbrain, striatum and limbic forebrain, respectively. The increases of [35S]GTP gamma S binding induced by kappa-opioid receptor agonists were completely reversed by the selective kappa-opioid receptor antagonist, norbinaltorphimine (norBNI), in all brain regions.

Dynorphinergic mechanism mediating endomorphin-2-induced antianalgesia in the mouse spinal cord.

We have previously demonstrated that both endomorphin-1 (EM-1) and endomorphin-2 (EM-2) at high doses (1.75-35 nmol) given intrathecally (i.t.

Spinal pretreatment with antisense oligodeoxynucleotides against exon-1, -4, or -8 of mu-opioid receptor clone leads to differential loss of spinal endomorphin-1-and endomorphin-2-induced antinociception in the mouse.

Intrathecal (i.t.) pretreatments with antisense oligodeoxynucleotides (AS ODNs) against exon-1, -4, or -8 of mu-opioid receptor clone (MOR-1) to knockdown different variants of MOR-1 on the antinociception induced by endomorphin-1, enomorphin-2, or [D-Ala(2),N-Me-Phe(4),Gly(5)-ol]-enkephalin (DAMGO) given i.