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PubMed2006

Determinants of the rate of nicotine metabolism and effects on smoking behavior.

BACKGROUND: Studies on cytochrome P450 (CYP) 2A6 suggest that genotype affects the rate of nicotine metabolism and, consequently, cigarette consumption. However, known alleles of CYP2A6 associated with fast or slow metabolism are relatively uncommon, and there remains considerable variation in metabolic activity among those with presumed wild-type CYP2A6 alleles, suggesting that other genetic or environmental factors also influence the rate of nicotine metabolism. METHODS: We investigated determinants of the rate of nicotine metabolism and effects on smoking behavior in a United Kingdom cohort who participated in a placebo-controlled trial of smoking cessation via nicotine replacement therapy. Those who continued to smoke cigarettes at the 8-year follow-up formed our study group (N = 545). The ratio of the nicotine metabolite trans-3'-hydroxycotinine to cotinine in plasma was used as an index of CYP2A6 activity and thus as a marker of the rate of nicotine metabolism. RESULTS: The nicotine metabolite ratio was associated with sex (P < .0001), CYP2A6 genotype (*1B, *2, *4, *9, and *12) (P < .0001), CYP2B6 haplotype (*4-dominant) (P = .02), plasma nicotine concentration (P < .0001), and age (P = .02) but was not associated with dependence score (P > .20). The ratio also predicted the number of cigarettes smoked at will per day, although the association was weak (F(1, 492) = 4.05, P = .04). CONCLUSION: In this cohort the rate of nicotine metabolism is related to age, sex, CYP2A6 genotype, and CYP2B6 genotype and may affect the level of tobacco consumption.

Adult↗
PubMed2006

Effect of grapefruit juice on cytochrome P450 2A6 and nicotine renal clearance.

BACKGROUND AND OBJECTIVE: Grapefruit juice is an inhibitor of the cytochrome P450 (CYP) 3A4 enzyme and transporters such as P-glycoprotein and organic anion transporting polypeptides, leading to clinically important interactions. Our objective was to study the effect of grapefruit juice on the pharmacokinetics of nicotine, which is primarily metabolized by the CYP2A6 enzyme. METHODS: Ten volunteers were given a 2-mg oral dose of deuterium-labeled nicotine on 3 occasions together with 1 L of water, full-strength grapefruit juice, or half-strength grapefruit juice. Concentrations of nicotine and its metabolites were analyzed in plasma and urine for 8 hours. RESULTS: Grapefruit juice inhibited the formation of cotinine from nicotine (area under the plasma cotinine concentration-time curve from 0 to 8 hours of 6807 min.ng/mL, 7805 min.ng/mL, and 8007 min.ng/mL for full-strength grapefruit juice, half-strength grapefruit juice, and water, respectively; repeated-measures ANOVA, P=.009). The time to peak plasma concentration of cotinine was delayed (216 minutes, 159 minutes, and 147 minutes, respectively; ANOVA, P=.011), and the peak plasma concentration was lower with grapefruit juice compared with water (18 ng/mL, 21 ng/mL, and 22 ng/mL, respectively; ANOVA, P=.010). Oral clearance, peak plasma concentration, and time to peak plasma concentration of nicotine were not affected. Grapefruit juice increased the renal clearance of nicotine (231 mL/min, 219 mL/min, and 123 mL/min, respectively; ANOVA, P=.045) and cotinine (19 mL/min, 14 mL/min, and 16 mL/min, respectively; ANOVA, P=.002). CONCLUSIONS: Grapefruit juice inhibits the metabolism of nicotine to cotinine, a pathway mediated by CYP2A6, and increases the renal clearance of nicotine and cotinine. Nicotine oral clearance is not affected by grapefruit juice because the inhibition of hepatic metabolism is offset by the increase in the renal clearance of nicotine. However, other compounds metabolized by CYP2A6, as well as other drugs excreted via renal clearance mechanisms similar to those of nicotine, may be susceptible to significant pharmacokinetic grapefruit juice interactions.

Administration, Oral↗
PubMed2006

CYP2A6 genotype and the metabolism and disposition kinetics of nicotine.

