Ch 23 (Development) - Behavioral Neuroscience

Cell death

the biological process by which a cell permanently ceases to carry out its functions. It is essential for maintaining tissue homeostasis, eliminating damaged or infected cells, and enabling embryonic development

trophic factors

specialized signaling molecules (proteins or hormones) that promote cell survival, proliferation, growth, and maturation. In neuroscience (where they are called neurotrophic factors), they act like the power grid of the nervous system, ensuring neurons receive the energy and chemical support required to function and communicate

neurotrophins

a family of small, secreted proteins that act as growth factors to regulate the survival, development, differentiation, and function of neurons in the central and peripheral nervous systems

apoptosis

a highly regulated form of programmed cell death (cellular suicide) used by multicellular organisms to eliminate damaged, old, or unnecessary cells without triggering inflammation

synaptic elimination

or synaptic pruning, is a vital developmental process where the brain removes weak or excess neuronal connections to increase neural network efficiency

synaptic rearrangement

the process where neural connections in the brain are refined by losing some synapses and establishing new ones

activity-dependent synaptic rearrangement

the process by which neural circuits are refined during development and plasticity, where active synapses are strengthened and stabilized while inactive or weak synapses are eliminated

synaptic segregation

a developmental process where neuronal connections (synapses) refine from an overlapping, diffuse state into distinct, non-overlapping territories on a target cell. It involves selective synapse elimination, branch withdrawal, and competition

Hebb synapses (Hebbian modifications)

Hebbian theory, introduced by Donald Hebb in 1949, states that synaptic connections strengthen when a presynaptic neuron repeatedly and persistently triggers a postsynaptic neuron to fire, often summarized as "neurons that fire together, wire together". This form of associative plasticity represents a key mechanism for learning and memory in the brain, creating positive feedback loops that increase synaptic efficacy

Ocular dominance columns

alternating, stripe-like bands of neurons in the primary visual cortex (V1) of mammals, including humans, that respond preferentially to input from either the left or right eye

Synaptic convergence

a neural mechanism where multiple presynaptic neurons send signals to a single postsynaptic neuron. It allows the brain to integrate information from diverse inputs, pool weak signals to enhance sensitivity, and make decisions based on combined information (funnel)

Ocular dominance shift

the brain changing which eye it favors for sensory input, a sign of neuroplasticity often triggered by short-term visual deprivation of one eye

synaptic competition (binocular competition)

an activity-dependent developmental process where neuronal inputs from the two eyes compete for limited resources (e.g., neurotrophins, space) to establish eye-specific connections in the brain's visual pathways

modulatory influences

processes that adjust, enhance, or inhibit neural activity, physiological states, or signals rather than directly causing them. In neuroscience, neuromodulators (like dopamine or serotonin) alter neuronal gain, changing how cells respond to input over seconds, rather than milliseconds. These influences regulate cognitive functions, including attention and emotion

cortical synaptic plasticity

the brain's ability to reorganize, strengthen, or weaken connections (synapses) between neurons in the cortex based on experience, learning, and sensory input. It involves long-term potentiation (LTP) and depression (LTD), as well as structural remodeling (formation/removal of synapses) to adapt to new environments

rules for synaptic modifications

activity-dependent plasticity, primarily driven by

1. Hebbian learning ("cells that fire together, wire together") and

2. Spike-Timing-Dependent Plasticity (STDP), which dictates that the precise timing of pre- and postsynaptic spikes determines whether a synapse strengthens (LTP) or weakens (LTD).

3. Key mechanisms include NMDA receptor activation, Ca\({}^{2+}\) influx, and neuromodulation, creating both long-term and short-term changes that shape neural circuits

NMDA receptor features

NMDA receptors (NMDARs) are crucial ionotropic glutamate receptors in the brain, playing a foundational role in synaptic plasticity, learning, and memory.

long-term potentiation

persistent strengthening of synapses based on recent patterns of activity. It produces a long-lasting increase in signal transmission between two neurons and is widely considered one of the primary cellular mechanisms the brain uses to learn and store memories

neurons that fire together wire together

long-term depression

a persistent, activity-dependent reduction in the efficacy of neuronal synapses, lasting hours or longer. It acts as the opposing process to long-term potentiation (LTP), weakening specific synaptic connections to prevent saturation and allow for new memory formation

neurons that fire out of sync lose their link

critical periods

a specific, limited developmental window during infancy or childhood when the brain is exceptionally receptive to specific environmental stimuli, essential for developing skills like language, vision, or social bonding

HIGH PLASTICITY

monocular deprivation

an experimental technique and clinical condition where visual input is restricted in one eye while the other remains open, often used to study neural plasticity.

. During a critical development period, this triggers long-term structural changes, including shrinkage of neurons related to the deprived eye, but it also causes rapid, reversible, homeostatic shifts in adult brain activity

immature muscles

mess of neuronal connections in muscles

neurons innervating 3 diff muscles

characterized by developing neuromuscular junctions (NMJs) that are not yet fully stabilized or efficient, relying on developmental plasticity to mature. This immature state involves smaller muscle fiber types, lingering embryonic isoforms, and reduced neurotransmitter release, making them highly vulnerable to metabolic demand or degenerative diseases