α4* Nicotinic Acetylcholine Receptors Modulate Experience-Based Cortical Depression in the Adult Mouse Somatosensory Cortex

Brown, Craig E.; Sweetnam, Danielle; Beange, Maddie; Nahirney, Patrick C.; Nashmi, Raad

doi:10.1523/jneurosci.4568-11.2012

Cited by 11 publications

(10 citation statements)

References 66 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In rat, nAChRs are not detectable in FS cells in visual (Xiang et al, 1998) and motor (Porter et al, 1999) cortex, but they are widely expressed in layer I interneurons, which regulate inhibition of interneurons in layers II/III (Christophe et al, 2002). Expression of α4 ∗ nAChRs was also observed in layer IV GABAergic neurons of somatosensory areas, but the specific cell-type distribution is unclear (Brown et al, 2012). In deep layers of medial PFC of mice (Couey et al, 2007) and rats (Gulledge et al, 2007), α4 ∗ nAChR expression is mainly restricted to non-FS cells.…”

Section: Discussionmentioning

confidence: 99%

α4β2 ∗ nicotinic receptors stimulate GABA release onto fast-spiking cells in layer V of mouse prefrontal (Fr2) cortex

et al. 2017

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

α4β2 ∗ nicotinic receptors stimulate GABA release onto fast-spiking cells in layer V of mouse prefrontal (Fr2) cortex

et al. 2017

View full text Add to dashboard Cite

show abstract

“…A similar analysis with different methodological approaches was recently performed on Layer IV of murine SS cortex. This demonstrated a low, but significant, degree of colocalization (7–10%) of α4 nAChR with glutamatergic cortical terminals (Brown et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…Although we did not perform a detailed quantitative analysis of nAChR distribution in SS and Fr2, our qualitative comparison broadly confirms previous results obtained in rodents' SS (Bravo and Karten, ; Hill et al, ; Nakayama et al, ; Schröder, ; Whiteaker et al, ). More recent observations aimed to better discriminate the laminar distribution and function of nAChRs in different neocortical regions of mice (Brown et al, ; Kawai et al, ; Poorthuis et al, ). However, the overall picture is still uncertain, because the anatomical studies focused on SS, whereas the electrophysiological approaches were mainly directed toward the prefrontal regions.…”

Section: Discussionmentioning

confidence: 99%

“…For coherence with literature, we retain the expression “prefrontal cortex,” although its appropriateness in rodents has been questioned, because of the difficulties of making comparisons with the immensely more complex dorsolateral prefrontal cortex in primates (Uylings et al, ). Expression of nAChRs on the soma of different interneuronal populations is established in the prefrontal cortex of rats (Christophe et al, ; Porter et al, ; Xiang et al, ), humans (Alkondon et al, ), and mice (Brown et al, ; Couey et al, ). Evidence of heteromeric nAChR expression in GABAergic terminals is also available, at least in mouse (Aracri et al, ; Klaassen et al, ).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Regulation of glutamate release by heteromeric nicotinic receptors in layer V of the secondary motor region (Fr2) in the dorsomedial shoulder of prefrontal cortex in mouse

