The role of interaction between orexin receptors and β2 adrenergic receptors in basolateral amygdala in dentate gyrus synaptic plasticity in male rats

2021 ◽  
Vol 177 ◽  
pp. 164-171
Author(s):  
Seyedeh Kebria Noorani ◽  
Vida Hojati ◽  
Esmaeil Akbari ◽  
Simin Ehsani ◽  
Takeshi Sakurai ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Dentate Gyrus ◽  
Adrenergic Receptors ◽  
Basolateral Amygdala ◽  
Male Rats ◽  
Orexin Receptors

scholarly journals Paired-Pulse Inhibition and Disinhibition of the Dentate Gyrus Following Orexin Receptors Inactivation in the Basolateral Amygdala

2021 ◽  
Vol 0 (0) ◽  
pp. 1-16
Author(s):  
Esmaeil Akbari ◽  
◽  
Narges Hosseinmardi ◽  
Motahareh Rouhi Ardeshiri ◽  
◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Dentate Gyrus ◽  
Dimethyl Sulfoxide ◽  
Rat Brain ◽  
Learning And Memory ◽  
Basolateral Amygdala ◽  
Local Interneuron ◽  
Paired Pulse ◽  
Orexin Receptors ◽  
Neuronal Transmission

The basolateral amygdala (BLA) has substantial effects on the neuronal transmission and synaptic plasticity processes through the dentate gyrus. Orexin neuropeptides play different roles in the sleep/wakefulness cycle, feeding, learning, and memory. The present study was conducted to investigate the function of the orexin receptors of the BLA in the hippocampal local interneuron circuits. For this, paired-pulse responses from dentate gyrus (DG) region were recorded. Within the procedure, SB-334867-A (12μg/0.5μl), and, TCS-OX2-29 (10μg/0.5μl (orexin 1 and 2 receptors antagonists, respectively), were administered into the both side of the BLA areas of the rat brain. Dimethyl sulfoxide (DMSO) was used as the solvent in the control animals with the volume of 0.5μl. Our data indicated that the paired-pulse (PP) responses were not affected by the inactivation of the orexin receptors of the BLA.

Role of transmitters in mediating hypothalamic control of electrolyte excretion

1977 ◽  
Vol 55 (5) ◽  
pp. 1143-1154 ◽  
Author(s):  
M. Morris ◽  
S. M. McCann ◽  
R. Orias
Keyword(s):  
Sodium Excretion ◽  
Adrenergic Receptors ◽  
Male Rats ◽  
Intraventricular Injection ◽  
Urinary Volume ◽  
Electrolyte Excretion ◽  
Hypothalamic Control ◽  
Adrenergic Blocker ◽  
Β Receptor

Changes in urinary volume and electrolyte excretion were monitored after the injection of cholinergic and monoaminergic drugs into the third cerebral ventricle of conscious male rats made diuretic by an intravenous infusion of 5% dextrose. A natriuretic and kaliuretic response was induced by the intraventricular injection of norepinephrine (NE) or carbachol, whereas dopamine (DA) had no effect. The β-receptor stimulator isoproterenol (ISO) induced an antinatriuretic and antikaliuretic effect.Intraventricular injection of the α-adrenergic blocker phentolamine abolished the natriuretic response to NE and carbachol and to intraventricular hypertonic saline (HS). By contrast, the β-adrenergic blocker propranolol induced a natriuresis and kaliuresis when injected alone and an additive effect when its injection was followed by NE or HS. Propranolol potentiated the natriuretic response to carbachol. Cholinergic blockade with atropine diminished the response to NE and blocked the natriuretic response to HS. It is suggested that sodium receptors in the ventricular wall can modify renal sodium excretion via a stimulatory pathway involving cholinergic and α-adrenergic receptors and can inhibit sodium excretion via a tonically active β-receptor pathway.

