scholarly journals Regulation of Drosophila Long-Term Courtship Memory by Ecdysis Triggering Hormone

2021 ◽  
Vol 15 ◽  
Author(s):  
Sang Soo Lee ◽  
Michael E. Adams
Keyword(s):  
Neural Circuit ◽  
Direct Action ◽  
Memory Performance ◽  
Corpus Allatum ◽  
Behavioral Changes ◽  
Brain Exposure ◽  
Circuit Components ◽  
Ecdysis Triggering Hormone ◽  
The Brain

Endocrine state is an important determinant of learning and memory in animals. InDrosophila, rejection of male courtship overtures by mated females leads to an aversive response manifested as courtship memory. Here we report that ecdysis triggering hormone (ETH) is an obligatory enabler of long-term courtship memory (LTM). ETH deficiency suppresses LTM, whereas augmented ETH release reduces the minimum training period required for LTM induction. ETH receptor knockdown either in the mushroom body (MB) γ lobe or in octopaminergic dorsal-anterior-lateral (DAL) neurons impairs memory performance, indicating its direct action in these brain areas. Consistent with these findings, brain exposure to ETH mobilizes calcium in MB γ lobe neuropils and DAL neurons. ETH receptor (ETHR) knockdown in the corpus allatum (CA) to create juvenile hormone (JH) deficiency also suppresses LTM, as does knockdown of the JH receptor Met in the MB γ lobe, indicating a convergence of ETH and JH signaling in this region of the brain. Our findings identify endocrine-enabled neural circuit components in the brain that are critical for persistent behavioral changes resulting from aversive social experience.

Long-Term Potentiation and Long-Term Depression

2018 ◽  
Author(s):  
Arianna Maffei
Keyword(s):  
Synaptic Plasticity ◽  
Neural Circuit ◽  
Long Term Potentiation ◽  
Synaptic Connections ◽  
Long Term Depression ◽  
Term Potentiation ◽  
Functional Implications ◽  
The Brain

Synaptic connections in the brain can change their strength in response to patterned activity. This ability of synapses is defined as synaptic plasticity. Long lasting forms of synaptic plasticity, long-term potentiation (LTP), and long-term depression (LTD), are thought to mediate the storage of information about stimuli or features of stimuli in a neural circuit. Since its discovery in the early 1970s, synaptic plasticity became a central subject of neuroscience, and many studies centered on understanding its mechanisms, as well as its functional implications.

scholarly journals Long-Term Safety of PEGylated Coagulation Factor VIII in the Immune-Deficient Rowett Nude Rat

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Caroline E. Rasmussen ◽  
Jette Nowak ◽  
Julie M. Larsen ◽  
Emma Moore ◽  
David Bell ◽  
...  
Keyword(s):  
Factor Viii ◽  
Hemophilia A ◽  
Coagulation Factor ◽  
Limit Of Quantification ◽  
Toxicity Studies ◽  
Clinical Observations ◽  
Brain Exposure ◽  
Human Proteins ◽  
The Brain

Turoctocog alfa pegol (N8-GP) is a glycoPEGylated human recombinant factor VIII for the treatment of hemophilia A. The safety profile of rFVIII, and polyethylene glycols (PEG) technology, is well-established. Conducting long-term toxicity studies in animals using human proteins can be complicated by anti-drug antibody (ADA) development. To evaluate long-term safety of N8-GP, 26- and 52-week toxicity studies were conducted in immune-deficient rats dosed intravenously every fourth day with 0, 50, 150, 500, or 1200 IU/kg N8-GP. Observations included clinical observations, body weight, ophthalmoscopy, hematology, chemistry, coagulation, urinalysis, toxicokinetics, antibody analysis, and macroscopic/microscopic organ examination. Immunohistochemical staining examined the distribution of PEG in the brain. No adverse test item-related findings were seen and PEG was not detected in the brain. Exposure was confirmed for ~75% of the animals dosed with 500 and 1200 IU/kg N8-GP; the high lower limit of quantification of the bioanalysis assay prevented confirmation of exposure in the lower doses. A small number of animals developed ADAs, and the proportion of animals surviving until scheduled termination was >80%. N8-GP was well tolerated, and the immune-deficient rat proved suitable for testing long-term toxicity of human proteins that are immunogenic in animals.

scholarly journals Diet and Age Interactions with Regards to Cholesterol Regulation and Brain Pathogenesis

