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Pineal Function
Published in Nate F. Cardarelli, The Thymus in Health and Senescence, 2019
N-acetyltransferase (NAT) is probably the rate-limiting step in melatonin synthesis.149 It catalyzes the serotonin-N-acetylserotonin reaction.150 NAT is found in the retina and apparently acts in the same manner.69 Both ocular and pineal NAT show a diurnal rhythm.66,69,70,149,151–153 NAT also is under feedback regulation.154 Cultured chick pineal glands under diurnal illumination show a diurnal NAT cycle.151 The NAT cycle is age dependent. NAT output from neonatal rat pineal in vitro will rise spontaneously under dark conditions, whereas adult rat glands in culture will not do so unless chemically stimulated.155 Administration of lithium chloride over a 5-week period suppressed NAT diurnal amplitude and may delay the peak of the cycle.156 Exposure of intact or blinded chicks to white light during the dark period led to a very rapid drop, a four- to fivefold decrease, T½ = 10 min of NAT in intact chicks, and a less severe decrease in blinded ones, indicating retinal involvement.152 Wild rats also show a rapid NAT decrease under similar experimental conditions, with a T½ = 2 min.157 The effect was noted at irradiance levels between 300 µW/cm2 and 0.01 µW/cm2 At 0.005 µW/cm2 there was no change.
Experimental Models of Status Epilepticus
Published in Steven L. Peterson, Timothy E. Albertson, Neuropharmacology Methods in Epilepsy Research, 2019
Pilocarpine at a dose of 400 mg/kg (i.p. or s.c.) does not always induce SE. In an attempt to enhance the action of pilocarpine several investigators pretreat animals with lithium chloride. Lithium chloride (Sigma, St. Louis, MO) is injected (3 mEq/kg or 3 mM/kg, i.p.) 19 to 24 h prior to the administration of a significantly lower dose of pilocarpine (25 to 30 mg/kg).13,80-84 Pretreatment with lithium chloride appears to potentiate the effect of pilocarpine, since lithium in combination with a 30 mg/kg dose of pilocarpine consistently induced SE.13,80-82 Behavioral and electrographic seizure activity and accompanying neuropathology after the combination of lithium and low-dose pilocarpine is the same as that observed after high-dose pilocarpine alone.13 There is less variability in the time of onset of behavioral seizures and an increase in the number of animals that go into SE with the combination of lithium and low-dose pilocarpine. Atropine sulfate pretreatment of lithium-treated rats blocks pilocarpine-induced seizures, suggesting cholinergic activation is still necessary for SE to occur. Neither lithium at 3 mM/kg or pilocarpine at a dose of 30 mg/kg when administered by themselves induced seizure activity.13,80
Physiology
Published in Stephen W. Carmichael, Susan L. Stoddard, The Adrenal Medulla 1986 - 1988, 2017
Stephen W. Carmichael, Susan L. Stoddard
O’Connor, Naylor, Cox et al. (1988) found that daily, intraperitoneal injections of lithium chloride significantly lowered systolic blood pressure in SHR rats but were without effect in WKY rats. In contrast, adrenal medullary epinephrine and norepinephrine values were significantly increased in lithium chloride-treated rats of both strains. The authors concluded that the antihypertensive effects of lithium chloride are independent of its action on adrenal medullary catecholamines.
