Response of nitrergic system in the brain of rat conditioned to intracranial self-stimulation.

The role of nitrergic system in modulating the action of psychostimulants on reward processing is well established. However, the relevant anatomical underpinnings and scope of the involved interactions with mesolimbic dopaminergic system have not been clarified. Using immunohistochemistry, we track the changes in neuronal nitric oxide synthase (nNOS) containing cell groups in the animals conditioned to intracranial self-stimulation (ICSS) via an electrode implanted in the lateral hypothalamus-medial forebrain bundle (LH-MFB) area.

Chronic agmatine treatment prevents olanzapine-induced obesity and metabolic dysregulation in female rats.

Antipsychotic-induced obesity affects millions of people and is a serious health condition worldwide. Olanzapine is the most widely prescribed antipsychotic agent with high obesogenic potential. However, the exact mechanism by which it causes its metabolic dysregulation remains poorly understood.

Encephalitis patient-derived monoclonal GABAA receptor antibodies cause epileptic seizures.

Autoantibodies targeting the GABAA receptor (GABAAR) hallmark an autoimmune encephalitis presenting with frequent seizures and psychomotor abnormalities. Their pathogenic role is still not well-defined, given the common overlap with further autoantibodies and the lack of patient-derived mAbs. Five GABAAR mAbs from cerebrospinal fluid cells bound to various epitopes involving the α1 and γ2 receptor subunits, with variable binding strength and partial competition.

Nicotine-induced Brain Stimulation Reward is Modulated by Melanocortin-4 Receptors in Ovariectomized Rats.

Apart from reproduction, estrogen influences a multitude of processes. Increase in estrogen levels in women is known to promote reward probably mediated via the melanocortin and dopamine systems. Reduced estrogen in post-menopausal women attenuates reward, evoking the need for stimulation with greater rewarding salience.

CART modulates the effects of levodopa in rat model of Parkinson's disease.

Parkinson's disease (PD) is an age-related disorder characterized by a progressive degeneration of dopaminergic neurons of substantia nigra (SN). The neuropeptide cocaine- and amphetamine-regulated transcript (CART) is known to closely interact with the dopamine system and regulate psychomotor activity. We screened the effectiveness of CART in reversing the symptoms of PD in a rat model.

Neuropeptide Y system in accumbens shell mediates ethanol self-administration in posterior ventral tegmental area.

Although modulatory effects of neuropeptide Y (NPY) on ethanol consumption are well established, its role in ethanol reward, in the framework of mesolimbic dopaminergic system, has not been studied. We investigated the influence of nucleus accumbens shell (AcbSh) NPYergic system on ethanol self-administration in posterior ventral tegmental area (p-VTA) using intracranial self-administration paradigm. Rats were stereotaxically implanted with cannulae targeted unilaterally at the right p-VTA and trained to self-administer ethanol (200 mg%) in standard two-lever (active/inactive) operant chamber, an animal model with high predictive validity to test the rewarding mechanisms.

CART in the brain of vertebrates: circuits, functions and evolution.

Cocaine- and amphetamine-regulated transcript peptide (CART) with its wide distribution in the brain of mammals has been the focus of considerable research in recent years. Last two decades have witnessed a steady rise in the information on the genes that encode this neuropeptide and regulation of its transcription and translation. CART is highly enriched in the hypothalamic nuclei and its relevance to energy homeostasis and neuroendocrine control has been understood in great details.

A simple and economical method of electrode fabrication for brain self-stimulation in rats.

Introduction: Intracranial self-stimulation (ICSS) is an operant paradigm in which rodents self-administer rewarding electrical stimulation through electrodes implanted into the brain. We describe a simple, inexpensive and reliable method to fabricate monopolar and bipolar electrodes, along with the swivel system, for delivery of electric pulses at the targeted sites in the brain of rat.

Methods: The system consists of an insulated stainless steel wire(s) (diameter: 0.

NPY mediates reward activity of morphine, via NPY Y1 receptors, in the nucleus accumbens shell.

Although the interaction between endogenous neuropeptide Y (NPY) and opioidergic systems in processing of reward has been speculated, experimental evidence is lacking. We investigated the role of NPY, and its Y1 receptors, in the nucleus accumbens shell (AcbSh) in morphine induced reward and reinforcement behavior. Rats were implanted with cannulae targeted at AcbSh for drug administration, and with stimulating electrode in the medial forebrain bundle (MFB).

Cocaine- and amphetamine-regulated transcript peptide (CART) in the central nucleus of amygdala potentiates behavioral and hormonal responses of the rat exposed to its predator.

Since cocaine- and amphetamine-regulated transcript peptide (CART) regulates anxiety and stress in amygdala, we hypothesized that the peptide may also process negative psychological experience like fear. During acute exposure to a cat, the rat showed freezing behavior and subsequently, profound signs of anxiety in social interaction test, and elevated serum cortisol concentration. While these behavioral effects were potentiated by the intracerebroventricular (icv) and intra-central nucleus of amygdala (intra-CeA) administration of CART peptide, they were blocked by CART antibody.

Neuroprotective effect of cocaine- and amphetamine-regulated transcript peptide in spinal cord injury in mice.