2010 ◽  
Vol 2010 ◽  
pp. 1-14 ◽  
Author(s):  
Romina M. Uranga ◽  
Jeffrey N. Keller
Keyword(s):  
Behavioral Changes ◽  
Western Society ◽  
Aging Brain ◽  
Cholesterol Levels ◽  
Cognitive Disturbances ◽  
Number Of Individuals ◽  
Cholesterol Regulation ◽  
The Brain ◽  
Brain Homeostasis

Cholesterol is an essential molecule for brain homeostasis; yet, hypercholesterolemia and its numerous complications are believed to play a role in promoting multiple aspects of brain pathogenesis. An ever increasing number of individuals in modern Western Society are regularly consuming diets high in fat which promote the development of hypercholesterolemia. Additionally, modern societies are becoming increasingly aged, causing a collision between increased hypercholesterolemia and increased aging, which will likely lead to the development of increased pathological conditions due to hypercholesterolemia, thereby promoting deleterious neurochemical and behavioral changes in the brain. Lastly, while beneficial in controlling cholesterol levels, the long-term use of statins itself may potentially promote adverse effects on brain homeostasis, although specifics on this remain largely unknown. This review will focus on linking the current understanding of diet-induced hypercholesterolemia (as well as statin use) to the development of oxidative stress, neurochemical alterations, and cognitive disturbances in the aging brain.

scholarly journals Neuropeptides as Primary Mediators of Brain Circuit Connectivity

2021 ◽  
Vol 15 ◽  
Author(s):  
Mathilde C. C. Guillaumin ◽  
Denis Burdakov
Keyword(s):  
Neural Circuit ◽  
Direct Action ◽  
Temporal Integration ◽  
Neuronal Membrane ◽  
Brain Functions ◽  
Neuronal Interactions ◽  
Evolutionarily Conserved ◽  
Neuronal Processing ◽  
G Protein Coupled ◽  
The Brain

Across sleep and wakefulness, brain function requires inter-neuronal interactions lasting beyond seconds. Yet, most studies of neural circuit connectivity focus on millisecond-scale interactions mediated by the classic fast transmitters, GABA and glutamate. In contrast, neural circuit roles of the largest transmitter family in the brain–the slow-acting peptide transmitters–remain relatively overlooked, or described as “modulatory.” Neuropeptides may efficiently implement sustained neural circuit connectivity, since they are not rapidly removed from the extracellular space, and their prolonged action does not require continuous presynaptic firing. From this perspective, we review actions of evolutionarily-conserved neuropeptides made by brain-wide-projecting hypothalamic neurons, focusing on lateral hypothalamus (LH) neuropeptides essential for stable consciousness: the orexins/hypocretins. Action potential-dependent orexin release inside and outside the hypothalamus evokes slow postsynaptic excitation. This excitation does not arise from modulation of classic neurotransmission, but involves direct action of orexins on their specific G-protein coupled receptors (GPCRs) coupled to ion channels. While millisecond-scale, GABA/glutamate connectivity within the LH may not be strong, re-assessing LH microcircuits from the peptidergic viewpoint is consistent with slow local microcircuits. The sustained actions of neuropeptides on neuronal membrane potential may enable core brain functions, such as temporal integration and the creation of lasting permissive signals that act as “eligibility traces” for context-dependent information routing and plasticity. The slowness of neuropeptides has unique advantages for efficient neuronal processing and feedback control of consciousness.

Vasopressin and oxytocin their presence in the central nervous system and their functional significance in brain processes related to behaviour and memory

1986 ◽  
Vol 113 (2_Suppla) ◽  
pp. S85-S94 ◽  
Author(s):  
Tj. B. van Wimersma Greidanus ◽  
J. P. H. Burbach ◽  
H. D. Veldhuis
Keyword(s):  
Direct Action ◽  
Memory Function ◽  
Animal Experiments ◽  
Physiological Role ◽  
Conditioned Avoidance ◽  
Male Rats ◽  
Memory Processes ◽  
Vasopressin Receptors ◽  
The Brain