Lithium upregulates growth-associated protein-43 (GAP-43) and postsynaptic density-95 (PSD-95) in cultured neurons exposed to oxygen-glucose deprivation and improves electrophysiological outcomes in rats subjected to transient focal cerebral ischemia following a long-term recovery period
Published in Neurological Research, 2022
Shih-Huang Tai, Sheng-Yang Huang, Liang-Chun Chao, Yu-Wen Lin, Chien-Chih Huang, Tian-Shung Wu, Yan-Shen Shan, Ai-Hua Lee, E-Jian Lee
The animal model was induced by intra-arterial suture occlusion of the proximal right middle cerebral artery (MCA), as described previously [15–18]. Briefly, a 4–0 nylon suture with its tip rounded by heating over a flame and subsequently coated with silicone (Merck KGaA, Darmstadt, Germany) was inserted from the external carotid artery into the internal carotid artery until the tip occluded the origin of the MCA. After 90 min, the suture was removed and reperfusion occurred. Laser Doppler flowmetry (LDF, Laserflo BMP2; Vasamedics, St Paul, MN, USA) was used for local cortical blood perfusion (LCBF) measurements. The LDF probes (model P436) were placed on two 1.5 mm diameter areas over bilateral parietal bones (AP −0.5 mm, ML 7 mm). The measured region was close to the core of the infarction caused by MCA occlusion (MCAO) on the operated side (right side). Another 1.5 mm diameter area over the right parietal bone (AP −2.0 mm, ML 2.5 mm) was thinned for additional LCBF measurements. This area has been identified as a representative ischemic penumbral area based on previous studies [19–21] and a rat brain atlas [22] for cerebral blood flow measurements. LCBF was serially measured before and during the MCAO, after a brief reperfusion period, and at 30 min after reperfusion onset. Animals were randomly assigned to the lithium treatment or control group. Lithium chloride was dissolved in normal saline (0.9% w/v) for administration. Lithium (1 mEq/kg) or vehicle (saline) was delivered through intraperitoneal injection to rats at 24, 48, and 72 h after reperfusion onset.
Neuroprotective Effect of Intravitreal Single-Dose Lithium Chloride after Optic Nerve Injury in Rats
Published in Current Eye Research, 2021
Moein Ala, Razieh Mohammad Jafari, Hossein Nematian, Mohammad Reza Ganjedanesh, Asieh Naderi, Mostafa Akbariani, Mehdi Sanatkar, Leila Satarian, Masoud Aghsaei Fard, Ahmad Reza Dehpour
While lithium is an old drug used for bipolar disorder, the results of neuroscience studies suggest that it can offer some protective effects on nervous system such as anti-inflammation, angiogenesis, neurogenesis, blood-brain barrier integrity preservation, and disease-specific neuroprotection.7 Lithium has those neuroprotective effects by inhibiting glycogen synthase kinase-3 (GSK-3β), modulating the excitotoxic response, regulating autophagy, expression of Bcl-2 and modulating neuronal growth factor.8 Inhibition of GSK-3β activates the β-catenin pathway9 which is known to improve cell viability and increase their resistance to death. This function of lithium chloride contributes to inhibit neurodegeneration and helps management of cognitive disorders.10
Glycyrrhizic acid renders robust neuroprotection in rodent model of vascular dementia by controlling oxidative stress and curtailing cytochrome-c release
Published in Nutritional Neuroscience, 2020
Yogeshkanna Sathyamoorthy, Kathiravan Kaliappan, Pradeepkumar Nambi, Rameshkumar Radhakrishnan
CCH was modelled using the two-vessel occlusion method (2VO) through permanent bilateral common carotid artery occlusion (bCCAO) [19]. The rats were anesthetized by 5% isoflurane in oxygen for induction and 2% for maintenance. For the sham group the above mentioned surgical procedures were performed, except bCCAO, moreover, the sham rats do not receive any vehicle. This study includes four experimental groups (n = 12), i.e. (i) Sham, (ii) CCH and (iii) GA treated- administration of GA (dissolved in distilled water) at a dosage of 20 mg/kg body weight intraperitoneally for 30 days daily following bCCAO, (iv) Li treated- administration of lithium chloride (dissolved in distilled water) at a dosage of 40 mg/kg body weight intraperitoneally for 30 days daily following bCCAO. Lithium chloride is a standard compound used for inhibition of GSK3β and thus could be used to compare GSK3β modulating effects of GA. After surgical procedures rats were maintained for a week under proper post-operative care.