Module 1-4 Flashcards
(68 cards)
What activity primes neural circuits before sensory experience, and in which retinal cells does it involve graded potentials?
Subthreshold patterned activity, occurring before sensory experience, primes circuits. This activity involves graded potentials in photoreceptors and bipolar/amacrine cells.
Name the three sequential neural stations that visual signals traverse to reach the cortex, and what alternating columnar arrangement forms from inputs of the two eyes within the cortex’s primary input layer?
Anatomical Pathway:
Retina → LGN → Primary Visual Cortex (V1)
In layer 4 of V1, afferents from both eyes create alternating “ocular dominance columns.”
Which layers of the primary visual cortex are primarily driven by one eye, and which layers integrate inputs from both eyes to exhibit graded binocular responsiveness?
Physiological Correlates:
* Layer 4 neurons: Primarily driven by one eye.
* Layers 2, 3, 5, 6: Integrate inputs from both eyes, exhibiting graded binocular responsiveness.
Ocular Dominance Groups
Ocular Dominance Groups:
o Neurons are classified into seven groups based on their response to either the contralateral or ipsilateral eye.
o Group 1: Responds only to the contralateral eye.
o Group 7: Responds only to the ipsilateral eye.
o Group 4: Responds equally to both eyes.
- Dark Rearing
- Rearing in total darkness without patterned light input delays—but does not prevent—normal development. Upon later light exposure (even after typical critical period), acuity and ocular dominance patterns can recover to near-normal, unlike monocular deprivation.
V1 consequence strabismus
- Loss of Binocularity in Supragranular and Infragranular Layers: In V1 layers 2–3 and 5–6, binocular neurons typically respond to both eyes. In strabismus, most neurons become monocular, responding only to one eye, disrupting binocular convergence.
Ubiquitin Ligase Ube3a:
Target specific proteins that typically helps remove AMPA receptors (AMPA-Rs) from the synapse, allowing these receptors to stay at the synapse.
Neurexins and Neuroligins
Neurexins (presynaptic) & Neuroligins (postsynaptic): These proteins mediate trans-synaptic adhesion, helping to organize the structure of the synaptic cleft and regulate synaptic function.
mTor Pathway:
This protein ensures that new receptors and structural proteins are produced where and when needed for plasticity.
Which signaling cascade is initiated by TrkB activation, and which transcription factor does it help activate in conjunction with CaMK signals?
BDNF released from active afferents binds TrkB, activating Ras → RAF → ERK cascade. Converges with CaMK signals to drive CREB-mediated gene expression, embedding plastic changes in the transcriptional state.
Four Principal Barriers to CNS Regeneration
Four Principal Barriers to CNS Regeneration
1. Neuron Loss: Local injury in brain tissue frequently triggers apoptosis or necrosis of neurons whose axons or cell bodies are damaged.
2. Glial Inhibition: Reactive astrocytes and oligodendrocytes secrete inhibitory molecules (e.g., chondroitin sulfate proteoglycans, myelin‐associated inhibitors) that actively block axon extension (hinder axon growth and repair). Preventing the regeneration of damaged neurons in the central nervous system (CNS).
3. Restricted Neural Stem Cells: Although adult neural stem‐cell niches exist (e.g., subventricular zone, hippocampal dentate gyrus), progenitors in most brain regions remain quiescent, with limited proliferation, migration, or differentiation into functional neurons.
4. Immune‐Mediated Cytokines: Microglia and astrocytes release inflammatory cytokines and reactive oxygen species that further impede regrowth and can exacerbate tissue damage.
Functional Reorganization After Stroke (No True Repair)*
Recovery without regrowth: Brain function improves even without tissue regeneration.
* Latent circuits unmasked: Nearby silent brain circuits activate to take over lost functions.
* Synaptic plasticity: Neuron connections get stronger or weaker to adapt.
* Modest sprouting: Some surviving neurons grow small new branches to help reconnect.
* Opposite hemisphere helps: The undamaged side of the brain supports the affected side
Three Types of Neuronal Repair
- Axonal Regrowth (Best in PNS)
o Surviving neurons regrow severed axons.
o It happens mostly in peripheral nerves.
o Involves reactivation of developmental growth programs. - Sprouting of Surviving Neurons (CNS)
o Damaged central neurons try to reconnect by growing new branches.
o Blocked by glial scars and inflammation, so repair is limited. - Neurogenesis (Rare)
o New neurons are made, mainly in olfactory system.
o Requires stem cells, supportive environment, and proper guidance cues.