Abstract. Vasopressin and oxytocin exert pronounced effects on behaviour by a direct action on the brain. A single injection of vasopressin results in a long-term inhibition of extinction of a conditioned avoidance response suggesting that vasopressin triggers a long-term effect on the maintenance of a learned response, probably by facilitation of memory processes. In addition vasopressin improves passive avoidance behaviour, delays extinction of appetitive discrimination tasks, affects approach behaviour to an imprinting stimulus in ducklings, improves copulation rewarded behaviour of male rats in a T-maze, prevents or reverses amnesia induced by electroconvulsive shoch. CO2 inhalation, pentylenetetrazol or puromycin. The majority of these effects of vasopressin in the various and sometimes relatively complex tasks may be explained by stimulatory influences of this neuropeptide on memory processes. Generally oxytocin exerts effects which are opposite to those of vasopressin and it has been suggested that oxytocin may be an amnesic neuropeptide. Various limbic system structures seem to act as the anatomical substrate for the bevavioural effects of vasopressin. In particular the amygdala, the dentate gyrus of the hippocampal complex, the ventral hippocampus and the dorsal septum seem to be involved. Evidence has been obtained from experiments with homozygous diabetes insipidus rats and from experiments in which antisera were applied that endogenous vasopressin and oxytocin play a physiological role in brain processes related to memory. It appears that highly active fragments can be generated from vasopressin and experiments in which a fragment of vasopressin ([pGlu4, Cyt6]AVP-(4–8)) as well as an AVP-antagonist were used, reveal that the vasopressin receptors mediating the behavioural effects are situated in the brain and differ in specificity from the peripheral (blood pressure) vasopressin receptors. Generally the clinical data obtained so far with vasopressin treatment are in agreement with the results from animal experiments and they support the notion on the involvement of vasopressin in memory function. The sometimes reported conflicting results on vasopressin effects in certain patients (Korsakoff or Alzheimer) may have to do with the wide-spread pathology in these diseases.

Diurnal rhythm returns to normal after elimination of portacaval shunting

1998 ◽  
Vol 274 (3) ◽  
pp. E426-E431 ◽  
Author(s):  
Paul A. Hawkins ◽  
Mary R. Dejoseph ◽  
Richard A. Hawkins
Keyword(s):  
Diurnal Rhythm ◽  
Time Course ◽  
Complete Recovery ◽  
Behavioral Changes ◽  
Behavioral Study ◽  
Hepatic Circulation ◽  
Long Period ◽  
Portacaval Shunting ◽  
The Brain

Previous studies showed that portacaval shunting causes metabolic and behavioral changes in rats. Most metabolic changes reversed within 1–2 wk after restoration of normal circulation. However, the rate of cerebral glucose metabolism (CMRGlc) remained depressed in some areas. The question arose whether complete recovery was possible. Therefore, a long-term behavioral study was undertaken to determine the time course of recovery. Diurnal activity was monitored for 48 h each week over a period of 14 wk: 2 wk before shunting, 6 wk after shunting, and 6 wk after restoration of normal hepatic circulation. Nighttime activity was depressed within 1 wk of shunting and did not change. Normal circulation to the liver was reestablished after 6 wk. The diurnal cycle was normal 3 wk later. Thus, although recovery of the diurnal rhythm is possible, the relatively long period necessary suggests the correction of a significant structural or chemical abnormality. A study of CMRGlcwas made using the behavioral study as an index of the time necessary for recovery. CMRGlcreturned to normal throughout the brain 6 wk after cessation of shunting except in the hippocampus and amygdala (7–8% decrease).

scholarly journals Behavioral and epigenetic consequences of oxytocin treatment at birth

2019 ◽  
Vol 5 (5) ◽  
pp. eaav2244 ◽  
Author(s):  
W. M. Kenkel ◽  
A.-M. Perkeybile ◽  
J. R. Yee ◽  
H. Pournajafi-Nazarloo ◽  
T. S. Lillard ◽  
...  
Keyword(s):  
Direct Action ◽  
Fetal Brain ◽  
Social Contact ◽  
The United States ◽  
Oxytocin Receptor ◽  
Epigenetic Mechanism ◽  
Long Term Effects ◽  
Socially Monogamous ◽  
The Brain

Oxytocin is used in approximately half of all births in the United States during labor induction and/or augmentation. However, the effects of maternal oxytocin administration on offspring development have not been fully characterized. Here, we used the socially monogamous prairie vole to examine the hypothesis that oxytocin exposure at birth can have long-term developmental consequences. Maternally administered oxytocin increased methylation of the oxytocin receptor (Oxtr) in the fetal brain. As adults, oxytocin-exposed voles were more gregarious, with increased alloparental caregiving toward pups and increased close social contact with other adults. Cross-fostering indicated that these effects were the result of direct action on the offspring, rather than indirect effects via postnatal changes in maternal behavior. Male oxytocin-exposed offspring had increased oxytocin receptor density and expression in the brain as adults. These results show that long-term effects of perinatal oxytocin may be mediated by an epigenetic mechanism.

scholarly journals A mechanism for synaptic copy between neural circuits

2018 ◽  
Author(s):  
Yuxiu Shao ◽  
Binxu Wang ◽  
Andrew T. Sornborger ◽  
Louis Tao
Keyword(s):  
Memory Consolidation ◽  
Information Transfer ◽  
Neural Circuits ◽  
Neural Circuit ◽  
Neural Systems ◽  
Long Term Memory ◽  
Cortical Oscillations ◽  
The Brain ◽  
Putative Mechanism

