Postnatal development of cannabinoid receptor type 1 expression in rodent somatosensory cortex

Deshmukh, Suvarna; Onozuka, Kaori; Bender, Kevin J.; Bender, Vanessa A.; Lutz, Beat; Feldman, Daniel E.

doi:10.1016/j.neuroscience.2006.11.033

Cited by 33 publications

(36 citation statements)

References 52 publications

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“…Coincident adolescent development of the cortical eCB system includes reduced CB1R expression (Deshmukh et al, 2007;Heng et al, 2011) and changes in eCB metabolism (Long et al, 2012). The highly dynamic nature of glutamatergic, GABAergic, and eCB system development parallels the maturation of cortical oscillations that are suppressed by cannabinoids, and may underlie the attenuation of cortical oscillations that we observe after adolescent cannabinoid exposure.…”

Section: Discussionmentioning

confidence: 67%

Adolescent Cannabinoid Exposure Permanently Suppresses Cortical Oscillations in Adult Mice

Raver

Haughwout

Keller

2013

Neuropsychopharmacol

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Regular marijuana use during adolescence, but not adulthood, may permanently impair cognition and increase the risk for psychiatric diseases, such as schizophrenia. Cortical oscillations are integral for cognitive processes and are abnormal in patients with schizophrenia. We test the hypothesis that adolescence is a sensitive period because of the active development of cortical oscillations and neuromodulatory systems that underlie them. The endocannabinoid system upon which marijuana acts is one such system. Here we test the prediction that adolescent cannabinoid exposure alters cortical oscillations in adults. Using in vitro local field potential, in vivo electrocorticogram recordings and cognitive behavioral testing in adult mice, we demonstrate that chronic adolescent, but not adult, cannabinoid exposure suppresses pharmacologically evoked cortical oscillations and impairs working memory performance in adults. The later-maturing prefrontal cortex is more sensitive to adolescent exposure than the earlier-maturing, primary somatosensory cortex. These data establish a link between chronic adolescent cannabinoid exposure and alterations in adult cortical network activity that underlie cognitive processes.

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Section: Discussionmentioning

confidence: 67%

Adolescent Cannabinoid Exposure Permanently Suppresses Cortical Oscillations in Adult Mice

Raver

Haughwout

Keller

2013

Neuropsychopharmacol

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“…S1). Low expression was observed in layer 4 of the somatosensory cortex (9), corresponding to the whisker barrels (Fig. 1C).…”

Section: Resultsmentioning

confidence: 97%

Cannabinoid receptor 1-expressing neurons in the nucleus accumbens

Winters

Kruger

Huang

et al. 2012

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

104

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Endocannabinoid signaling critically regulates emotional and motivational states via activation of cannabinoid receptor 1 (CB1) in the brain. The nucleus accumbens (NAc) functions to gate emotional and motivational responses. Although expression of CB1 in the NAc is low, manipulation of CB1 signaling within the NAc triggers robust emotional/motivational alterations related to drug addiction and other psychiatric disorders, and these effects cannot be exclusively attributed to CB1 located at afferents to the NAc. Rather, CB1-expressing neurons in the NAc, although sparse, appear to be critical for emotional and motivational responses. However, the cellular properties of these neurons remain largely unknown. Here, we generated a knock-in mouse line in which CB1-expressing neurons expressed the fluorescent protein tdTomato (tdT). Using these mice, we demonstrated that tdTpositive neurons within the NAc were exclusively fast-spiking interneurons (FSIs). These FSIs were electrically coupled with each other, and thus may help synchronize populations/ensembles of NAc neurons. CB1-expressing FSIs also form GABAergic synapses on adjacent medium spiny neurons (MSNs), providing feed-forward inhibition of NAc output. Furthermore, the membrane excitability of tdT-positive FSIs in the NAc was up-regulated after withdrawal from cocaine exposure, an effect that might increase FSI-to-MSN inhibition. Taken together with our previous findings that the membrane excitability of NAc MSNs is decreased during cocaine withdrawal, the present findings suggest that the basal functional output of the NAc is inhibited during cocaine withdrawal by multiple mechanisms. As such, CB1-expressing FSIs are targeted by cocaine exposure to influence the overall functional output of the NAc.C annabinoid receptor type 1 (CB1) has been extensively implicated in a variety of psychological and psychiatric disorders, including drug addiction (1, 2). Recent studies suggest that CB1 within the nucleus accumbens (NAc), a key component of the brain reward circuit, plays a particularly important role in the development and maintenance of cocaine-induced behavioral alterations (3). Compared with the extensive expression of CB1 in the striatum, the mRNA and protein levels of CB1 within the NAc are sparse, leading to the notion that CB1 at afferent terminals projecting to the NAc are largely responsible for intraNAc, CB1-dependent, cocaine-induced behaviors (4-6). However, a recent study primarily targeting CB1-expressing neurons demonstrates that inhibiting the expression of CB1 within the NAc antagonizes cocaine-induced reward responses (7). This and other results (8) suggest that CB1-expressing neurons in the NAc, although sparse, are critical for cellular and behavioral alterations induced by cocaine and other drugs of abuse.To examine these putative CB1-expressing neurons within the NAc, we generated a knock-in mouse line in which CB1-expressing neurons expressed the fluorescent protein td-Tomato (tdT). Our results show that tdT-positive neurons within the N...