BACKGROUND AND OBJECTIVE: The liver enzyme cytochrome P450 (CYP) 2A6 is primarily responsible for the metabolism of nicotine. Variants in the CYP2A6 gene have been associated with altered nicotine metabolism and with effects on smoking behavior. Our objective was to determine the relationship between variant CYP2A6 genotypes and the disposition and metabolism of nicotine administered intravenously. METHODS: Intravenous infusions of deuterium-labeled nicotine and cotinine were administered to 278 healthy twin volunteers, most of whom were white. They were genotyped for CYP2A6*1, CYP2A6*2, CYP2A6*4, CYP2A6*7, CYP2A6*8, CYP2A6*9, CYP2A6*10, and CYP2A6*12. RESULTS: On the basis of the fractional clearance of nicotine to cotinine and on the plasma ratio of 3'-hydroxycotinine to cotinine, both shown to be indicators of CYP2A6 enzymatic activity, subjects were classified into 3 groups. Group 1 included wild-type variant CYP2A6*1/*1 (n=215) and was assumed to have 100% activity. Group 2 included *1/*9 (n=21) and *1/*12 (n=12), which averaged about 80% of normal activity. Group 3 included *1/*2 (n=10), *1/*4 (n=2), *9/*12 (n=3), *9/*4 (n=2), and *9/*9 (n=3), which averaged about 50% of normal activity. The mean total plasma clearance of nicotine (+/-SD) was 18.8+/-6.0, 15.5+/-4.9, and 11.7+/-5.1 mL.min-1.kg-1 in groups 1, 2, and 3, respectively, and group 1 had significantly faster clearance than group 2 (P<.05) and group 3 (P<.01). Overall, groups 2 and 3 also had lower total clearance of cotinine, had longer half-lives for nicotine and cotinine, and excreted in the urine a greater fraction of the nicotine dose as unchanged nicotine and nicotine glucuronide and excreted less as 3'-hydroxycotinine compared with group 1. CONCLUSIONS: We provide novel pharmacokinetic and metabolic data on nicotine after systemic dosing in relation to common CYP2A6 genotypes. Our data will enhance the interpretation of CYP2A6 genotypic data as used in association studies of smoking behavior and its health consequences.

Adolescent↗
PubMed2003

Comprehensive deficits in performance of an attentional task produced by co-administering alcohol and nicotine to rats.

BACKGROUND: Nicotine can improve and alcohol can impair attentional performance in rats, but little is known about the effects of mixtures of the two drugs with respect to attention. AIMS: The aims were to investigate the effects of alcohol and nicotine alone and when co-administered on performance of a five-choice serial reaction time task, and to examine the impact of task difficulty by varying durations of the limited hold (LH) for availability of the reinforcer. METHODS: Male hooded rats were trained to respond (nose-poke) to a 0.5 s light stimulus presented randomly in one of five apertures to obtain food reinforcers. Three groups of rats trained with different LH values were used (n = 10). RESULTS: The first experiment showed that training at different LH values had little effect on performance when the LH value during testing was held constant. Experiment 2 showed that alcohol (0.4-1.6 g/kg, i.p.) had no effect on the percentage of correct responses (accuracy) but it impaired all speed-related indices. In the third experiment, the effects of nicotine (0.1 and 0.2 mg/kg, s.c.) were determined alone and on the dose-response curve for alcohol (0.4-1.2 g/kg, i.p.). Nicotine alone produced small improvements in performance whereas co-administration of nicotine and alcohol produced large decrements at doses of alcohol that themselves only slightly impaired performance. These decrements included impairments of accuracy as well as of anticipatory responding, omission errors, response latencies and reinforcers earned. There were no marked or consistent interactions of drug effects with LH values. CONCLUSIONS: Task performance was disrupted to a much greater extent by co-administration of alcohol and nicotine than by alcohol alone; therefore, it seems unlikely that an ability of nicotine to reverse the effects of alcohol can account for associations between the use of the two substances.

Animals↗
PubMed2006

Non-treatment-seeking heavy drinkers: effects of chronic cigarette smoking on brain structure.