We explored the effect of cocaine- and amphetamine-regulated transcript peptide (CART), alone and in combination with methylprednisolone (MP), on the cellular pathology and locomotor recovery of mice following spinal cord injury (SCI). While cellular pathology was evaluated in terms of spinal cord histology and profile of astrocytes following immunolabeling with antibodies against glial fibrillary acidic protein (GFAP), locomotor recovery was monitored using hindlimb motor function scoring system. At 24 h post-SCI, there was a massive loss of motor function and cysts formation in the spinal cord.

Nicotine evoked improvement in learning and memory is mediated through NPY Y1 receptors in rat model of Alzheimer's disease.

We investigated the role of endogenous neuropeptide Y (NPY) system in nicotine-mediated improvement of learning and memory in rat model of Alzheimer's disease (AD). Intracerebroventricular (icv) colchicine treatment induced AD-like condition in rats and showed increased escape latency (decreased learning), and amnesic condition in probe test in Morris water maze. In these rats, nicotine (0.

CART peptide in the nucleus accumbens shell acts downstream to dopamine and mediates the reward and reinforcement actions of morphine.

The opioid-mesolimbic-dopamine circuitry operates between ventral tegmental area (VTA) and nucleus accumbens (Acb) and serves as a major reward pathway. We hypothesized that the neuropeptide cocaine- and amphetamine-regulated transcript (CART) is involved in the natural reward action mediated by the circuitry. Therefore, the modulation of opioid-mesolimbic-dopamine reward circuitry by CART was investigated using pellet self-administration paradigm in operant chamber.

Evidence for the participation of cocaine- and amphetamine-regulated transcript peptide (CART) in the fluoxetine-induced anti-hyperalgesia in neuropathic rats.

Cocaine- and amphetamine-regulated transcript peptide (CART) has a role in chronic pain, and also in the actions of selective serotonin reuptake inhibitors (SSRIs) employed in the treatment of neuropathic pain. Herein, we test the hypothesis that CART may mediate the anti-hyperalgesic effect of the SSRI, fluoxetine, in neuropathic rats. Sciatic nerve in the right hind paw of rat was ligated to induce neuropathic pain, and the paw withdrawal latency was evaluated using Hargreaves apparatus.

Cocaine- and amphetamine-regulated transcript peptide increases spatial learning and memory in rats.

Aim: We investigated the involvement of cocaine- and amphetamine-regulated transcript peptide (CART) in spatial learning and memory.

Main Methods: Rats were intracerebroventricularly injected with CART or CART-antibody, with or without intraperitoneal scopolamine, for a period of 4 days, during which they were subjected to the acquisition protocol in Morris water maze (MWM). In retrieval protocols, at 24 h and 15 days post-acquisition time points similar treatments were given to trained rats and subjected to MWM.

Effect of alpha-melanocyte stimulating hormone on locomotor recovery following spinal cord injury in mice: Role of serotonergic system.

The present study underscores the effect of serotonergic antagonist on alpha-melanocyte stimulating hormone (α-MSH) induced neuronal regeneration. Swiss-albino mice were subjected to experimental spinal cord injury (ESCI) and treated with serotonergic antagonist, ritanserin, alone or in combination with α-MSH, and the locomotor recovery was investigated. ESCI was induced at thoracic T(10-12) level by compression method.

Neuropeptide Y Y1 receptors in the central nucleus of amygdala mediate the anxiolytic-like effect of allopregnanolone in mice: Behavioral and immunocytochemical evidences.

Since allopregnanolone (ALLO) elicits anxiolytic-like action and increases neuropeptide Y Y1 (NPY Y1) receptors gene expression in the amygdala, we were interested in studying the involvement of NPY Y1 receptors in the anxiolytic-like actions of ALLO. The anxiety-like behavior was evaluated in mice using Vogel's conflict test (VCT), in which number of shocks were measured. ALLO and NPYergic agents, alone or in combinations, were administered bilaterally into the central nucleus of amygdala (CeA).

Involvement of neuropeptide Y in the acute, chronic and withdrawal responses of morphine in nociception in neuropathic rats: behavioral and neuroanatomical correlates.

Although morphine is a potent antinociceptive agent, its chronic use developed tolerance in neuropathic pain (NP). Furthermore, opioid antagonist naloxone attenuated the antinociceptive effect of neuropeptide Y (NPY). The present study investigated the role of NPY and NPY Y1/Y5 receptors in acute and chronic actions of morphine in neuropathic rats using thermal paw withdrawal test and immunocytochemistry.

Neuropeptide Y modulates the antidepressant activity of imipramine in olfactory bulbectomized rats: involvement of NPY Y1 receptors.

Since long-term treatment with imipramine increases the neuropeptide Y (NPY) levels in the frontal cortex and hypothalamus, the possibility exists that the antidepressant action of imipramine may be mediated via the NPY Y1 receptors. Bilateral olfactory bulbectomy (OBX) resulted in hyperactivity (increased number of ambulation, rearing and grooming episodes) in open field test (OFT) suggesting a depression-like condition. Chronic (14 days) administration of NPY, NPY Y1/Y5 receptor agonist [Leu(31), Pro(34)]-NPY (intracerebroventricular, i.

Central administration of selective melanocortin 4 receptor antagonist HS014 prevents morphine tolerance and withdrawal hyperalgesia.

Major problem involved in treatment of chronic pain with morphine is the development of tolerance and dependence. Previous studies have demonstrated the participation of melanocortin (MC) system in the development of tolerance to antinociceptive effect of morphine. However, the impact of supraspinal MC4 receptors (MC4 R) modulation on this phenomenon and morphine withdrawal hyperalgesia remained unexplored.