- Necessary Criteria for CNS Replacement:
o Presence of Multipotent Stem Cells
o Permissive Microenvironment: Local cues that support proliferation, differentiation, and survival of new neurons.
o Recapitulation of Developmental Processes: Migratory pathways, process outgrowth, synaptogenesis, and long‐distance targeting must be preserved or reestablished.
Recovery of Sensory Function After Nerve Injury
* Protopathic Sensation
(basic touch, pressure)→ Recovers quickly
→ Uses large, simple fibers
→ Fast but imprecise regrowth
* Epicritic Sensation (fine touch, temperature, pain)
→ Recovers slowly
→ Uses small, specialized fibers
→ Needs precise molecular guidance for accurate reconnection
- Epicritic Sensation
(fine touch, temperature, pain) → Recovers slowly
→ Uses small, specialized fibers
→ Needs precise molecular guidance for accurate reconnection
Peripheral Nerve Repair
- Schwann Cells:
o Form “bands of Büngner” to guide regrowing axons
o Secrete growth factors (early: protopathic, later: epicritic)
o Provide a growth-friendly surface - Macrophages:
o Clear damaged myelin (Wallerian degeneration)
o Release signals to support Schwann cells - Wallerian Degeneration:
o Damaged distal axon breaks down
o Basal lamina remains and acts as a scaffold for regeneration
CNS Injury
Glial Cell Responses and Scar Formation
* Astrocytes: Hypertrophy, and proliferation around lesion border.
o Glial Scar: Astrocyte processes interweave, depositing molecules that inhibit axon extension.
Why the Adult CNS Doesn’t Regenerate Well
* No Pro-Growth Signals: CNS neurons don’t activate growth genes like PNS neurons do.
* No Schwann-Like Help: Lacks bands-of-Büngner, ECM support, and growth factors.
* Multiple Barriers:
o Neuron death, excitotoxicity, autophagy issues
o Glial scars block axon growth
o Missing developmental cues
* Result: Axons avoid the injury site and fail to reconnect.
* BBB Breakdown: Injury opens the blood–brain barrier, letting immune cells and proteins into the brain, worsening damage.
Neurogenesis SVZ Subventricular Zone and SGZ (Sugranular zone in hippocampus)
Neural stem cells (NSCs) still exist, but only in specific regions:
* SVZ (Subventricular Zone) → new neurons migrate to the olfactory bulb (important for smell).
* SGZ (Subgranular Zone in the hippocampus) → new neurons become part of the hippocampus, which is important for memory.
Neurogenic Response to Injury: Limited and region-specific; injury can transiently boost proliferation in niche zones, but few new neurons survive or integrate outside these areas.
Newborn neurons (neuroblasts) travel to the olfactory bulb through a pathway called the RMS.
Long-Term Memory Subtypes . Nondeclarative (Implicit)
- Nondeclarative (Implicit)
* Unconscious; “knowing how”
* Types:
o Motor skills (e.g., biking)
o Perceptual skills (e.g., sound discrimination)
o Habits (e.g., conditioning)
* Brain areas: Basal ganglia, cerebellum, sensorimotor cortex
Declarative (Explicit)
- Conscious; “knowing that”
- Types:
o Episodic: Personal events; time-stamped (hippocampus)
o Semantic: Facts and concepts; decontextualized (temporal/frontal cortex)
Amygdala and Fear Learning
Amygdala learns fear by pairing a neutral sound with a shock.
* After learning, the sound alone causes fear (like freezing).
* Tone and shock info go to the lateral amygdala.
* Learning happens because connections get stronger when both signals arrive together.
* Then, the amygdala tells the hypothalamus (for stress) and brainstem (for freezing) what to do.
Universal Role of NMDA-AMPA in LTP
*
Hippocampus: Needed for memory formation.
* Amygdala: Needed for fear learning.
* Cortex & Basal Ganglia: Needed for habits and perception
- Transcortical Pathway
(for new or conscious actions)
* Used when you’re learning, thinking, or following instructions
* Involves prefrontal cortex (planning) and hippocampus (explicit memory)
* Route: Sensory → motor association areas → motor cortex → action