We previously reported [Cardenas, V.A., Studholme, C., Meyerhoff, D.J., Song, E., Weiner, M.W., 2005. Chronic active heavy drinking and family history of problem drinking modulate regional brain tissue volumes. Psychiatry Res. 138, 115-130] that non-treatment-seeking, active heavy drinkers (HD) demonstrated smaller regional neocortical gray matter volumes compared to light drinking controls; however, the potential effects of chronic cigarette smoking on regional brain volumes were not addressed. The goal of this retrospective analysis was to determine if chronic smoking affected brain structure in the non-treatment-seeking heavy drinking sample from our earlier report (i.e., Cardenas et al., 2005). Regional volumetric comparisons were made among age-matched smoking HD (n=17), non-smoking HD (n=16), and non-smoking light drinkers (nsLD; n=20) from our original sample. Quantitative volumetric measures of neocortical gray matter (GM), white matter (WM), subcortical structures, and cerebral spinal fluid (CSF) were derived from high-resolution magnetic resonance imaging. Smoking HD demonstrated smaller volumes than nsLD in the frontal, parietal, temporal GM, and for total neocortical GM. Smoking HD also demonstrated smaller temporal and total GM volumes than non-smoking HD. Non-smoking HD and nsLD did not differ significantly on GM volumes. Further, the three groups did not differ on lobar WM, subcortical structures or regional CSF volumes. These retrospective analyses indicate neocortical GM volume reductions in non-treatment-seeking smoking HD, but not in non-smoking HD, which are consistent with our studies in recently detoxified treatment-seeking alcohol-dependent samples.

Adult↗
PubMed2003

Pre- and postsynaptic dopamine mechanisms after repeated nicotine: effects of adrenalectomy.

The reinforcing properties of nicotine may be related to its ability to release dopamine in the nucleus accumbens and to increase locomotor activity in experimental animals. Both these effects are sensitized following repeated drug exposure, a phenomenon that may underlie important aspects of addiction. Adrenal steroids may be involved both in positive reinforcement and in sensitization. Adrenalectomy hampers, e.g., the induction of locomotor sensitization to nicotine, and cross-sensitization between stress and psychostimulants may develop. Here, the effect of adrenalectomy on postsynaptic and presynaptic changes of the mesolimbic dopamine system in association with nicotine sensitization was examined. Adrenalectomy or sham-operated rats received daily nicotine (0.4 mg/kg s.c.) or vehicle for 15 days, after which the locomotor responses to nicotine (0.2 mg/kg s.c.) and the dopamine D1/D2 receptor agonist apomorphine (1.0 mg/kg s.c. or 100 microM in the nucleus accumbens by reversed microdialysis) were recorded. In addition, accumbal dopamine output was monitored by in vivo microdialysis after nicotine challenge. Sham/nicotine animals showed a sensitized locomotor response to systemic and local apomorphine compared to all other groups, including the adrenalectomized/nicotine group. Nicotine increased accumbal dopamine output in all animals. In contrast, nicotine induced a pronounced increase in locomotor activity in the sham/nicotine animals compared to the other vehicle group and the adrenalectomized animals. These results indicate that adrenal steroids are involved in the induction of the postsynaptic component of nicotine sensitization, whereas their involvement in tentative presynaptic changes remains unclear.

Adrenalectomy↗
PubMed2005

Extended blockade of the discriminative stimulus effects of nicotine with low doses of ethanol.

The aim of the present study was to further evaluate effects of ethanol on nicotine discrimination and to correlate these effects with blood ethanol levels. Rats were trained to discriminate 0.3 mg/kg nicotine from its vehicle in the standard two-lever operant procedure. In antagonism tests, small doses of ethanol (0.25-0.5 g/kg) were injected either 5 or 50 min before nicotine. Both doses of ethanol partially antagonized the nicotine cue regardless of the pre-treatment time. Ethanol attenuated also inhibitory effects of nicotine on the rate of responding. Suppression of the cueing effects of nicotine was noted even 60 min after the injection of 0.25 g/kg ethanol, i.e. at the time point when the blood ethanol level was close to zero. Ethanol-induced antagonism of the nicotine cue disappeared when longer time (110 min) was allowed to elapse between the ethanol (0.5 g/kg) and nicotine injection. Concluding, the present results may indicate that the effects of ethanol on nicotine discrimination are not primarily related to blood ethanol levels.

Animals↗
PubMed2006

Potentiation of nicotinic currents by bradykinin in the paratracheal ganglia neurons of rats.