Aracri

Amadeo

Pasini

et al. 2013

Synapse

View full text Add to dashboard Cite

We studied how nicotinic acetylcholine receptors (nAChRs) regulate glutamate release in the secondary motor area (Fr2) of the dorsomedial murine prefrontal cortex, in the presence of steady agonist levels. Fr2 mediates response to behavioral situations that require immediate attention and is a candidate for generating seizures in the frontal epilepsies caused by mutant nAChRs. Morphological analysis showed a peculiar chemoarchitecture and laminar distribution of pyramidal cells and interneurons. Tonic application of 5 mM nicotine on Layer V pyramidal neurons strongly increased the frequency of spontaneous glutamatergic excitatory postsynaptic currents. The effect was inhibited by 1 mM dihydro-b-erythroidine (which blocks a4-containing nAChRs) but not by 10 nM methyllicaconitine (which blocks a7-containing receptors). Excitatory postsynaptic currents s were also stimulated by 5-iodo-3-[2(S)-azetidinylmethoxy]pyridine, selective for b2-containing receptors, in a dihydro-b-erythroidine -sensitive way. We next studied the association of a4 with different populations of glutamatergic terminals, by using as markers the vesicular glutamate transporter type (VGLUT) 1 for corticocortical synapses and VGLUT2 for thalamocortical projecting fibers. Immunoblots showed higher expression of a4 in Fr2, as compared with the somatosensory cortex. Immunofluorescence showed intense VGLUT1 staining throughout the cortical layers, whereas VGLUT2 immunoreactivity displayed a more distinct laminar distribution. In Layer V, colocalization of a4 nAChR subunit with both VGLUT1 and VGLUT2 was considerably stronger in Fr2 than in somatosensory cortex. Thus, in Fr2, a4b2 nAChRs are expressed in both intrinsic and extrinsic glutamatergic terminals and give a major contribution to control glutamate release in Layer V, in the presence of tonic agonist levels. Synapse 67:338-357, 2013. V C 2013 Wiley Periodicals, Inc.

show abstract

“…It has been shown that propagation, but not induction, of retinal spreading depression is suppressed by acetylcholine [16]. Increased expression of cholinergic receptors in sensory-deprived cortex mediates inhibition of sensory responses via hyperexcitability of GABAergic inhibitory neurons [17]. This potentially can explain inhibition of CSD in response to high acetylcholine levels.…”

Section: Discussionmentioning

confidence: 99%

Behavior in the open field predicts the number of KCl-induced cortical spreading depressions in rats

Bogdanov

Bogdanova

Koulchitsky

et al. 2013

Behavioural Brain Research

View full text Add to dashboard Cite

Anxiety disorders are known to be comorbid with migraine, and cortical spreading depression (CSD) is the most likely cause of the migraine aura. To search for possible correlations between susceptibility to CSD and anxiety we used the open field test in male Sprague-Dawley rats chronically treated with the preventive anti-migraine drugs valproate or riboflavin. Animals avoiding the central area of the open field chamber and those with less exploratory activity (i.e. rearing) were considered more anxious. After 4 weeks of treatment CSDs were elicited by application of 1 M KCl over the occipital cortex and the number of CSDs occurring over a 2 hour period was compared to the previously assessed open field behaviour. Higher anxiety-like behaviour was significantly correlated with a higher frequency of KCl-induced CSDs. In saline-treated animals, fewer rearings were found in animals with more frequent CSDs (R= −1.00). The duration of ambulatory episodes in the open field center correlated negatively with number of CSDs in the valproate group (R= −0.83; p<0.005) and in riboflavin treated group (R= −0.69; p<0.05) as well as total time spent in the open field center in both groups (R= −0.75; p<0.05 and R= −0.58; p<0.1 respectively). These results suggest that anxiety symptoms are associated with susceptibility to CSD and might explain why it can be an aggravating factor in migraine with aura.

show abstract

α4* Nicotinic Acetylcholine Receptors Modulate Experience-Based Cortical Depression in the Adult Mouse Somatosensory Cortex

Cited by 11 publications

References 66 publications

α4β2 ∗ nicotinic receptors stimulate GABA release onto fast-spiking cells in layer V of mouse prefrontal (Fr2) cortex

α4β2 ∗ nicotinic receptors stimulate GABA release onto fast-spiking cells in layer V of mouse prefrontal (Fr2) cortex

Regulation of glutamate release by heteromeric nicotinic receptors in layer V of the secondary motor region (Fr2) in the dorsomedial shoulder of prefrontal cortex in mouse

Behavior in the open field predicts the number of KCl-induced cortical spreading depressions in rats

Contact Info

Product

Resources

About