Effects of administration of sertraline, clozapine, amitriptyline and imipramine on brain serotonin, liver enzymes and blood chemistry of rabbit

Ebuehi, Oat; Ikanone, C. E. O.; Balogun, AA; Akinwande, A. I.; Oo, Famuyiwa

doi:10.4314/ijbcs.v3i1.42739

Cited by 3 publications

(4 citation statements)

References 22 publications

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“…Serotonin does not cross the blood-brain barrier; however, it is abundantly present also in the peripheral tissues (e.g., gut), is accumulated by blood platelets, and uses the same transporter to cross membranes in the periphery as it does in the CNS. It has been shown that, following the fluoxetine administration, serotonin levels increase in blood plasma and serum (35,36) while they decrease in the platelets (36). The opposite result reached by Alvarez et al (37) may be due to difficulties entirely separating platelets and plasma (38).…”

Section: Discussionmentioning

confidence: 93%

“…SSRI drugs such as fluoxetine are commonly thought to function by inhibiting the serotonin transporter SERT, a membrane protein involved in the transport of neurotransmitter serotonin from the synaptic cleft, thereby changing the serotonin levels and persistence in the synaptic cleft (34). It has been shown that administration of the SSRI drug Sertraline for 28 d in rabbits increases the serotonin levels in brain (35). Serotonin does not cross the blood-brain barrier; however, it is abundantly present also in the peripheral tissues (e.g., gut), is accumulated by blood platelets, and uses the same transporter to cross membranes in the periphery as it does in the CNS.…”

Section: Discussionmentioning

confidence: 99%

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An experimental test of the ovulatory homolog model of female orgasm

Pavličev

Zupan

Barry

et al. 2019

Proc. Natl. Acad. Sci. U.S.A.

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The ovulatory homolog model of female orgasm posits that the neuro-endocrine mechanisms underlying female orgasm evolved from and are homologous to the mechanisms mediating copulation-induced ovulation in some mammals. This model predicts that pharmacological agents that affect human orgasm, such as fluoxetine, should also affect ovulation in animals with copulation-induced ovulation, such as rabbits. We tested this prediction by treating rabbits with daily doses of fluoxetine for 2 wk and found that fluoxetine treatment reduces the number of ovulations postcopulation by 30%. In a second experiment we tested whether this result was mediated by an effect on the brain or via peripheral serotonin functions. We treated animals with fluoxetine and induced ovulation with a single injection of human chorionic gonadotropin. In this experiment ovulation rate was nominally reduced by only 8%, which is statistically not significant. We conclude that the effect of fluoxetine on copulation-induced ovulation rate supports the ovulatory homolog model of female orgasm, suggesting that female orgasm has very deep evolutionary roots among the early eutherian mammals.

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

An experimental test of the ovulatory homolog model of female orgasm

Pavličev

Zupan

Barry

et al. 2019

Proc. Natl. Acad. Sci. U.S.A.

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“…One of the key factors on which brain function depends is the availability of neurotransmitter molecule for release into synapse, this alteration in the neurotransmitter scale may therefore underlie the functional deficit displayed by the protein malnourished groups. In addition, dopamine alteration perturbs neural encoding, this suggests a clinical association with other dysfunctions such as anxiety and psychosis (Ebuehi et al, 2001, 2009; Kelly et al, 2017). In malnutrition condition, free radicals mediate tissue damage, due to the inadequate protective and repair mechanisms in the protein-deficient models (Feoli et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Neurodevelopment and Cognitive Impairment in Parents and Progeny of Perinatal Dietary Protein Deficiency Models

