Hi there :) I'm currently doing a Bsc of neuroscience, and I just wanted to thank you for posting such relevant and inspiring articles. I've been stuck on which topic to choose for a neurobiology assignment, but thanks to you I'm feeling inspired and ready to get my write on (and spoiled for topical choice) :D So thanks again, lovie!
You’re very welcome. Let me know what topic you end up writing about.
Even though PTSD is triggered by a stressful incident, it is really a disease of memory. The problem isn’t the trauma—it’s that the trauma can’t be forgotten. Most memories, and their associated emotions, fade with time. But PTSD memories remain horribly intense, bleeding into the present and ruining the future. So, in theory, the act of sharing those memories is an act of forgetting them.
In the past decade, scientists have come to realize that our memories are not inert packets of data and they don’t remain constant. Even though every memory feels like an honest representation, that sense of authenticity is the biggest lie of all.
Every memory begins as a changed set of connections among cells in the brain. If you happen to remember this moment—the content of this sentence—it’s because a network of neurons has been altered, woven more tightly together within a vast electrical fabric. This linkage is literal: For a memory to exist, these scattered cells must become more sensitive to the activity of the others, so that if one cell fires, the rest of the circuit lights up as well. Scientists refer to this process as long-term potentiation, and it involves an intricate cascade of gene activations and protein synthesis that makes it easier for these neurons to pass along their electrical excitement. Sometimes this requires the addition of new receptors at the dendritic end of a neuron, or an increase in the release of the chemical neurotransmitters that nerve cells use to communicate. Neurons will actually sprout new ion channels along their length, allowing them to generate more voltage. Collectively this creation of long-term potentiation is called the consolidation phase, when the circuit of cells representing a memory is first linked together. Regardless of the molecular details, it’s clear that even minor memories require major work. The past has to be wired into your hardware.
I just found this online and could not be more proud that I know and am professionally associated to these people. I’ve actually had the pleasure of meeting Dr. Karim Nader (he’s the coolest) at a GRC conference and hearing all he has to say about memory reconsolidation and zeta. And as for Joe Le Doux, well he’s the director for our institute (EBI).
Anyhow, the link above is a strongly encouraged read, as it explains the persistence of PTSD (and traumatic memories) as well as memory mechanisms like reconsolidation. The molecular player in question, PKMzeta, is actually at the centerpiece of one of our current collaborations.
Astrocytes are a special kind of stellate-shaped brain cells that are found throughout the central nervous system and that play a supportive role for neurons. For a long time, astrocytes were thought of as merely providing “assistance” for neuron function and survival. However, the discovery that astrocytes express voltage-gated channels and neurotransmitter receptors suggests the possibility of an active role for astrocytes in neuronal communication. Astrocytes primarily originate come from either radial glia cells or from cells in the sub ventricular zone and can be visualized with glial fibrillary acidic protein (GFAP). Below is an image of GFAP staining for astrocytes.
Other groups of glia:
Oligodendrocytes: Provide myelin sheath in neurons present in the central nervous system (CNS). Each oligodendrocyte can myelinate multiple axons.
Schwann Cells: Myelinate axons of neurons present in the peripheral nervous system (PNS). Schwan cells, however, only myelinate one axon.
Microglia: Derived from bone marrow and function as antigen presenting cells. Microglia have phagocytic activity, which means they “eat up” (or clear) cellular debris and their roles are predominantly host defense.
Regulation of brain extracellular pH via secretion of acid into the extracellular space (aka potassium buffering). Other regulatory functions of astrocytes include limiting the rise of both extracellular potassium (K+) and pH during neural activity. In addition, astrocytes can take up potassium in a variety of ways: Na+-K+ exchange, K+-Cl- cotransport and other K+ channels characterized by distinct properties.
Regulating the uptake of glutamate near the synaptic cleft.
Astrocytes can serve as signaling elements within an astrocyte network, between astrocytes and blood vessels, and/or between astrocytes and neurons. For example, astrocytes can signal to other neurons via Ca+2 oscillations (otherwise known as calcium waves). These calcium waves can come about in two ways: they are either triggered by neural activity (such as activation of astrocyte glutamate receptors) or spontaneoulsy via calcium release from internal stores and activation of IP3 receptors. Astrocytes may also serve as neurotransmitter transporters and receptors as well as aiding in neurotransmitter catabolism.
Modulate synaptic and neural activity via “gliotransmission”. Known gliotransmitters (chemicals that can act on neighboring neurons, glial cells or vessels) include glutamate, cytokines, ATP, and D-serine. As illustrated below, astrocyte processes govern the amount of neurotransmitter spillage around synapse, thus controlling lateral spread of excitation.
Modulation of brain vascular tone (i.e. vasodilation/vasoconstriction) and promotion of neurovascular coupling. Basically, astrocytes regulate cerebral blood flow. Moreover, vascular tone depends on the release of vascular agents into the perivascular space.
Control of synapse formation, stabilization and function as well as neurogenesis. These roles have been predominantly explored in the context of brain pathology and psychiatric disorders like ALS, Alzheimer’s, brain tumors, traumatic brain injury and ischemia.
Chesler, Mitch. Properties of the brain, extracellular space and astrocyte function. Lecture given as part of the cellular neuroscience course. Fall 2009.