Lecture 2

Central Control and Somatosensory Cortex

Central Control of Somatosensory Information

• Sensory signals undergo extensive modification before reaching higher CNS levels.

• Modification mechanisms:

  • Inhibition via collaterals from other ascending neurons (lateral inhibition).

  • Descending pathways from higher brain centers.

  • Synapses on axon terminals of primary afferent neurons (presynaptic inhibition).

  • Indirectly via interneurons affecting other sensory pathway neurons.

• The cortex inhibits sensory fibers and projection neurons, effectively reducing the impact of stimuli.

• Removing cortical inhibition amplifies the response to sensory input.

• Lateral inhibition is a gating mechanism in the CNS.

• Pain pathways are continuously inhibited to allow modulation of signal transmission.

Central Control of Afferent Information

• Sensory neuron with branches in the skin (e.g., nociceptor).

• Afferent neuron synapses with a projection neuron in the spinal cord, ascending to higher brain centers, including the cortex.

• Descending excitatory neurons from the cortex synapse onto inhibitory interneurons.

• Inhibitory neurons release inhibitory neurotransmitters onto projection neurons or sensory afferent neurons which reduces glutamate release or its effect.

• CNS cells receive thousands of synapses, both excitatory and inhibitory.

• Inhibitory inputs reduce the projection neuron's response to stimuli.

• Gating of sensory stimulation varies based on the situation.

Neural Pathways of the Somatosensory System

• Information from the periphery travels to the somatosensory cortex via projection neurons.

• Different pathways for different types of information:

  • Anterolateral system (spinothalamic tract): pain, hot/cold.

  • Dorsal column system: fine touch, mechanoreception.

Anterolateral System/Spinothalamic Tract

• Painful stimulus activates free neuron endings.

• Action potentials travel via mixed peripheral nerve.

• First synapse: sensory receptor neuron and a second neuron in the dorsal horn of the grey matter of the spinal cord on the same side of the body which was stimulated.

• Second neuron crosses the spinal cord immediately and ascends on the contralateral side.

• Synapses in the thalamus with a cortically projecting neuron.

• Pain information crosses immediately and travels up the contralateral side of the body.

Dorsal Column System

• A tap activates mechanoreceptors.

• Action potentials in mechanoreceptors travel via sensory neuron to the dorsal horn on the same side.

• Sensory neuron ascends to the brainstem on the same side.

• Sensory neuron synapses with a secondary neuron in the brainstem.

• Secondary neuron crosses over at the level of the brainstem.

• Secondary neuron synapses with a projection neuron in the thalamus.

• Touch information travels up the spinal cord on the same side of the body as the stimulation.

• Both pathways end in the somatosensory cortex on the contralateral side of the body.

• One pathway crosses immediately (anterolateral system), the other ascends and crosses at the brainstem (dorsal column system).

The Somatosensory Cortex

• All sensory information goes from the thalamus to the somatosensory cortex.

• Located behind the motor cortex and the central sulcus.

• Somatosensory cortex neurons activate motor cortex neurons, controlling movement.

• Motor cortex neurons descend to motor neurons, activating them.

• The somatosensory cortex is the main region for processing somatic information.

• Each body region maps to a specific area in the somatosensory cortex.

• Representation size is determined by sensory receptor density.

• Fingers, thumb, and face have the largest areas due to dense innervation.

• Lips have densely packed receptors, occupying a large cortical area.

• Neck, trunk, and hips have few receptors, taking up a small region.

• Smaller, more densely packed receptors lead to larger cortical regions due to more projection neurons.

Vision and the Anatomy of the Eye

Vision

• Photoreceptors are depolarized at rest and hyperpolarized when activated.

• Eyes have optical and neural components.

  • Optical: focuses the visual image on receptor cells.

  • Neural: transforms the visual image into graded potentials and action potentials.

Visible Light

• We see light reflected off objects hitting photoreceptors.

Anatomy of the Human Eye

• Sclera: the white part of the eye.

• Extraocular muscle: controls eye movements.

• Cornea: clear part of the sclera at the front; refracts light waves.

  • Light waves bend and converge where photoreceptors are located.

• Pupil: hole allowing light to pass through.

• Iris: regulates pupil size and light entry; gives eye color.

  • Innervated by the autonomic nervous system (parasympathetic constricts, sympathetic dilates).

• Lens: focuses the visual image on the retina with the cornea; changes shape.

• Zonular fibers: attach the lens to ciliary muscles.

• Ciliary muscles: contract/relax to change lens shape.

  • Lens changes shape to focus on objects close to the eye.

• Retina: location of photoreceptors.

• Photoreceptors: rods and cones.

  • Rods: activated in low light, monochromatic.

  • Cones: activated in more light, responsible for color vision.

• Retinal ganglion cells: activated by rods and cones; send information to the brain.

