Nicotine exposure during adolescence: cognitive performance and brain gene expression in adult heterozygous reeler mice

Romano, Emilia; Angelis, Federica De; Ulbrich, Lisa; Jaco, Antonella De; Fuso, Andrea; Laviola, Giovanni

doi:10.1007/s00213-013-3388-y

Cited by 13 publications

(19 citation statements)

References 103 publications

(130 reference statements)

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“…While a complete summary is beyond the scope of this review, a number of papers have documented that adolescent nicotine results in persisting changes in signaling systems associated with synapses. Signaling systems with persisting changes include catecholaminergic (Trauth et al, 2001), serotonergic, and cholinergic systems , hippocampal and striatal cannabinoid CB1 and mu opiate receptors (Marco et al, 2007), adenylyl cyclase , and gene expression (Doura et al, 2008), including expression for reelin, GAD67, and BDNF (Romano et al, 2014). These may be merely associated with changes in robusticity of existing synapses, but these findings would also be consistent with the formation of new synapses.…”

Section: Adolescent Nicotine Synaptic Connectivity and Information mentioning

confidence: 93%

“…Spaeth et al (2010) found impairments in contextual fear conditioning after adolescent nicotine, consistent with the DG cell changes we (Ehlinger et al, 2012) have found. Romano et al (2014) reported persistent modulation of cognition in mice, along with increased BDNF mRNA expression after adolescent nicotine. Mateos et al (2012) reported persisting effects on memory of adolescent nicotine (or a cannabinoid agonist), tested in the novel object test.…”

Section: Cognitionmentioning

confidence: 99%

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Adolescent nicotine induces persisting changes in development of neural connectivity

Smith

McDonald

Bergstrom

et al. 2015

Neuroscience & Biobehavioral Reviews

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Section: Adolescent Nicotine Synaptic Connectivity and Information mentioning

confidence: 93%

Section: Cognitionmentioning

confidence: 99%

Adolescent nicotine induces persisting changes in development of neural connectivity

Smith

McDonald

Bergstrom

et al. 2015

Neuroscience & Biobehavioral Reviews

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“…Long term behavioral effects and molecular changes in brain mechanisms are resultant from nicotine exposure either through smoke or tobacco chewing. This is often evident and prominent in the adolescence humans (Romano et al, 2013). Depression is a characteristic long term behavior that may result from nicotine addiction (van der Meer et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Smoke and ethanolic extract of nicotiana tabacum altered hippocampal histology and behaviour in mice

Adeniyi¹,

Ogundele²

2014

J. Cell Anim. Biol.

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The effects of tobacco use on human health are well known and are documented in scientific reports. When tobacco is smoked or chewed, nicotine is absorbed by the lungs and oral cavity and quickly moved into the bloodstream where it is distributed rapidly through the circulatory system to reach the brain and peripheral nervous system. Male and female adult mice (N=32) were used for this study. The animals were randomly divided in to four (4) groups, A, B, C and D, of eight (n=8) animals each. Group A animals were treated by oral administration of 10.72 mg of the extract, B 10.72 mg of the tobacco smoke exposure for 3 min (in a controlled air chamber), C were given 0.2 ml of normal saline and D were expose to equal weight (0.02 g) of cotton wool for 3 min, for 21 experimental days. The mice were sacrificed 4 h after the last administration and the brains excised, blotted, weighed and fixed in formol calcium for histological analysis, using Haematoxylin and Eosin. There was a significant decrease in the body weight, brain weight and relative brain weight in the treatment groups. The pyramidal and granular cell layers showed changes in cell count scores; significant at p<0.05 when compared with the control. The results suggested that the consumption of Nicotiana tabacum leaves; either smoking or chewing may lead to alterations in cell count, brain weight and neurobehavioral patterns. Weight loss was also observed in the treatment and was found to be dependent on the route of administration.