The effects of bradykinin on nicotine-induced responses were investigated in neurons dissociated from rat paratracheal ganglia using the nystatin-perforated patch-clamp recording technique. When bradykinin (10(-9) to 10(-8) M) was pretreated and then simultaneously applied with 10(-5) M nicotine, bradykinin potentiated the nicotine-induced currents. The potentiation was mimicked by [Hyp3]-bradykinin and inhibited by HOE-140, pertussis toxin, neomycin and U-73122, but not U-73433. These results suggest that bradykinin potentiates nicotinic currents via bradykinin B2 receptor, pertussis toxin-sensitive G-protein and phospholipase C. Since bradykinin inhibits the M-current via bradykinin B2 receptor and pertussis toxin-insensitive G-protein [Mochidome, T., Ishibashi, H., Takahama, K., 2001. Bradykinin activates airway parasympathetic ganglion neurons by inhibiting M-currents. Neuroscience 105, 785-791.], it seemed that bradykinin B2 receptor activated two distinct signal transduction pathways in the paratracheal ganglia neurons. This effect of bradykinin might cause enhanced synaptic transmission in paratracheal ganglia neurons and contribute to the aggravation of pathological conditions of the lower airway via enhanced acetylcholine release from the postganglionic nerve terminals.

Animals↗
PubMed2006

Effect of quinpirole on striatal dopamine release and locomotor activity in nicotine-treated mice.

The effect of chronic oral nicotine treatment which in its intermittent delivery resembles human smoking was studied on the sensitivity of dopamine autoreceptors in mice. On the 50th day of nicotine administration in the drinking water or after 23-25 h withdrawal quinpirole (D2/D3 agonist, 0.01-0.1 mg/kg s.c.) was given, and accumbal and dorsal striatal dopamine outflow, locomotor activity and body temperature were measured. Dorsal striatal extracellular dopamine concentration and locomotor activity were found to be elevated during nicotine administration. Chronic nicotine did not alter the effects of small, autoreceptor preferring doses of quinpirole on accumbal or dorsal striatal dopamine, locomotor activity or body temperature. However, quinpirole's locomotor activity reducing effect was slightly diminished in mice treated repeatedly with nicotine (0.4 mg/kg twice daily for 10 days s.c.). Thus, although repeated nicotine treatment for 5-14 days decreases dopamine autoreceptor sensitivity, after long-term oral nicotine treatment such a decrease is not seen. Thus, the changes occurring in the sensitivity of D2-like dopamine receptors probably play a minor role in regulating the dopaminergic transmission during long-term nicotine administration.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2006

Activation of orexin neurons by acute nicotine.

The hypothalamus is a prominent central site of action of nicotine but the phenotype of nicotine-sensitive neurons in this region has not been fully described. Hypothalamic orexin neurons are important regulators of state-dependent behavior, arousal and feeding. Here, we treated rats with acute nicotine and quantitated Fos expression as a marker of neuronal activation. Nicotine increased the percentage of orexin neurons expressing Fos without a significant effect on non-orexin neurons. This effect was attenuated by the nicotinic antagonists mecamylamine and dihydro-beta-erythroidine, implicating alpha4beta2-containing nicotinic receptors. The orexin system is likely to play an important role in the coordination of physiological and behavioral responses to acute nicotine treatment.

Animals↗
PubMed2006

Influence of ATP-dependent K+ channels on nicotine-induced inhibition of withdrawal in morphine-dependent mice.

In the present study, we have investigated the effect of nicotine and diazoxide, a potassium channel opener and glibenclamide, a potassium channel (K(ATP)) blocker on naloxone-precipitated physical withdrawal signs, including jumping and diarrhea. Then, the interactions of nicotine with diazoxide and glibenclamide were tested. Mice were rendered dependent on morphine by subcutaneous (s.c.) injections of morphine sulphate 3 times a day for 3 days, and jumping behavior and diarrhea were induced by intraperitoneal (i.p.) administration of naloxone 2 h after the 10th injection of morphine sulphate on day 4. Nicotine was administered 15 min and diazoxide and glibenclamide 30 min before naloxone injection. Nicotine (0.01-1 mg/kg, s.c.) and (0.1-1 mg/kg) reduced withdrawal jumping and diarrhea respectively. Diazoxide (8-64 mg/kg, i.p.) decreased jumping behavior significantly, but had no significant effect on diarrhea. On the other hand glibenclamide (0.25-1 mg/kg i.p.) and (1 mg/kg) augmented jumping and diarrhea respectively. The response of nicotine on jumping or on diarrhea was potentiated by diazoxide and decreased by glibenclamide pretreatment. The isobolographic analysis revealed synergistic interaction between diazoxide and nicotine on decreasing physical withdrawal signs including jumping and diarrhea in morphine-dependent mice. According to these results the interaction of nicotine with the K(ATP) channel opener and blocker in morphine physical withdrawal signs could be explained by direct and indirect effects of nicotine on membrane potassium currents.