• Optic nerve: axons of retinal ganglion cells, leading to the thalamus and cortex.

• Aqueous humor: gelatinous fluid between the lens and cornea.

• Vitreous humor: gelatinous fluid behind the lens.

The Optics of Vision

The Optics of Vision

• Refraction: change in direction (bending) of light.

  • Light bends when traveling from a less dense to a more dense medium.

  • In the eye, light travels from air to the eyeball.

• The cornea is primarily responsible for refraction; the lens adjusts to focus the image on the retina.

Ciliary Muscles

• Lens: focuses the visual image on the retina.

• Iris: regulates light entering the eyeball.

  • Pupil size is controlled by the iris.

• Zonular fibers connect the lens to the ciliary muscle.

• Ciliary muscle contraction causes the lens to become fatter and shorter, increasing refraction to focus on close objects.

Accommodation

• The process of using ciliary muscles and the lens to focus on near objects.

• The ability to accommodate decreases around 45 years of age due to ciliary muscle breakdown.

"Defects" in Vision

• Presbyopia: loss of lens elasticity, impairing near vision; due to ciliary muscle breakdown; age-related.

• Myopia: nearsightedness.

  • Can focus on close objects but not far away.

  • The eyeball is too long; the image is reconstructed in front of the retina.

  • Corrected with concave lenses or laser surgery to reduce refraction.

• Hyperopia: farsightedness.

  • Can focus on far objects but not up close.

  • The eyeball is too short; the image is reconstructed behind the retina.

  • Corrected with convex lenses or laser surgery to increase refraction.

• Astigmatism: oblong shape of the eyeball.

  • Corrected with glasses or laser surgery.

• Glaucoma: damage to photoreceptors due to increased intraocular pressure.

  • Buildup of aqueous humor pushes on the lens, then the vitreous humor, damaging the retina.

  • Prognosis is poor for maintaining long-term vision.

• Cataracts: clouding of the lens.

  • Age-related.

  • Cell death and debris buildup cause graying of the lens.

  • Treated by replacing the lens with a silicone or fake lens, which cannot accommodate.

The Retina and Phototransduction

Organization of the Retina

• Photoreceptors: rods and cones.

  • Rods: low light vision.

  • Cones: color vision in bright light.

• Connected to interneurons: horizontal, bipolar, and amacrine cells.

  • Interneurons transfer information to retinal ganglion cells.

  • Axons of retinal ganglion cells form the optic nerve.

• Bipolar cells: interneurons that transmit information from photoreceptors to retinal ganglion cells.

Phototransduction

Cones

• Synaptic terminals make contact with bipolar cells.

• Consist of a cell body, inner segment, and outer segment.

• The outer segment contains disks where visual information is processed.

Dark Environment (No Light)

• Guanylyl cyclase converts GTP to cyclic GMP (cGMP).

• Cyclic GMP-gated cation channels are present in the membrane.

• cGMP binds to the cation channel, opening it and allowing sodium and calcium to enter the cell.

• Photoreceptor depolarizes.

• Photoreceptors are relatively depolarized in the dark (-35mV).

Light Present

• The disk of the cones contains a photopigment with a chromophore called retinal.

• Light causes retinal to change conformation from cis to trans, activating cyclic GMP phosphodiesterase.

• Cyclic GMP phosphodiesterase breaks down cGMP into GMP.

• cGMP is removed from the ion channel, and the channel closes.

• Sodium and calcium can no longer enter the cell; thus, the photoreceptor hyperpolarizes.

• Photoreceptor is relatively hyperpolarized (-75mV) when light is present.

Phototransduction: ON and OFF Pathways

• Retinal ganglion cells send information from the retina to the cortex.

• Activation of a single cone activates two bipolar cells and two retinal ganglion cells.

• Photoreceptors constantly provide information via retinal ganglion cells: "yes, light is hitting me" or "no, light is not hitting me."

OFF Pathway: "No, I do Not Have Any Light Hitting Me"

• No light → relative depolarization of the photoreceptor (-35mV).

• Graded potentials are generated, resulting in glutamate release.

• Glutamate activates the OFF bipolar cell and inhibits the ON bipolar cell.

• OFF bipolar cell activation leads to glutamate release onto the OFF retinal ganglion cell → action potential generated in the OFF retinal ganglion cell.

• No action potential is generated in the ON retinal ganglion cell because it's inhibited.

ON Pathway: "Yes, I Have Light Hitting Me"

• Light present → relative hyperpolarization of the photoreceptor.

• cGMP is broken down by cGMP phosphodiesterase.

• Little glutamate is released; the OFF pathway is not activated.

• Reduced glutamate release causes the ON bipolar cell to be released from inhibition.

• ON bipolar cell is activated → glutamate release from the ON bipolar cell activates the ON retinal ganglion cell → action potential generated in the retinal ganglion cell.