The role of dentate gyrus dopaminergic receptors in the lateral hypothalamic-induced antinociception during persistent inflammatory pain in male rats

2021 ◽  
pp. 113434
Author(s):  
Farbod Torkamand ◽  
Ali-Mohammad Aghakhani-Lobnani ◽  
Hossein Khaleghzadeh-Ahangar ◽  
Mina Rashvand ◽  
Mohammad Rahban ◽  
...  
Keyword(s):  
Dentate Gyrus ◽  
Inflammatory Pain ◽  
Male Rats ◽  
Dopaminergic Receptors ◽  
Lateral Hypothalamic

scholarly journals A ketogenic diet reduces long-term potentiation in the dentate gyrus of freely behaving rats

2011 ◽  
Vol 106 (2) ◽  
pp. 662-666 ◽  
Author(s):  
Jessica L. Koranda ◽  
David N. Ruskin ◽  
Susan A. Masino ◽  
J. Harry Blaise
Keyword(s):  
Synaptic Plasticity ◽  
Dentate Gyrus ◽  
Ketogenic Diet ◽  
Long Term Potentiation ◽  
Male Rats ◽  
Ketogenic Diets ◽  
Neuronal Inhibition ◽  
Term Potentiation ◽  
Freely Behaving

Ketogenic diets are very low in carbohydrates and can reduce epileptic seizures significantly. This dietary therapy is particularly effective in pediatric and drug-resistant epilepsy. Hypothesized anticonvulsant mechanisms of ketogenic diets focus on increased inhibition and/or decreased excitability/excitation. Either of these consequences might not only reduce seizures, but also could affect normal brain function and synaptic plasticity. Here, we characterized effects of a ketogenic diet on hippocampal long-term potentiation, a widely studied form of synaptic plasticity. Adult male rats were placed on a control or ketogenic diet for 3 wk before recording. To maintain the most physiological conditions possible, we assessed synaptic transmission and plasticity using chronic in vivo recordings in freely behaving animals. Rats underwent stereotaxic surgery to chronically implant a recording electrode in the hippocampal dentate gyrus and a stimulating electrode in the perforant path; they recovered for 1 wk. After habituation and stable baseline recording, 5-Hz theta-burst stimulation was delivered to induce long-term potentiation. All animals showed successful plasticity, demonstrating that potentiation was not blocked by the ketogenic diet. Compared with rats fed a control diet, rats fed a ketogenic diet demonstrated significantly diminished long-term potentiation. This decreased potentiation lasted for at least 48 h. Reduced potentiation in ketogenic diet-fed rats is consistent with a general increase in neuronal inhibition (or decrease in excitability) and decreased seizure susceptibility. A better understanding of the effects of ketogenic diets on synaptic plasticity and learning is important, as diet-based therapy is often prescribed to children with epilepsy.

scholarly journals Role of prefrontal cortex projections to the nucleus accumbens core in mediating the effects of ceftriaxone on cued cocaine relapse

2020 ◽  
Author(s):  
Allison R. Bechard ◽  
Carly N. Logan ◽  
Javier Mesa ◽  
Yasmin Padovan Hernandez ◽  
Harrison Blount ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Nucleus Accumbens ◽  
Basolateral Amygdala ◽  
Male Rats ◽  
Self Administration ◽  
Nucleus Accumbens Core ◽  
Cocaine Seeking ◽  
Context Cues ◽  
Glutamate Efflux

AbstractCeftriaxone is an antibiotic that reliably attenuates the reinstatement of cocaine-seeking after extinction while preventing the nucleus accumbens (NA) core glutamate efflux that drives reinstatement. However, when rats undergo abstinence without extinction, ceftriaxone attenuates context-primed relapse but NA core glutamate efflux still increases. Here we sought to determine if the same would occur when relapse is prompted by both context and discrete cues (context+cues) after cocaine abstinence. Male rats self-administered intravenous cocaine for 2 hr/day for 2 weeks. Cocaine delivery was accompanied by drug-associated cues (light+tone). Rats were then placed into abstinence with daily handling but no extinction training for two weeks. Ceftriaxone (200 mg/kg IP) or vehicle was administered during the last 6 days of abstinence. During a context+cue relapse test, microdialysis procedures were conducted. Rats were perfused at the end of the test for later Fos analysis. A separate cohort of rats was infused with the retrograde tracer cholera toxin B in the NA core and underwent the same self-administration and relapse procedures. Ceftriaxone increased baseline glutamate and attenuated both context+cue-primed relapse and NA core glutamate efflux during this test. Ceftriaxone reduced Fos expression in regions sending projections to the NA core (prefrontal cortex, basolateral amygdala, ventral tegmental area) and specifically reduced Fos in prelimbic cortex and not infralimbic cortex neurons projecting to the NA core. Thus, when relapse is primed by drug-associated cues and context, ceftriaxone is able to attenuate relapse by preventing NA core glutamate efflux, likely through reducing activity in prelimbic NA core-projecting neurons.

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