Banisteriopsis caapi extract: Implications for neuroinflammatory pathways in Locus coeruleus lesion rodent model.

Ethnopharmacology Relevance: Ayahuasca is a beverage obtained from the decoctions of Banisteriopsis caapi (Spruce ex Griseb.) Morton and Psychotria viridis Ruiz & Pav., used throughout the Amazon as a medicinal beverage for healing and spiritual exploration.

Behavioral effects of 6-hydroxydopamine-induced damage to nigro-striatal pathway and Locus coeruleus as a rodent model of Parkinson's disease.

Parkinson's disease (PD) is a chronic and progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons in the Substantia nigra pars compacta (SNpc), which leads to motor and non-motor symptoms (NMS). NMS can appear many years before the classical motor symptoms and are associated with the neurodegeneration of several nuclei; in this work, we highlight the neurodegeneration of Locus coeruleus (LC) in PD. The aim was to investigate the effects of depleting SNpc and LC catecholaminergic neurons on behavioral and neurobiological endpoints.

Oxidative Stress Inhibition Via Apocynin Prevents Medullary Respiratory Neurodegeneration and Respiratory Pattern Dysfunction in a 6-Hydroxydopamine Animal Model of Parkinson's Disease.

Parkinson's Disease (PD) is a neurogenerative disorder characterized by the death of dopaminergic neurons in the Substantia Nigra pars compacta (SNpc), leading to motor, cognitive, learning, and respiratory dysfunctions. New evidence revealed that breathing impairment in PD mainly results from oxidative stress (OS) that initiates apoptotic signaling in respiratory neurons. Here, we investigated the role of OS inhibition using apocynin (non-specific NADPH oxidase inhibitor) in a 6-OHDA PD animal model in the neural control of breathing.

Depletion of hypothalamic hypocretin/orexin neurons correlates with impaired memory in a Parkinson's disease animal model.

Parkinson's disease (PD) is a progressive and chronic neurodegenerative disorder characterized by loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and affects multiple neurotransmission systems such as hypocretin/orexin (HO) release and can lead to cognitive and memory deficits. The HO neurons located in lateral hypothalamus/perifornical area (LH/PeF) are involved with consolidation and memory processes. Here we verified the involvement of HO deficit in learning and memory process in an animal model of PD induced by bilateral intra-striatal injections of 6-hydroxydopamine (6-OHDA).

Kinin B1 receptor mediates memory impairment in the rat hippocampus.

The bradykinin (BK) receptors B1R and B2R are involved in inflammatory responses and their activation can enhance tissue damage. The B2R is constitutively expressed and mediates the physiologic effects of BK, whereas B1R expression is induced after tissue damage. Recently, they have been involved with Alzheimer's disease, ischemic stroke and traumatic brain injury (TBI).

Chronic Microdose Lithium Treatment Prevented Memory Loss and Neurohistopathological Changes in a Transgenic Mouse Model of Alzheimer's Disease.

The use of lithium is well established in bipolar disorders and the benefits are being demonstrated in neurodegenerative disorders. Recently, our group showed that treatment with microdose lithium stabilized the cognitive deficits observed in Alzheimer's disease (AD) patients. In order to verify the lithium microdose potential in preventing the disease development, the aim of this work was to verify the effects of chronic treatment with microdose lithium given before and after the appearance of symptoms in a mouse model of a disease similar to AD.

Chronic infusion of amyloid-β peptide and sustained attention altered α7 nicotinic receptor density in the rat brain.

It is already known that progressive degeneration of cholinergic neurons in brain areas such as the hippocampus and the cortex leads to memory deficits, as observed in Alzheimer's disease. This work verified the effects of the infusion of amyloid-β (Aβ) peptide associated to an attentional rehearsal on the density of α7 nicotinic cholinergic receptor (nAChR) in the brain of male Wistar rats. Animals received intracerebroventricular infusion of Aβ or vehicle (control - C) and their attention was stimulated weekly (Stimulated Aβ group: S-Aβ and Stimulated Control group: SC) or not (Non- Stimulated Aβ group: N-SAβ and Non-Stimulated Control group: N-SC), using an active avoidance apparatus.

Influence of anabolic steroid treatment associated to physical exercise in the ultrasonic vocalization of rats.

Unlike humans, who communicate in frequency bands between 250 Hz and 6 kHz, rats can communicate in frequencies above 18 kHz. Their vocalization types depend on the context and are normally associated to subjective or emotional states. It was reported significant vocal changes due to administration of replacement testosterone in a trained tenor singer with hypogonadism.

Change in central kinin B2 receptor density after exercise training in rats.

Cardiovascular responses elicited by the stimulation of kinin B2 receptors in the IV cerebral ventricle, paratrigeminal nucleus or in the thoracic spinal cord are similar to those observed during an exercise bout. Considering that the kalikrein-kinin system (KKS) could act on the cardiovascular modulation during behavioral responses as physical exercise or stress, this study evaluated the central B2 receptor densities of Wistar (W) and spontaneously hypertensive rats (SHR) after chronic moderate exercise. Animals were exercise-trained for ten weeks on a treadmill.

Role of kinin B1 and B2 receptors in memory consolidation during the aging process of mice.

Under physiological conditions, elderly people present memory deficit associated with neuronal loss. This pattern is also associated with Alzheimer's disease but, in this case, in a dramatically intensified level. Kinin receptors have been involved in neurodegeneration and increase of amyloid-beta concentration, associated with Alzheimer's disease (AD).

Participation of kinin receptors on memory impairment after chronic infusion of human amyloid-beta 1-40 peptide in mice.

Chronic infusion of human amyloid-beta 1-40 (Abeta) in the lateral ventricle (LV) of rats is associated with memory impairment and increase of kinin receptors in cortical and hippocampal areas. Deletion of kinin B1 or B2 receptors abolished memory impairment caused by an acute single injection of Abeta in the LV. As brain tissue and kinin receptors could unlikely react to acute or chronic administration of a similar quantity of Abeta, we evaluated the participation of B1 or B2 receptors in memory impairment after chronic infusion of Abeta.