2019

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There is an absolute dependence of the concept of development on supply of adequately balanced nutrients especially during the perinatal age which is critical to development. Therefore, an upgraded nutrition is specially required during gestation and lactation, as this is the critical period of neurodevelopment. This study sought to investigate the effect of protein deficiency during gestation (F0) and lactation through to adolescence on neurological functions of subsequent (F1 and F2) generations, establishing the possible consequential mechanistic association. Rats in four groups were fed different rations of protein diets (PD) as formulated: 21% PD, 10% PD, 5% PD and control diet (standard rat chow, containing 16–18% protein), from adolescent through to gestation and lactation, next generations were weaned to the maternal diet group. Neurobehavioral studies (which include; Surface righting reflex, Negative geotaxis, Learning and Memory tests), brain oxidative stress and quantification of serotonin and dopamine levels in the brain were conducted. Result shows significantly altered neurobehavior, reflected in the reduction of reflex response and postural reaction score at P ≤ 0.05. There was also a transgenerational cognitive impairment of brain function in the F-generations, following perinatal protein malnutrition as shown in the Y-maze result, measuring spatial memory and Morris water maze result (cognition), providing a background for the observed sensorimotor response. The significant increase in dopamine level, decrease in the antioxidant capacity of the protein deficient brain groups are consistent with significantly altered serotonin system, critical to neurodevelopment and functional activities of learning and memory. Therefore, persistent early life protein deficiency mediates dysfunction in neurodevelopment and this involves life-long changes in key neurotransmitters and the brain redox status underlying the neurobehavioral display.

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“…It is suggested that tricyclic drugs could reverse HVS in a physiological way through their improvement in brain serotonin and then subsequently be discontinued [31]. Ebuehi previously reported that malnutrition, marijuana smoking and ethanol consumption all decreased serotonin in experimental animals [32][33][34], while the tricyclic drugs (Impramine or amitriptyline) produces a more pronounced increase in brain serotonin levels compared with antidepressants such as sertraline [35]. These observations suggest that serotonin is important in the condition of HVS and offers a possible explanation for the observed benefits of amitriptyline.…”

Section: Discussionmentioning

confidence: 99%

The beneficial effects of oral amitriptyline in anxiety-induced hyperventilation syndrome; a case series

Varney¹,

Parnell²,

Quirke³

2016

Clin Case Rep Rev

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We describe 12 breathless patients all referred to respiratory outpatients where a final diagnosis of anxiety-induced chronic hyperventilation syndrome was made. Many had received treatments for asthma or COPD or cardiac disease without benefit and had attended their GP and A&E departments repeatedly without a clear diagnosis being made; despite raised oxygen saturations and respiratory rate at rest. Referrals to rapid access chest pain clinics were also common leading to multiple other investigations with yet further patient anxiety and prolonged periods away from work.The cases show that a clear diagnosis could have been made at the outset by a careful history particularly recognizing the circumstances at the onset of the condition, along with the presence of significant insomnia and anxiety-like symptoms with admission to panic if enquiries made.All cases responded promptly to oral amitriptyline that was commenced at 10 mg nocte and increased until full sleep was restored and hyperventilation ceased.In this case series we review the topic of anxiety-induced hyperventilation and discuss data suggesting that carbon-dioxide sensitivity in the brain-stem (respiratory centre) changes during slow wave sleep. Serotonergic neurons influence this, causing respiratory depression and tricyclic drugs enhance the activity of these neurons and are described to alleviate symptomatic hyperventilation by restoring slow wave sleep. This would be a reasonable treatment trial for doctors to commence in patients with insomnia and a picture of hyperventilation. It would be expected to give clinical improvement once the dose restores sleep, confirming the likely diagnosis and avoiding time away from work with protracted symptoms and possibly unwarranted investigations and referrals.

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Effects of administration of sertraline, clozapine, amitriptyline and imipramine on brain serotonin, liver enzymes and blood chemistry of rabbit

Cited by 3 publications

References 22 publications

An experimental test of the ovulatory homolog model of female orgasm

An experimental test of the ovulatory homolog model of female orgasm

Neurodevelopment and Cognitive Impairment in Parents and Progeny of Perinatal Dietary Protein Deficiency Models

The beneficial effects of oral amitriptyline in anxiety-induced hyperventilation syndrome; a case series

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