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“…In adolescent heterozygous reeler mice, subchronic (6 day) nicotine free choice drinking ameliorates hyperlocomotion, perseverative behaviour and cognitive impairment [138,139]. Furthermore, in heterozygous reeler mice, subchronic nicotine restores mRNA levels of reelin and GAD67 in the cortex, hippocampus, striatum and cerebellum to WT-like levels [138,139]. Together, this suggests protective effects of subchronic nicotine in the heterozygous reeler mouse.…”

Section: Nicotinementioning

confidence: 95%

“…Reelin deficits have been observed in schizophrenia [132], and heterozygous reeler mice exhibit hyperlocomotion, PPI and cognitive deficits, and perseverative behaviour [133][134][135], as well as a loss of Purkinje cells of the cerebellum, which is also observed in patients with schizophrenia [136,137]. In adolescent heterozygous reeler mice, subchronic (6 day) nicotine free choice drinking ameliorates hyperlocomotion, perseverative behaviour and cognitive impairment [138,139]. Furthermore, in heterozygous reeler mice, subchronic nicotine restores mRNA levels of reelin and GAD67 in the cortex, hippocampus, striatum and cerebellum to WT-like levels [138,139].…”

Section: Nicotinementioning

confidence: 99%

Schizophrenia and drug addiction comorbidity: recent advances in our understanding of behavioural susceptibility and neural mechanisms

Menne

Chesworth

2020

Neuroanatomy and Behaviour

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Schizophrenia is a severe psychiatric disorder which is worsened substantially by substance abuse/addiction. Substance abuse affects nearly 50% of individuals with schizophrenia, extends across several drug classes (e.g. nicotine, cannabinoids, ethanol, psychostimulants) and worsens overall functioning of patients. Prominent theories explaining schizophrenia and addiction comorbidity include the primary addiction hypothesis (i.e. schizophrenia susceptibility primes drug reward circuits, increasing drug addiction risk following drug exposure), the two-hit hypothesis (i.e. drug abuse and other genetic and/or environmental risk factors contribute to schizophrenia development) and the self-medication hypothesis (i.e. drug use alleviates schizophrenia symptoms). Animal models can be used to evaluate the utility and validity of these theories. Since this literature was last reviewed by Ng and colleagues in 2013 [Neurosci Biobehav Rev, 37(5)], significant advances have been made to our understanding of schizophrenia and substance abuse comorbidity. Here we review advances in the field since 2013, focussing on two key questions: 1) Does schizophrenia susceptibility increase susceptibility to drug addiction (assessing the primary addiction hypothesis), and 2) Do abused drugs exacerbate or ameliorate schizophrenia symptoms (assessing the two-hit hypothesis and the self-medication hypothesis). We addressed these questions using data from several schizophrenia preclinical models (e.g. genetic, lesion, neurodevelopmental, pharmacological) across drug classes (e.g. nicotine, cannabinoids, ethanol, psychostimulants). We conclude that addiction-like behaviour is present in several preclinical schizophrenia models, and drugs of abuse can exacerbate but also ameliorate schizophrenia-relevant behaviours. These behavioural changes are associated with altered receptor system function (e.g. dopaminergic, glutamatergic, GABAergic) critically implicated in schizophrenia and addiction pathology.

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Nicotine exposure during adolescence: cognitive performance and brain gene expression in adult heterozygous reeler mice

Abstract: These findings support the hypothesis of pre-existing vulnerability (based on haploinsufficiency of reelin) to brain and behavioral disorders and regulative short- and long-term effects associated with nicotine modulation.

Cited by 13 publications

References 103 publications

Adolescent nicotine induces persisting changes in development of neural connectivity

Adolescent nicotine induces persisting changes in development of neural connectivity

Smoke and ethanolic extract of nicotiana tabacum altered hippocampal histology and behaviour in mice

Schizophrenia and drug addiction comorbidity: recent advances in our understanding of behavioural susceptibility and neural mechanisms

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