The brain has a central, short-term learning module, the hippocampus, which transfers what it has learned to long-term memory in cortex during non-REM sleep. The putative mechanism responsible for this type of memory consolidation invokes hierarchically nested hippocampal ripples (100-250 Hz), thalamo-cortical spindles (7-15 Hz), and cortical slow oscillations (< 1 Hz) to enable transfer. Suppression of, for instance, thalamic spindles has been shown to impair hippocampus-dependent memory consolidation. Cortical oscillations are central to information transfer in neural systems. Significant evidence supports the idea that coincident spike input can allow the neural threshold to be overcome, and spikes to be propagated downstream in a circuit. Thus, an observation of oscillations in neural circuits would be an indication that repeated synchronous spiking is enabling information transfer. However, for memory transfer, in which synaptic weights must be being transferred from one neural circuit (region) to another, what is the mechanism? Here, we present a synaptic transfer mechanism whose structure provides some understanding of the phenomena that have been implicated in memory transfer, including the nested oscillations at various frequencies. The circuit is based on the principle of pulse-gated, graded information transfer between neural populations.PACS numbers: 87.18.Sn,87.19.lj,87.19.lm,87.19.lq

Long-Term Pathologic and Behavioral Changes in Mice after Focal Deuteron Irradiation of the Brain

1963 ◽  
Vol 20 (1) ◽  
pp. 30 ◽  
Author(s):  
J. M. Ordy ◽  
T. Samorajski ◽  
W. Zeman ◽  
R. L. Collins ◽  
H. J. Curtis
Keyword(s):  
Behavioral Changes ◽  
Deuteron Irradiation ◽  
The Brain

scholarly journals Behavioral alterations in long-term Toxoplasma gondii infection of C57BL/6 mice are associated with neuroinflammation and disruption of the blood brain barrier

PLoS ONE ◽  
2021 ◽  
Vol 16 (10) ◽  
pp. e0258199
Author(s):  
Leda Castaño Barrios ◽  
Ana Paula Da Silva Pinheiro ◽  
Daniel Gibaldi ◽  
Andrea Alice Silva ◽  
Patrícia Machado Rodrigues e Silva ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Brain Tissue ◽  
Blood Brain Barrier ◽  
Behavioral Changes ◽  
Brain Barrier ◽  
Behavioral Alterations ◽  
Compulsive Disorder ◽  
Blood Brain ◽  
The Brain

The Apicomplexa protozoan Toxoplasma gondii is a mandatory intracellular parasite and the causative agent of toxoplasmosis. This illness is of medical importance due to its high prevalence worldwide and may cause neurological alterations in immunocompromised persons. In chronically infected immunocompetent individuals, this parasite forms tissue cysts mainly in the brain. In addition, T. gondii infection has been related to mental illnesses such as schizophrenia, bipolar disorder, depression, obsessive-compulsive disorder, as well as mood, personality, and other behavioral changes. In the present study, we evaluated the kinetics of behavioral alterations in a model of chronic infection, assessing anxiety, depression and exploratory behavior, and their relationship with neuroinflammation and parasite cysts in brain tissue areas, blood-brain-barrier (BBB) integrity, and cytokine status in the brain and serum. Adult female C57BL/6 mice were infected by gavage with 5 cysts of the ME-49 type II T. gondii strain, and analyzed as independent groups at 30, 60 and 90 days postinfection (dpi). Anxiety, depressive-like behavior, and hyperactivity were detected in the early (30 dpi) and long-term (60 and 90 dpi) chronic T. gondii infection, in a direct association with the presence of parasite cysts and neuroinflammation, independently of the brain tissue areas, and linked to BBB disruption. These behavioral alterations paralleled the upregulation of expression of tumor necrosis factor (TNF) and CC-chemokines (CCL2/MCP-1, CCL3/MIP-1α, CCL4/MIP-1β and CCL5/RANTES) in the brain tissue. In addition, increased levels of interferon-gamma (IFNγ), TNF and CCL2/MCP-1 were detected in the peripheral blood, at 30 and 60 dpi. Our data suggest that the persistence of parasite cysts induces sustained neuroinflammation, and BBB disruption, thus allowing leakage of cytokines of circulating plasma into the brain tissue. Therefore, all these factors may contribute to behavioral changes (anxiety, depressive-like behavior, and hyperactivity) in chronic T. gondii infection.

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