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“…For example, it was reported that the level of mRNA expression of CB 1 R in the rat cerebral cortex measured by in situ hybridization was high at P1 and P5 and became very low in the adult, although the specific CB 1 R binding assessed by radioautography in the adult was higher than that at P1 and P5 (Berrendero et al, 1999). By immunohistochemistry, however, it was reported that CB 1 R immunoreactivity appeared in layer II/III of the rat somatosensory cortex around P6, becoming very intense by P12-P16, and then remained high in the adult (Deshmukh et al, 2007). Thus, the developmental changes in the expression level of CB 1 Rs assessed by different methods in the cerebral cortex seemed not completely consistent with each other, and the disappearance of hetero-LTD in the adult might not be explained solely by the developmental changes in CB 1 Rs in the visual cortex.…”

Section: Developmental Changes In Hetero-ltdmentioning

confidence: 93%

Roles of Endocannabinoids in Heterosynaptic Long-Term Depression of Excitatory Synaptic Transmission in Visual Cortex of Young Mice

Huang¹,

Yasuda²,

Sarihi³

et al. 2008

J. Neurosci.

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Tetanic stimulation of one of two afferent pathways converging to neurons in the visual cortex induces long-term depression (LTD) of synaptic transmission in the other, nonactivated pathway under a certain condition. This form of synaptic plasticity called heterosynaptic LTD (hetero-LTD) was not systematically investigated in previous studies, whereas homosynaptic LTD has been extensively studied. To determine whether hetero-LTD is induced in visual cortical slices of mice and, if so, through what mechanisms, we recorded EPSPs evoked in layer II/III neurons by alternating test stimulation of two sites in layer IV at 0.05 Hz. After theta-burst stimulation of one site, EPSPs evoked by test stimulation of the other site were depressed for a long time in most of the neurons, whereas homosynaptic long-term potentiation was induced at activated synapses. Such a hetero-LTD was induced in most mice at postnatal day 7-20 (P7-P20), but not induced in mice at P35-P41. Tests using the paired-pulse stimulation protocol and coefficient of variation analysis suggested that hetero-LTD was expressed at presynaptic sites. Pharmacological analysis indicated that this form of LTD was induced through activation of the type 5 of metabotropic glutamate receptors, not through the NMDA type of glutamate receptors. Additional analysis using a cannabinoid type 1 receptor agonist and an antagonist suggested that endocannabinoids (eCBs) are involved in this type of LTD. Moreover, results suggest that brain-derived neurotrophic factor, which may be released from strongly activated presynaptic sites, prevents eCBs from suppressing the release of transmitters from these sites.

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Postnatal development of cannabinoid receptor type 1 expression in rodent somatosensory cortex

Cited by 33 publications

References 52 publications

Adolescent Cannabinoid Exposure Permanently Suppresses Cortical Oscillations in Adult Mice

Adolescent Cannabinoid Exposure Permanently Suppresses Cortical Oscillations in Adult Mice

Cannabinoid receptor 1-expressing neurons in the nucleus accumbens

Roles of Endocannabinoids in Heterosynaptic Long-Term Depression of Excitatory Synaptic Transmission in Visual Cortex of Young Mice

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