Mind, Brain & Behavior Monday January 27, 2003

Connections Among Neurons  The growing tip of an axon is called a growth cone.  Lamellipodia – flaps at the edge of the growth cone. Fold in to become the terminal synapse at destination. Filopodia – spikes take hold of the extracellular material and pull the cone forward.

Pathway Formation  Axons stick together due to fasciculation – expression of cell adhesion molecules (CAM).  Chemical markers in the axon and the targets guide axon growth.  Diffusable molecules called netrins also attract axons.  Absence of laminin at target may retard further growth.

Synapse Formation  Proteins are secreted by both the growth cone and the target membrane in a layer – basal lamina.  Interaction between these proteins results in receptor formation. Agrin reception attracts ACh receptors. Ca 2 enters the growth cone and triggers neurotransmitter release.

Naturally Occurring Cell Die Off  Cells compete to innervate targets. Those not used die off.  Cell survival depends on activation at the target.  Neurotrophins travel back from target tissue to neuron cell body promoting survival. Nerve growth factor (NGF) Brain-derived neurotrophic factor (BDNF).

Activity-Dependent Rearrangement  At first cells are in no particular order and send axons everywhere.  Neural activity causes rearrangement of cells and synapses.  Hebb synapses – synapses that are active at the same time as the target is active are strengthened. Things that fire together, wire together.

Plasticity  Critical periods are periods of plasticity.  Plasticity ends when axon growth ends.  Plasticity ends when synaptic transmission matures.  Plasticity diminishes when cortical activation is constrained. Reduction of ACh or NE (norepinephrine)

Aging and the Brain  To study normal aging of the brain, researchers must control for health conditions.  Abnormal aging is affected by: Dementia – usually caused by artherosclerosis (hardening of arteries) Alzheimer’s disease

Mental Changes in Old Age  Cognitive processes slow down Neuronal speed of transmission may be affected by loss of myelin NMDA receptors decrease by 30% (important to learning & memory)  Variability is greater at 60 than at other times of life.  Loss of functioning is relative to someone’s original level of functioning.

Longitudinal Studies  Scores on IQ tests show little decline until age 70.  Declines in motor movements are not dramatic or disabling.  Remaining intellectually active protects against some cognitive decline. Elderly professors do better than same-age controls, even on memory tasks.

Sensory Loss  Age-related changes in hearing and vision can affect performance.  Decline in sensory accuity affects: Amount of information received Rate at which information can be processed

Behavioral Consequences  Most elderly compensate for the gradual changes during aging so that no performance difference occurs.  Other ways can be found to do most tasks.  Elderly may continuously increase in “wisdom,” social and emotional skills, experience-based understanding.

Ion Channels Chapter 7

Ion Channels  Found in all cells throughout the body.  Open and close in response to signals. Selectively permeable to specific ions High rate of flow (conductance)  Resting channels – usually open  Gated channels – open and close Refractory period – temporarily cannot be opened

Control of Gating  Binding of neurotransmitters, hormones, or second messengers from within the cell.  Phosphorylation – energy comes from a phosphate that binds with the channel. Dephosphorylation – removal of the phosphate.  Voltage-gated – responds to a change in the membrane potential.  Stretch or pressure gated – mechanical forces.

Effects of Drugs  Exogenous ligands – drugs that come from outside the body.  Endogenous ligands – naturally occurring  Agonist – binds with and opens a channel. Endogenous or exogenous (e.g., drug)  Antagonist – binds with and closes a channel. Reversible (curare) or irreversible (snake venom)

Importance of Calcium  Voltage-gated calcium (CA 2 ) channels permit CA to enter the cell.  As CA 2 rises, it binds with the neuron, preventing additional calcium from entering.  Increased calcium concentrations can cause dephosphorylation or permanent inactivation of a channel.  Calcium signals neurotransmitter release.