Adenosine Triphosphate↗
PubMed2006

Nicotine increases dopamine transporter function in rat striatum through a trafficking-independent mechanism.

In previous in vivo voltammetry studies, acute nicotine administration increased striatal dopamine clearance. The current study aimed to determine whether nicotine also increases [(3)H]dopamine uptake across the time course of the previous voltammetry studies and whether dopamine transporter trafficking to the cell surface mediates the nicotine-induced augmentation of dopamine clearance in striatum. Rats were administered nicotine (0.32 mg/kg, s.c.); striatal synaptosomes were obtained 5, 10, 40 or 60 min later. Nicotine increased (25%) the V(max) of [(3)H]dopamine uptake at 10 and 40 min. To determine whether the increase in V(max) was due to an increase in dopamine transporter density, [(3)H]GBR 12935 (1-(2-[bis(4-fluorophenyl)methoxy]ethyl)-4-(3-phenylpropyl)piperazine dihydrochloride) binding was performed using rat striatal membranes; no differences were found between nicotine and saline-control groups at 5, 10 or 40 min post-injection, indicating that nicotine did not increase striatal dopamine transporter density; however, [(3)H]GBR 12935 binding assays determine both cell surface and intracellular dopamine transporter. Changes in cellular dopamine transporter localization in striatum were determined using biotinylation and subfractionation approaches; no differences between nicotine and saline-control groups were observed at 10 and 40 min post-injection. These results suggest that the nicotine-induced increase in dopamine uptake and clearance in striatum may occur via a trafficking-independent mechanism.

Animals↗
PubMed2006

Effects of nicotine and vitamin E on glutathione reductase activity in some rat tissues in vivo and in vitro.

Effects of nicotine, and nicotine+vitamin E on glutathione reductase (Glutathione: NADP(+) oxidoreductase, EC 1.8.1.7) activity in the muscle, heart, lungs, testicles, kidney, stomach, brain and liver tissues were investigated in vivo and also in vitro. The groups were: nicotine [0.5 mg/kg/day, intraperitoneal (i.p.)]; nicotine+vitamin E [75 mg/kg/day, intragastric (i.g.)]; and control group (receiving only vehicles). There were eight rats per group and supplementation period was 3 weeks. The results showed that nicotine (0.5 mg/kg, i.p.) inhibited glutathione reductase activity significantly in the liver, lungs, heart, stomach, kidney, and testicles by approximately 61.5%, approximately 65%, approximately 70.5%, approximately 72.5%, approximately 64% and approximately 71.5%, respectively, while it had activated glutathione reductase activity in the brain by approximately 11.8%, and had no effect on the muscle glutathione reductase activity. Vitamin E supplementation prevented this nicotine-induced decrease in glutathione reductase activity in liver, lungs, heart, stomach, and kidney. However, it did not prevent this nicotine-induced decrease in testicles. In vitro studies were also carried out to elucidate the effects of nicotine and vitamin E on glutathione reductase activity. In vitro results correlated well with in vivo experimental results in liver, lungs, heart, stomach, and testicular tissues. These results show that vitamin E administration generally restores the inactivation of glutathione reductase activity due to nicotine administration in various rat tissues in vivo, and also in vitro.

Animals↗
PubMed2006

Interactive effects of the mGlu5 receptor antagonist MPEP and the mGlu2/3 receptor antagonist LY341495 on nicotine self-administration and reward deficits associated with nicotine withdrawal in rats.

