Thalamocortical Physiology Flashcards
Describe why the thalamus, which is a deep structure and therefore cannot contribute directly to the EEG, does contribute to the signals recorded in an EEG and recognize that the contribution of thalamus to EEG recording is due to thalamocortical connections.
because the thalamus through thalamic relay neurons connects to the cortex and excites the cortex
what is the frequency of the delta wave?
3 Hz
Are T type Ca2+ channels closed or open at -55mV?, is this an awake state or an asleep state?
closed, awake
What happens when you are asleep? what is the resting membrane potential are T type Ca 2+ channels open or closed?
reticular cells inhibit thalamic relay neurons–>membrane potential is hyperpolarized at -85 mV. ca2+ channels are activated and Ca2+ flows into the neurons -> slow action potential. As Ca2+ flows in, VNa+ channels open—-> Ca2+ spikes with several fast action potentials on top of the Ca2+ spikes from VNa+ channels
Describe how thalamorcortical connections – between the thalamic relay neurons and the pyramidal cortical neurons – are such that the Ca2+ spikes occurring in thalamic relay neurons at the delta frequency give rise to a slow wave in the delta frequency in the EEG
Thalamic relay neurons form excitatory, glu synapses on cortical neurons. Slow Ca2+ spikes in thalamic relay neurons–> to the synaptic terminal–>release of glu–> excites cortical neuron. every time Ca2+ spike fired in relay neuron, AP is propagated to the synapse, glu is released–> AP fired in the cortical neuron. The AP in the cortical neuron is of the same frequency of the relay neuron, generating a slow wave that is detectable by EEG.
what allows thalamic relay neurons to be hyperpolarized?
inhibitory interneurons in the thalamic reticular nuclei
Discuss how slow EEG waves recorded in absence epilepsy (3 Hz) are thought to stem from thalamorcortical oscillatory activity, describe why a mutation in the T type Ca2+ channel could give rise to this type of epilepsy.
Absence epilepsy (sudden staring spells, absence of activity). EEGs look similar to person in slow wave sleep. These patterns occur abnormally in awake patient due to defects in T-type Ca2+ channels on thalamic relay nuclei. Normally, this channel is inactivated by the depolarized (-55 mV) membrane potential while awake. Patients with absence epilepsy, inactivation gate is abnormally open at depolarized resting membrane potentials.= Ca2+ spikes normally of slow phase sleep are fired while awake. predisposition for absence seizures in families with T-type Ca2+ channel mutations.
Recognize that ascending brain-stem circuits sending axons to the thalamus regulate the thalamorcortical circuit.
role ACH, NE, and 5HT neurons
Regulation occurs via cholinergic, noradrenergic and serotonergic neurons
What drugs are used to control epilepsy, by inhibiting T type Ca2+ channels
valproic acid and ethosuximide
role of ACH neurons in thalamorcortical circuit.
-ACH neurons from reticular activating system (neuronal circuits between brainstem and cortex through thalamus): stimulation–> ACh release in thalamus and awakening from sleep and disruption to slow waves in EEG
role of NE neurons in thalamorcortical circuit.
NE neurons from the locus coeruleus (a nucleus in the pons responsible for responses to stress and panic): during “flight or fight” response–> NE release into thalamus
role of 5HT neurons in thalamorcortical circuit.
-5HT neurons from raphe nucleus (5HT-releasing nucleus in brainstem): release serotonin into thalamus and plays a role in sleep/wake cycles
