The course will explore how we sense, feel, motivate, behave, learn and remember. The processes and neural basis of sensation, cognition, motivation and behaviour, and the ways they may be studied (deconstructed) at systems, cellular and molecular levels will be illustrated by coverage of specific ...
1. Somatosensory system: Focus on pain and pain processing hyperalgesia, analgesia.
Question: Describe different forms of analgesia within the somatosensory system and
discuss the neural mechanisms underlying them. Provide an example for each type of
analgesia.
a) Congenital Analgesia: This form of analgesia, also known as congenital insensitivity to
pain (CIP), is characterized by the inability to perceive physical pain from birth. The neural
mechanism underlying congenital analgesia involves genetic mutations affecting nociceptive
pathways. For example, mutations in the SCN9A gene encoding a sodium channel critical for
nociception can lead to congenital insensitivity to pain. An example of congenital analgesia is
hereditary sensory and autonomic neuropathy (HSAN) type IV, caused by mutations in
SCN9A.
b) Context-Induced Analgesia: Context-induced analgesia refers to a reduction in pain
perception in specific environmental or situational contexts. The neural mechanism involves
activation of descending pain modulatory pathways, particularly the periaqueductal gray
(PAG) and rostral ventromedial medulla (RVM) in the brainstem. These regions release
endogenous opioids that inhibit pain transmission. For instance, during intense physical
activity or sports, the release of endorphins can lead to reduced pain perception promoting
anagelsia. In that situation believed to be more adaptive to ignore the pain and carry on e.g.
finish the marathon race than attending to the pain immediately.
c) Placebo Analgesia: Placebo analgesia is the phenomenon where pain relief occurs after
receiving an inert treatment (placebo) due to the belief that it is effective. The neural
mechanism of placebo analgesia involves brain regions associated with expectation and pain
modulation, such as the prefrontal cortex, anterior cingulate cortex (ACC), and insula.
Activation of these regions can trigger the release of endogenous opioids. For example, in
clinical trials, patients may experience reduced pain after receiving a placebo pill due to
psychological factors influencing pain perception.
2. Olfactory system, neuropeptides, and behavior Question: How can specific odors affect
behavior, and what receptors and circuits are involved? Discuss the influence of
neuropeptides on olfactory processing and behavior.
Effects of Specific Odors on Behavior:
Specific odors can influence behavior through olfactory receptors located in the olfactory
epithelium of the nasal cavity. Each odorant molecule binds to specific olfactory receptors,
initiating signaling cascades that transmit information to the olfactory bulb and then to higher
brain regions involved in processing emotions, memories, and behaviors.
Receptors and Circuits Involved:
Olfactory receptors are G-protein coupled receptors (GPCRs) located on olfactory sensory
neurons. These neurons send axons to the olfactory bulb, where they synapse with mitral and
tufted cells. The olfactory bulb projects to brain regions like the amygdala (emotion),
hippocampus (memory), and orbitofrontal cortex (behavioral responses to odors).
Influence of Neuropeptides:
, Neuropeptides such as oxytocin and vasopressin can modulate olfactory processing and
behavior. For example, oxytocin enhances social bonding and recognition of familiar odors,
while vasopressin influences aggression and territorial behaviors. Neuropeptides act on
receptors in the brain to regulate neural circuits involved in olfactory perception and
behavior.
3. Long-term potentiation Question: How is the strength of a synapse modulated in the
context of long-term potentiation (LTP)? Provide evidence supporting the phenomenon of
LTP.
Long-term potentiation (LTP) is a phenomenon of synaptic plasticity characterized by a long-
lasting increase in synaptic strength following high-frequency stimulation of synapses. The
modulation of synaptic strength during LTP involves several molecular and cellular
mechanisms that contribute to the enhancement of synaptic transmission. Here's a detailed
explanation of how the strength of a synapse is modulated in the context of LTP, along with
evidence supporting this phenomenon:
Mechanisms of Synaptic Modulation in LTP:
1. Glutamate Receptor Activation:
o LTP typically involves the activation of glutamate receptors, particularly the
NMDA (N-methyl-D-aspartate) receptors. These receptors are ionotropic and
require both glutamate binding and postsynaptic depolarization (removal of
the Mg2+ block) to open their ion channels.
o Calcium influx through activated NMDA receptors is a key trigger for the
induction of LTP.
2. Calcium Signalling:
o The rise in intracellular calcium levels due to NMDA receptor activation
activates various signalling pathways involved in LTP. Calcium binds to
calmodulin, leading to the activation of calcium/calmodulin-dependent protein
kinase II (CaMKII) and other downstream effectors.
3. AMPAR Trafficking:
o AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptors
play a crucial role in synaptic transmission. During LTP, there is an increased
insertion of AMPA receptors into the postsynaptic membrane.
o This process is mediated by signalling cascades triggered by calcium influx,
leading to the phosphorylation of AMPA receptors and their recruitment to the
synapse.
4. Synaptic Structural Changes:
o LTP can induce structural changes at the synapse, such as the enlargement of
dendritic spines and the formation of new synaptic connections.
o These changes contribute to the long-lasting enhancement of synaptic strength
by providing a physical basis for increased neurotransmitter release and
responsiveness.
Evidence Supporting LTP:
1. Electrophysiological Recordings:
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