Stimulatory actions of nicotine on mesocorticolimbic dopamine transmission are partly mediated by nicotine-induced glutamate release acting on ionotropic and metabotropic glutamate (mGlu) receptors. Because both presynaptic inhibitory mGlu2/3 and postsynaptic excitatory mGlu5 receptors provide potential targets for treatment of aspects of nicotine dependence, we examined interacting effects of mGlu5 (2-methyl-6-(phenylethynyl)-pyridine, MPEP) and mGlu2/3 (LY341495) receptor antagonists on nicotine self-administration and brain reward threshold elevations associated with spontaneous nicotine withdrawal in rats. We hypothesized that increasing glutamate transmission by blocking presynaptic inhibitory mGlu2/3 autoreceptors would antagonize MPEP-induced decreases in nicotine self-administration. We also hypothesized that blocking postsynaptic actions of glutamate on mGlu5 receptors would exacerbate nicotine withdrawal-induced reward deficits, and that this effect would be attenuated by co-administration of the mGlu2/3 receptor antagonist LY341495. MPEP selectively decreased nicotine, but not food, self-administration in rats. LY341495 slightly decreased both nicotine and food self-administration. Co-administration of LY341495 with MPEP attenuated the effectiveness of MPEP in decreasing nicotine intake, although MPEP was still effective. Spontaneous nicotine withdrawal induced somatic signs of withdrawal and reward threshold elevations indicating reward deficits. MPEP increased somatic signs and reward deficits in both nicotine- and saline-withdrawing rats. Thus, while mGlu5 receptor antagonists may be therapeutically useful in decreasing tobacco smoking, they worsen nicotine withdrawal. Co-administration of LY341495 reduced MPEP-induced reward deficits in both nicotine- and saline-withdrawing rats. Thus, increasing glutamate transmission via mGlu2/3 autoreceptor blockade reduces the effects of mGlu5 receptor blockade on nicotine self-administration and MPEP-induced exacerbation of brain reward deficits associated with nicotine withdrawal.

Amino Acids↗
PubMed2004

Clinical and attentional effects of acute nicotine treatment in Tourette's syndrome.

Evidence from pre-clinical infrahuman investigations, open-label clinical trials, and a single controlled trial found acute nicotine treatment potentiated up to 4 weeks neuroleptic-induced reductions of dyskinetic symptoms characterizing Tourette's syndrome (TS). Given the attentional disturbances associated with this syndrome, and the improvements in attentional processes reported with nicotine, this randomized, double-blind, placebo-controlled trial examined the acute (4 h) and sustained (2 weeks) effects of a single dose of transdermal nicotine on clinical (i.e., tics), attentional (continuous performance task, event-related potential, patient and parental reports) and behavioral symptoms in 23 children and adolescents with TS receiving neuroleptic treatment. In the 14 evaluable patients with complete primary efficacy data, nicotine (compared to placebo) failed to alter symptoms at 4 h but counteracted ERP-P300 signs of diminished attention seen 2 weeks following placebo treatment. Secondary efficacy measures, including patient self-reports and parental ratings, found nicotine to reduce complex tics and improve behaviors related to inattention. Additional work with intermittent dosing schedules is required to characterize optimal clinical and cognitive effects with nicotine treatment.

Administration, Cutaneous↗
PubMed2004

The effectiveness of nicotine-patch therapy for smoking cessation in patients with schizophrenia.

The purpose of this study was to determine the effectiveness of nicotine-patch therapy for smoking cessation in patients with schizophrenia. This was a longitudinal study and sixty-eight schizophrenic patients were assigned to 8 weeks of a nicotine-patch therapy program or a control group. The generalized estimating equation analysis revealed that there were significant reductions in the subjects' nicotine dependence (Fagerstrom Tolerance Questionnaire), the number of cigarettes per day, and CO levels over an 8-week period of nicotine-patch therapy and 3-month follow-up. The point-prevalence rates of abstinence from smoking were an abstinence of 26.9% at 8 weeks and 26.9% at a 3-month follow-up. At the 3-month follow-up, the rate of continuous smoking abstinence in the nicotine-patch group was 23.1%.

Administration, Cutaneous↗
PubMed2006

Adolescents' perceptions about quitting and nicotine replacement therapy: findings from the California Tobacco Survey.

We collected data from 5,857 adolescent (12-17 y) respondents in California to assess their perception about quitting smoking and nicotine replacement therapy use. In multivariate models, never smokers were less likely than established or experimenter smokers to believe that if they were to smoke they could quit anytime but were more likely to believe that nicotine replacement therapy is a sure way to quit.

Adolescent↗
PubMed2005

Retinal coding of visual scenes -- repetitive and redundant too?

Visual information reaches the brain by way of a fine cable, the optic nerve. The million or so axons in the optic nerve represent an information bottleneck in the visual pathway-where the fewest number of neurons convey the visual scene. It has long been thought that to make the most of the optic nerve's limited capacity the retina may encode visual information in an optimally efficient manner. In this issue of Neuron, Puchalla et al. report a test of this hypothesis using multielectrode recordings from retinal ganglion cells stimulated with movies of natural scenes. The authors find substantial redundancy in the retinal code and estimate that there is an approximately 10-fold overrepresentation of visual information.

Animals↗