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Cy3-AffiniPure Goat Anti-Guinea Pig IgG (H+L) antibody

RRID:AB_2337423

Antibody ID

AB_2337423

Target Antigen

Guinea Pig IgG (H+L)

Proper Citation

(Jackson ImmunoResearch Labs Cat# 106-165-003, RRID:AB_2337423)

Clonality

polyclonal antibody

Vendor

Jackson ImmunoResearch Labs Go To Vendor

Cat Num

106-165-003

Active Protection: Learning-Activated Raf/MAPK Activity Protects Labile Memory from Rac1-Independent Forgetting.

  • Zhang X
  • Neuron
  • 2018 Apr 4

Literature context:


Abstract:

Active forgetting explains the intrinsic instability of a labile memory lasting for hours. However, how such memory maintains stability against unwanted disruption is not completely understood. Here, we report a learning-activated active protection mechanism that enables labile memory to resist disruptive sensory experiences in Drosophila. Aversive olfactory conditioning activates mitogen-activated protein kinase (MAPK) transiently in the mushroom-body γ lobe, where labile-aversive memory is stored. This increased MAPK activity significantly prolongs labile memory retention and enhances its resistance to disruption induced by heat shock, electric shock, or odor reactivation. Such experience-induced forgetting cannot be prevented by inhibition of Rac1 activity. Instead, protection of Rac1-independent forgetting correlates with non-muscle myosin II activity and persistence of learning-induced presynaptic structural changes. Increased Raf/MAPK activity, together with suppressed Rac1 activity, completely blocks labile memory decay. Thus, learning not only leads to memory formation, but also activates active protection and active forgetting to regulate the formed memory.

Funding information:
  • NCI NIH HHS - R01 CA107349-03(United States)

Serotonin axons in the neocortex of the adult female mouse regrow after traumatic brain injury.

  • Kajstura TJ
  • J. Neurosci. Res.
  • 2017 May 10

Literature context:


Abstract:

It is widely held that injured neurons in the central nervous system do not undergo axonal regrowth. However, there is mounting evidence that serotonin axons are a notable exception. Serotonin axons undergo long-distance regrowth in the neocortex after amphetamine lesion, and, following a penetrating stab injury, they can regrow from cut ends to traverse the stab rift. Traumatic brain injury (TBI) is clinically prevalent and can lead to pathologies, such as depression, that are related to serotonergic dysfunction. Thus, whether serotonin axons can regrow after TBI is an important question. We used two models for TBI-a persistent open skull condition and controlled cortical impact-to evoke injury in adult female mouse neocortex, and assessed serotonin axon density 1 week, 1 month, and 3 months after injury by serotonin transporter immunohistochemistry. We found that after both forms of TBI, serotonin axon density is decreased posterior but not anterior to the injury site when measured in layer 1 at 1 week post surgery, and that serotonin axons are capable of regrowing into the distal zone to increase density by 1 month post surgery. This pattern is consistent with the anterior-to-posterior course of serotonin axons in the neocortex. TBI in these models is associated with significant reactive astrogliosis both anterior and posterior to the impact, but the degree of reactive astrogliosis is not correlated with serotonin axon density when measured 1 week after TBI. Microglial density remains constant following both types of injuries, but microglial condensation was detected 1 week after controlled cortical impact.

Funding information:
  • NINDS NIH HHS - R21 NS081467()

Regrowth of Serotonin Axons in the Adult Mouse Brain Following Injury.

  • Jin Y
  • Neuron
  • 2016 Aug 17

Literature context:


Abstract:

It is widely believed that damaged axons in the adult mammalian brain have little capacity to regrow, thereby impeding functional recovery after injury. Studies using fixed tissue have suggested that serotonin neurons might be a notable exception, but remain inconclusive. We have employed in vivo two-photon microscopy to produce time-lapse images of serotonin axons in the neocortex of the adult mouse. Serotonin axons undergo massive retrograde degeneration following amphetamine treatment and subsequent slow recovery of axonal density, which is dominated by new growth with little contribution from local sprouting. A stab injury that transects serotonin axons running in the neocortex is followed by local regression of cut serotonin axons and followed by regrowth from cut ends into and across the stab rift zone. Regrowing serotonin axons do not follow the pathways left by degenerated axons. The regrown axons release serotonin and their regrowth is correlated with recovery in behavioral tests.

Colocalization of allatotropin and tachykinin-related peptides with classical transmitters in physiologically distinct subtypes of olfactory local interneurons in the cockroach (Periplaneta americana).

  • Fusca D
  • J. Comp. Neurol.
  • 2015 Jul 1

Literature context:


Abstract:

In the insect antennal lobe different types of local interneurons mediate complex excitatory and inhibitory interactions between the glomerular pathways to structure the spatiotemporal representation of odors. Mass spectrometric and immunohistochemical studies have shown that in local interneurons classical neurotransmitters are likely to colocalize with a variety of substances that can potentially act as cotransmitters or neuromodulators. In the antennal lobe of the cockroach Periplaneta americana, gamma-aminobutyric acid (GABA) has been identified as the potential inhibitory transmitter of spiking type I local interneurons, whereas acetylcholine is most likely the excitatory transmitter of nonspiking type IIa1 local interneurons. This study used whole-cell patch clamp recordings combined with single-cell labeling and immunohistochemistry to test if the GABAergic type I local interneurons and the cholinergic type IIa1 local interneurons express allatotropin and tachykinin-related neuropeptides (TKRPs). These are two of the most abundant types of peptides in the insect antennal lobe. GABA-like and choline acetyltransferase (ChAT)-like immunoreactivity were used as markers for GABAergic and cholinergic neurons, respectively. About 50% of the GABA-like immunoreactive (-lir) spiking type I local interneurons were allatotropin-lir, and ∼ 40% of these neurons were TKRP-lir. About 20% of nonspiking ChAT-lir type IIa1 local interneurons were TKRP-lir. Our results suggest that in subpopulations of GABAergic and cholinergic local interneurons, allatotropin and TKRPs might act as cotransmitters or neuromodulators. To unequivocally assign neurotransmitters, cotransmitters, and neuromodulators to identified classes of antennal lobe neurons is an important step to deepen our understanding of information processing in the insect olfactory system.

Funding information:
  • NHLBI NIH HHS - HL107147(United States)
  • NIDDK NIH HHS - R01 DK057038(United States)